部分阻断腹主动脉治疗急性脑梗死的实验研究
|
摘要
目的：研究新西兰大白兔脑动脉造影解剖及颅底动脉环（Willis环）的变异。方法：对50只新西兰大白兔行经股动脉途径选择性颈内动脉插管脑血管造影检查。具体方法如下：手术暴露右侧股动脉置入4F导管鞘，经鞘内送入4F单弯导管行主动脉弓造影后选择性进入右侧颈总动脉，经4F单弯导管插入3F微导管至颈内动脉造影。观察脑血管造影解剖及Willis环的常见变异。结果：由于对侧颈内动脉及椎动脉血流冲击，兔颈总动脉造影时颈内动脉及Willis环显影欠佳，只有选择性颈内动脉造影才能充分显示Willis环。50只兔中49只成功行选择性颈内动脉造影，其中2只由于血管痉挛导致右侧颈内动脉插管失败，但成功行对侧颈内动脉插管。选择性颈内动脉数字减影血管造影能清晰显示兔脑血管解剖细节。Willis环变异包括血管发育不良（22.4%），双大脑中动脉（20.4%），后循环不对称者（16.3%），完整对称的Willis环仅占41.9%。此外，枕动脉起源于颈内动脉者占30.1%。结论：经股动脉途径采用同轴导管技术对新西兰大白兔进行选择性颈内动血管造影可行，结果可靠。新西兰大白兔Willis环变异非常常见，熟悉其脑血管造影解剖及Willis环变异，有利于建立更加稳定脑缺血模型。
目的：经股动脉途径行选择性颈内动脉插管注射血栓建立兔大脑中动脉（MCA）栓塞模型，并评价其技术可行性及模型的稳定性。方法：新西兰大白兔30只，不限雌雄，平均兔龄14个月，体重4.1kg。实验组20只，对照组10只。经股动脉途径行选择性颈内动脉插管、脑血管造影（DSA），实验组于颈内动脉内注射1~5枚血栓，对照组不注射血栓仅注射造影剂。以DSA检查明确脑血管闭塞情况，用改良Bederson评分法评价神经功能缺损，CT灌注成像观察脑血流动力学改变，磁共振扩散加权成像（DWI）、TTC染色明确脑梗死情况。结果：实验组20只兔16只（80%）成功栓塞右侧大脑中动脉主干，其中2只眼动脉代偿、3只大脑后动脉软脑膜支代偿使大脑中动脉显影，余大脑中动脉及分支不显影。4只兔右侧颈内动脉远端栓塞，其中3只大脑动脉环良好，大脑中动脉经大脑前动脉代偿显影良好，血流无明显影响。实验组16只兔表现为神经功能缺损，15只手术侧大脑中动脉供血区明显CT灌注异常，14只兔表现为不同程度DWI信号异常及TTC染色异常。对照组影像学及病理学均无异常。两组CT灌注参数差异明显（P 目的：研究Forgarty导管部分阻断腹主动脉对正常兔脑血流灌注的影响。方法：实验兔5只，暴露右侧股动置入4F导管鞘，经鞘置入4F Forgarty取栓导管，于肾动脉近端水平充盈球囊阻断腹主动脉约70%，维持1小时。以CT灌注扫描评估腹主动脉部分阻断前后兔脑血流量的变化。腹主动脉部分阻断前后不同时间点脑血流量（CBF）比较采用方差分析。结果：充盈球囊部分阻断腹主动脉后兔脑血流量明显增加，约29.4%～39.8%，抽瘪球囊解除阻断后脑血流量有下降趋势，但较基线比较仍明显增加，为23.4%。部分阻断腹主动脉前后不同时间点脑血流量差异有统计学意义（P＜0.05）。结论：部分阻断腹主动脉可显著增加兔脑血流灌注。尽管阻断解除后脑血流灌注有下降的趋势，但较高水平的脑血流仍能持续维持至12小时。
目的：研究高位部分腹主动脉阻断对兔血流动力学及生存情况的影响。方法：实验兔5只，暴露右侧股动置入4F导管鞘，经鞘置入4F Forgarty取栓导管，于肾动脉近端水平充盈球囊阻断腹主动脉约70%，维持1小时。观察腹主动脉阻断前后血压、呼吸、中心静脉压的变化，及术后一周动物的生存情况。结果：实验兔腹主动脉部分阻断后BP、CVP均较阻断前有轻度升高；阻断解除后BP、CVP及HR则逐渐恢复至阻断前水平并趋于平稳。各观察指标于腹主动脉阻断前后及解除阻断后差异均无统计学意义。术后１周5只兔子均健康成活，下肢功能、饮食及大小便无异常表现。结论：部分阻断兔腹主动脉1小时安全，对血流动力学影响轻微。
目的：研究部分阻断腹主动脉能否增加脑缺血模型脑血流灌注、降低脑梗死体积。方法：对20只兔经股动脉途径行选择性颈内动脉插管注射血栓建立大脑中动脉栓塞模型。模型成功建立1h后，对实验组模型兔行部分阻断腹主动脉治疗并维持1h，对照组不予任何特殊处理。两组模型兔分别于模型制作成功后30min、3h、6h、12h、24h行CT灌注扫描。24h后处死模型兔行TTC染色。实验组及对照组间同一时间点CBF比较及24h后脑梗死体积比较采用t检验。结果：大脑中动脉栓塞模型成功建立22只，对照组7只，实验组15只。对照组CBF动态变化主要表现为低灌注程度随时间延长逐渐加剧或在较低水平上波动。实验组CBF的动态变化主要表现为三种情况：（1）低灌注在3h呈不同程度恢复，然后轻度下降并维持在相对较高水平；（2）低灌注程度随时间延长逐渐加剧或在较低水平上波动；（3）低灌注在3h呈不同程度恢复，然后下一时间又逐渐降低并随着时间延长进一步加剧。实验组部分腹主动脉阻断前后各时间点CBF与对照组比较差异均有统计学意义（P＜0.05）。实验组平均脑梗死体积（263.2±36.2）mm3，明显小于对照组平均脑梗死体积（299.9±35.3）mm3，两组间差异有统计学意义（t=2.234，P＜0.05）。结论：部分阻断腹主动脉可增加脑缺血区侧支血流灌注，而随着腹主动脉阻断的解除，相对较高水平的脑血流灌注仍能在一定时间内持续维持，进而降低脑梗死体积。部分阻断腹主动脉增加脑缺血区血流灌注可能与兔侧支循环解剖基础密切相关，即此方法仅能增强现有的侧支循环，而无法有效建立新的侧支循环，所以，对那些侧支循环基础差的动物无效。
Objective: To study the cerebral angiographic anatomy and variationsin the circle of Willis(COW) of the new zealand white rabbit. Methods: Subselectivetransfemoral internal carotid digital subtraction angiography was performed in50NewZealand White Rabbits. Specific methods are as follows: The right common femoral arterywas exposed and a4-F angiographic sheath was placed. A4-F angle-tip catheter wasadvanced to the aortic arch, and preliminary arch angiography and carotid artery selectionis performed. Then,3F microcatheter was employed through the4-F catheter to select theICA. Results: Common carotid artery injections provided poor filling of the COWbecause competitive flow from the opposite side and posterior circulation blocked fullCOW filling. Only with subselection of the ICA could the COW be fully displayed.49of50rabbits had subselective angiography with injections in the ICA and magnificationimaging. Two attempts at selecting the ICA on right side were not successful due to spasm,but the opposite side attempt in the same animal succeeded. Selective internal carotiddigital subtraction angiography can provide detailed images of cerebral vessels. TheVariations in the Circle of Willis include hypoplasia in22.4%, duplication of the middlecerebral artery in20.4%, asymmetries of the posterior region in16.3%. The completeclassical symmetric Circle of Willis without significant variation is present in only41.9%of animals. In addition, the occipital artery originated from the internal carotid artery in30.1%of all animals. Conclusion: Selective transfemoral internal carotid angiography ofthe rabbit is reliable. The variations of New Zealand White Rabbits are very common.With recognition of the cerebral angiography anatomy and variations of New ZealandWhite Rabbits, an improved model for embolic stroke could be obtained.
Objective: To establish rabbit model of embolic middle cerebral artery（MCA） occlusion stroke with clots through selective transfemoral internal carotidchatheterization, and evaluate the technique feasibility and stability. Method:30NewZealand White rabbits of either gender, averaging14months old，weighing4.1kg onaverage， were divided into control group(n=10) and experimental group(n=20). Bothgroups received selective transfemoral internal carotid chatheterization and angiography.1-5clots were injected in experimental group and only the contrast media was injected incontrol group. DSA was used to observe the cerebral vascular obstruction, the modifiedBederson scoring was used to observe neurologic impairment, CT perfusion was used toobserve cerebral blood perfusion, and DWI and TTC staining were used to observecerebral infarction. Result: MCA were successfully embolized in16(80%) rabbits inexperimental group, in which MCA received compensation from ophthalmic artery in2rabbits and leptomeningeal collaterals of posterior cerebral artery in3rabbits. ICA wereembolized in4rabbits in experimental group, and because of good COW, the flow ofMCA is normal in3rabbits. There were neurologic deficits in16rabbits, abnomalities ofCT perfusion in15rabbits, and abnomalities of DWI and TTC staining in14rabbits. Noabnormal findings were found for control animals．There was obvious difference of CTPparameters between the two groups（P<0.01）. Conclusion: The established rabbit modelsof embolic middle cerebral arteries occlusion stroke with clots through selectivetransfemoral internal carotid chatheterization is simple, microinvasive and reliable. Tochoose appropriate clots and get familiar with the anatomy and variation of ICA canobviously improve the stability and reproducibility of focal cerebral ischemia model inrabbits..
Objective: To study the effect of partial aortic occlusion on cerebralperfusion in nonstroke rabbit model using the Forgarty catheter. Methods: Five rabbitswere studied. The right common femoral artery was exposed and a4-F angiographic sheathwas placed. A4-F Forgarty catheter was advanced to the abdominal aorta above renalartery, and the balloon was filled to occlude the abdominal aorta about70%. CT perfusionscanning was used to determine cerebral blood flow (CBF) before and after sequentialpartial aortic occlusion. CBF at different time before and after partial aortic occlusion wascompared using analysis of variance. Results: CBF increased significantly(29.4%～39.8%) with inflation of the balloon and remained elevated by23.4%12h after deflation.The difference of CBF before and after partial aortic occlusion was significant(P＜0.05).Conclusions: Partial aortic occlusion can increase cerebral perfusion significantly.Although there was a trend to return to baseline flows, the increased flows weremaintained to12after deflation.
Objective: To investigate the changes of hemodynamics and thesurvival conditions after partial abdominal aortic occlusion and then provide referencematerials for clinical abdominal aorta interruption in rabbits. Methods: Five rabbits werestudied. The right common femoral artery was exposed and a4-F angiographic sheath wasplaced. A4-F Forgarty catheter was advanced to the abdominal aorta above renal artery,and the balloon was filled to occlude the abdominal aorta about70%for one hour. Heartrate(HR)，blood pressure(BP) and central venous pressure(CVP) before and after partialabdominal aortic occlusion were measured, and the survival condition in the followingweek was observed. Results: The results of hemodynamic changes in the group show that BP and CVP increased and HR slowed down slightly after the partial abdominal aorticocclusion. When the occlusion was removed, BP, CVP and HR were gradually restored tothe former level. The difference among the main outcome measures before and after partialabdominal aortic occlusion and after withdrawal was not significant. All rabbits survived,and the posterior limbs function, stool and urine and feed situation was normal in thefollowing week. Conclusions: Partial abdominal aortic occlusion for one hour is safeand has minor effect on hemodynamics.
Objective: To investigate wether partial aortic occlusion can increaseCBF and reduce cerebral infarction volume in a rabbit focal embolic stroke model.Methods: To establish the model of embolic MCA occlusion stroke with clots throughselective transfemoral internal carotid chatheterization in20rabbits. One hour after theembolic rabbit stroke models were established successfully, the models in experimentalgroup received the treatment of partial aortic occlusion for one hour and the models incontrol group did not received any treatment. All the rabbit models underwent CTperfusion imaging(CTPI) at0.5h,3h,6h,12h, and24h respectively after the embolic rabbitstroke models were established successfully. TTC staining were used to observe cerebralinfarction24h after stroke models were established. The CBF at the same point in time andcerebral infarction volume between two groups were compared using t test. Results: Theembolic rabbit stroke models were established successfully in22, which were grouped intoexperimental group(15) and control group(7) randomly. The changes of CBF in controlgroup were mainly characterized by an increasingly and sustained reduction over time. Thechanges of CBF in experimental group were manifested as three kinds of status.(1)Thelower cerebral perfusion recovered to some extent at3h and maintained relatively highlevel.(2) The lower cerebral perfusion reduced increasingly over time.(3) The lowercerebral perfusion recovered to some extent at3h and followed by increasingly andsustained reduction over time. The mean CBF at different points in experimental group were higher than those in control group, and the differences were significant(P＜0.05). Themean cerebral infarction volume in experimental group(263.2±36.2mm3) was less thanthat of control group(299.9±35.3mm3), and the difference was significant(t=2.234, P＜0.05). Conclusions: Partial aortic occlusion can increase cerebral collateral circulationperfusion significantly in the rabbit stroke models and the increased flows were maintainedfor some time, which resulted in the reduction of cerebral infarction volume. The increasedcerebral perfusion by partial aortic occlusion might be closely related to the existence ofcollateral circulation. In other words, partial aortic occlusion could not increase cerebralperfusion for the stroke model without collateral circulation..
目的：经股动脉途径行选择性颈内动脉插管注射血栓建立兔大脑中动脉（MCA）栓塞模型，并评价其技术可行性及模型的稳定性。方法：新西兰大白兔30只，不限雌雄，平均兔龄14个月，体重4.1kg。实验组20只，对照组10只。经股动脉途径行选择性颈内动脉插管、脑血管造影（DSA），实验组于颈内动脉内注射1~5枚血栓，对照组不注射血栓仅注射造影剂。以DSA检查明确脑血管闭塞情况，用改良Bederson评分法评价神经功能缺损，CT灌注成像观察脑血流动力学改变，磁共振扩散加权成像（DWI）、TTC染色明确脑梗死情况。结果：实验组20只兔16只（80%）成功栓塞右侧大脑中动脉主干，其中2只眼动脉代偿、3只大脑后动脉软脑膜支代偿使大脑中动脉显影，余大脑中动脉及分支不显影。4只兔右侧颈内动脉远端栓塞，其中3只大脑动脉环良好，大脑中动脉经大脑前动脉代偿显影良好，血流无明显影响。实验组16只兔表现为神经功能缺损，15只手术侧大脑中动脉供血区明显CT灌注异常，14只兔表现为不同程度DWI信号异常及TTC染色异常。对照组影像学及病理学均无异常。两组CT灌注参数差异明显（P
目的：研究高位部分腹主动脉阻断对兔血流动力学及生存情况的影响。方法：实验兔5只，暴露右侧股动置入4F导管鞘，经鞘置入4F Forgarty取栓导管，于肾动脉近端水平充盈球囊阻断腹主动脉约70%，维持1小时。观察腹主动脉阻断前后血压、呼吸、中心静脉压的变化，及术后一周动物的生存情况。结果：实验兔腹主动脉部分阻断后BP、CVP均较阻断前有轻度升高；阻断解除后BP、CVP及HR则逐渐恢复至阻断前水平并趋于平稳。各观察指标于腹主动脉阻断前后及解除阻断后差异均无统计学意义。术后１周5只兔子均健康成活，下肢功能、饮食及大小便无异常表现。结论：部分阻断兔腹主动脉1小时安全，对血流动力学影响轻微。
目的：研究部分阻断腹主动脉能否增加脑缺血模型脑血流灌注、降低脑梗死体积。方法：对20只兔经股动脉途径行选择性颈内动脉插管注射血栓建立大脑中动脉栓塞模型。模型成功建立1h后，对实验组模型兔行部分阻断腹主动脉治疗并维持1h，对照组不予任何特殊处理。两组模型兔分别于模型制作成功后30min、3h、6h、12h、24h行CT灌注扫描。24h后处死模型兔行TTC染色。实验组及对照组间同一时间点CBF比较及24h后脑梗死体积比较采用t检验。结果：大脑中动脉栓塞模型成功建立22只，对照组7只，实验组15只。对照组CBF动态变化主要表现为低灌注程度随时间延长逐渐加剧或在较低水平上波动。实验组CBF的动态变化主要表现为三种情况：（1）低灌注在3h呈不同程度恢复，然后轻度下降并维持在相对较高水平；（2）低灌注程度随时间延长逐渐加剧或在较低水平上波动；（3）低灌注在3h呈不同程度恢复，然后下一时间又逐渐降低并随着时间延长进一步加剧。实验组部分腹主动脉阻断前后各时间点CBF与对照组比较差异均有统计学意义（P＜0.05）。实验组平均脑梗死体积（263.2±36.2）mm3，明显小于对照组平均脑梗死体积（299.9±35.3）mm3，两组间差异有统计学意义（t=2.234，P＜0.05）。结论：部分阻断腹主动脉可增加脑缺血区侧支血流灌注，而随着腹主动脉阻断的解除，相对较高水平的脑血流灌注仍能在一定时间内持续维持，进而降低脑梗死体积。部分阻断腹主动脉增加脑缺血区血流灌注可能与兔侧支循环解剖基础密切相关，即此方法仅能增强现有的侧支循环，而无法有效建立新的侧支循环，所以，对那些侧支循环基础差的动物无效。
Objective: To study the cerebral angiographic anatomy and variationsin the circle of Willis(COW) of the new zealand white rabbit. Methods: Subselectivetransfemoral internal carotid digital subtraction angiography was performed in50NewZealand White Rabbits. Specific methods are as follows: The right common femoral arterywas exposed and a4-F angiographic sheath was placed. A4-F angle-tip catheter wasadvanced to the aortic arch, and preliminary arch angiography and carotid artery selectionis performed. Then,3F microcatheter was employed through the4-F catheter to select theICA. Results: Common carotid artery injections provided poor filling of the COWbecause competitive flow from the opposite side and posterior circulation blocked fullCOW filling. Only with subselection of the ICA could the COW be fully displayed.49of50rabbits had subselective angiography with injections in the ICA and magnificationimaging. Two attempts at selecting the ICA on right side were not successful due to spasm,but the opposite side attempt in the same animal succeeded. Selective internal carotiddigital subtraction angiography can provide detailed images of cerebral vessels. TheVariations in the Circle of Willis include hypoplasia in22.4%, duplication of the middlecerebral artery in20.4%, asymmetries of the posterior region in16.3%. The completeclassical symmetric Circle of Willis without significant variation is present in only41.9%of animals. In addition, the occipital artery originated from the internal carotid artery in30.1%of all animals. Conclusion: Selective transfemoral internal carotid angiography ofthe rabbit is reliable. The variations of New Zealand White Rabbits are very common.With recognition of the cerebral angiography anatomy and variations of New ZealandWhite Rabbits, an improved model for embolic stroke could be obtained.
Objective: To establish rabbit model of embolic middle cerebral artery（MCA） occlusion stroke with clots through selective transfemoral internal carotidchatheterization, and evaluate the technique feasibility and stability. Method:30NewZealand White rabbits of either gender, averaging14months old，weighing4.1kg onaverage， were divided into control group(n=10) and experimental group(n=20). Bothgroups received selective transfemoral internal carotid chatheterization and angiography.1-5clots were injected in experimental group and only the contrast media was injected incontrol group. DSA was used to observe the cerebral vascular obstruction, the modifiedBederson scoring was used to observe neurologic impairment, CT perfusion was used toobserve cerebral blood perfusion, and DWI and TTC staining were used to observecerebral infarction. Result: MCA were successfully embolized in16(80%) rabbits inexperimental group, in which MCA received compensation from ophthalmic artery in2rabbits and leptomeningeal collaterals of posterior cerebral artery in3rabbits. ICA wereembolized in4rabbits in experimental group, and because of good COW, the flow ofMCA is normal in3rabbits. There were neurologic deficits in16rabbits, abnomalities ofCT perfusion in15rabbits, and abnomalities of DWI and TTC staining in14rabbits. Noabnormal findings were found for control animals．There was obvious difference of CTPparameters between the two groups（P<0.01）. Conclusion: The established rabbit modelsof embolic middle cerebral arteries occlusion stroke with clots through selectivetransfemoral internal carotid chatheterization is simple, microinvasive and reliable. Tochoose appropriate clots and get familiar with the anatomy and variation of ICA canobviously improve the stability and reproducibility of focal cerebral ischemia model inrabbits..
Objective: To study the effect of partial aortic occlusion on cerebralperfusion in nonstroke rabbit model using the Forgarty catheter. Methods: Five rabbitswere studied. The right common femoral artery was exposed and a4-F angiographic sheathwas placed. A4-F Forgarty catheter was advanced to the abdominal aorta above renalartery, and the balloon was filled to occlude the abdominal aorta about70%. CT perfusionscanning was used to determine cerebral blood flow (CBF) before and after sequentialpartial aortic occlusion. CBF at different time before and after partial aortic occlusion wascompared using analysis of variance. Results: CBF increased significantly(29.4%～39.8%) with inflation of the balloon and remained elevated by23.4%12h after deflation.The difference of CBF before and after partial aortic occlusion was significant(P＜0.05).Conclusions: Partial aortic occlusion can increase cerebral perfusion significantly.Although there was a trend to return to baseline flows, the increased flows weremaintained to12after deflation.
Objective: To investigate the changes of hemodynamics and thesurvival conditions after partial abdominal aortic occlusion and then provide referencematerials for clinical abdominal aorta interruption in rabbits. Methods: Five rabbits werestudied. The right common femoral artery was exposed and a4-F angiographic sheath wasplaced. A4-F Forgarty catheter was advanced to the abdominal aorta above renal artery,and the balloon was filled to occlude the abdominal aorta about70%for one hour. Heartrate(HR)，blood pressure(BP) and central venous pressure(CVP) before and after partialabdominal aortic occlusion were measured, and the survival condition in the followingweek was observed. Results: The results of hemodynamic changes in the group show that BP and CVP increased and HR slowed down slightly after the partial abdominal aorticocclusion. When the occlusion was removed, BP, CVP and HR were gradually restored tothe former level. The difference among the main outcome measures before and after partialabdominal aortic occlusion and after withdrawal was not significant. All rabbits survived,and the posterior limbs function, stool and urine and feed situation was normal in thefollowing week. Conclusions: Partial abdominal aortic occlusion for one hour is safeand has minor effect on hemodynamics.
Objective: To investigate wether partial aortic occlusion can increaseCBF and reduce cerebral infarction volume in a rabbit focal embolic stroke model.Methods: To establish the model of embolic MCA occlusion stroke with clots throughselective transfemoral internal carotid chatheterization in20rabbits. One hour after theembolic rabbit stroke models were established successfully, the models in experimentalgroup received the treatment of partial aortic occlusion for one hour and the models incontrol group did not received any treatment. All the rabbit models underwent CTperfusion imaging(CTPI) at0.5h,3h,6h,12h, and24h respectively after the embolic rabbitstroke models were established successfully. TTC staining were used to observe cerebralinfarction24h after stroke models were established. The CBF at the same point in time andcerebral infarction volume between two groups were compared using t test. Results: Theembolic rabbit stroke models were established successfully in22, which were grouped intoexperimental group(15) and control group(7) randomly. The changes of CBF in controlgroup were mainly characterized by an increasingly and sustained reduction over time. Thechanges of CBF in experimental group were manifested as three kinds of status.(1)Thelower cerebral perfusion recovered to some extent at3h and maintained relatively highlevel.(2) The lower cerebral perfusion reduced increasingly over time.(3) The lowercerebral perfusion recovered to some extent at3h and followed by increasingly andsustained reduction over time. The mean CBF at different points in experimental group were higher than those in control group, and the differences were significant(P＜0.05). Themean cerebral infarction volume in experimental group(263.2±36.2mm3) was less thanthat of control group(299.9±35.3mm3), and the difference was significant(t=2.234, P＜0.05). Conclusions: Partial aortic occlusion can increase cerebral collateral circulationperfusion significantly in the rabbit stroke models and the increased flows were maintainedfor some time, which resulted in the reduction of cerebral infarction volume. The increasedcerebral perfusion by partial aortic occlusion might be closely related to the existence ofcollateral circulation. In other words, partial aortic occlusion could not increase cerebralperfusion for the stroke model without collateral circulation..
引文
[1] Schellinger PD, Fiebach JB, Mohr A,et al.Thrombolytic therapy for ischemic stroke-a review.Part I: intravenous thrombolysis.Crit Care Med,2001,29:1812-1818.
[2] Mitka M. Rapid stroke treatment an elusive goal. JAMA,2008,299:1653-1654.
[3] Wang Y, Liao X, Zhao X, et a1. Using recombinant tissue plasminogen activator lotreal acute ischemic stroke in China：analysis of the results from the chinese nationalstroke registry(CNSR). Stroke,2011,42:1658-1664.
[4] Hacke W, Kaste M, Bluhmki E, et a1. Thmmbolysis with alteplase3to4.5hours afteracute ischemic stroke. N Engl J Med,2008,359:1317-1329.
[5] Furlan A, Higashida R, Wechsler L, et al. Intra-arterial prourokinase for acuteischemic stroke, the PROACT II study: a randomized controlled trial-Prolyse in AcuteCerebral Thromboembolism. JAMA,1999,282:2003-2011.
[6] Del Zoppo GJ, Higashida RT, Furlan AJ, et al. PROACT: a phase II randomized trialof recombinant pro-urokinase by direct arterial delivery in acute middlecerebral.artery stroke. Stroke,1998,29:4-11.
[7] Nogueira RG, Schwamm LH, Hirsch JA. Endovascular approaches to acute stroke,part1: Drugs, devices, and data. AJNR Am J Neuroradiol,2009,30:649-661.
[8] Nogueira RG, Yoo AJ, Buonanno FS, et al. Endovascular approaches to acute stroke,part2: a comprehensive review of studies and trials. AJNR Am J Neuroradiol,2009,30:859-875.
[9] Arnold M, Schroth G, Nedeltchev K, et al. Intra-arterial thrombolysis in100patientswith acute stroke due to middle cerebral artery occlusion. Stroke,2002,33:1828-1833.
[10] Eckert B, Kucinski T, Pfeiffer G, et al. Endovascular therapy of acute vertebrobasilarocclusion: early treatment onset as the most important factor. Cerebrovasc Dis,2002,14:42-50.
[11] IMS Study Investigators. Combined intravenous and intra-arterial recanalization foracute ischemic stroke: the Interventional Management of Stroke Study. Stroke,2004,35:904-911.
[12] Jauch EC, Saver JL, Adams HP Jr, et al. Guidelines for the early management ofpatients with acute ischemic stroke: a guideline for healthcare professionals from theAmerican Heart Association/American Stroke Association. Stroke,2013,44:870-947.
[13] Sorimachi T, Fujii Y, Tsuchiya N, et al. Recanalization by mechanical embolusdisruption during intra-arterial thrombolysis in the carotid territory. Am J Neuroradiol,2004,25:1391-1402.
[14] Kim DJ, Kim DI, Byun JS, et al. Simple microwire and microcatheter mechanicalthrombolysis with adjuvant intraarterial urokinase for treatment of hyperacuteischemic stroke patients. Acta Radiol,2008,49:351-357.
[15] Yoon W, Park MS, Cho KH. Low-dose intra-arterial urokinase and aggressivemechanical clot disruption for acute ischemic stroke after failure of intravenousthrombolysis. AJNR Am J Neuroradiol,2010,31:161-164.
[16] Qureshi AI, Siddiqui AM, Suri MF, et al. Aggressive mechanical clot disruption andlow-dose intra-arterial third-generation thrombolytic agent for ischemic stroke: aprospective study. Neurosurgery,2002,51:1319-1327.
[17] Ikushima I, Ohta H, Hirai T, et al. Balloon catheter disruption of middle cerebralartery thrombus in conjunction with thrombolysis for the treatment of acute middlecerebral artery embolism. AJNR Am J Neuroradiol,2007,28:513-517.
[18] Nogueira RG, Schwamm LH, Buonanno FS, et al. Low-pressure balloon angioplastywith adjuvant pharmacological therapy in patients with acute ischemic stroke causedby intracranial arterial occlusions. Neuroradiology,2008,50:331-340.
[19]刘振生,王苇,张新江,等.球囊碎栓辅助动脉溶栓治疗急性大脑中动脉闭塞.介入放射学杂志,2009,18:84-86.
[20] Hitchcock KE，Holland CK. Ultrasound-assisted thrombolysis for stroke therapy:better thrombus break-up with bubbles. Stroke,2010,41(10Suppl):50-53.
[21] Tomsick T, Broderick J, Carrozella J, et a1. Revascularization results in theInterventional Management of Stroke II trial. AJNR Am J Neuroradiol,2008,29:582-587.
[22] Smith WS, Sung G, Sawer J, et a1. Mechanical thrombectomy for acute ischemicstroke：final results of the Multi MERCI trial.Stroke,2008,39:1205-1212.
[23] Nogueira RG, Smith WS; MERCI and Multi MERCI Writing Committee. Safety andefficacy of endovascular thrombectomy in patients with abnormal hemostasis: pooledanalysis of the MERCI and multi MERCI trials. Stroke,2009,40:516-522.
[24] Alshekhlee A, Pandya DJ, English J, et al. Merci mechanical thrombectomy retrieverfor acute ischemic stroke therapy: literature review. Neurology,2012,25:79(13Suppl1):S126-34.
[25] Almekhlafi MA, Menon BK, Freiheit EA, et al. A meta-analysis of observationalintra-arterial stroke therapy studies using the Merci device, Penumbra system, andretrievable stents. AJNR Am J Neuroradiol,2013,34:140-145.
[26] Tenser MS, Amar AP, Mack WJ. Mechanical thrombectomy for acute ischemic strokeusing the MERCI retriever and penumbra aspiration systems. World Neurosurg,2011,76(6Suppl):S16-23.
[27] Fields JD, Lutsep HL, Smith WS; MERCI Multi MERCI Investigators. Higherdegrees of recanalization after mechanical thrombectomy for acute stroke areassociated with improved outcome and decreased mortality: pooled analysis of theMERCI and Multi MERCI trials. AJNR Am J Neuroradiol,2011,32:2170-2174.
[28] Nogueira RG, Smith WS, Sung G, et al. Effect of time to reperfusion on clinicaloutcome of anterior circulation strokes treated with thrombectomy: pooled analysis ofthe MERCI and Multi MERCI trials. Stroke,2011,42:3144-3149.
[29] Nogueira RG, Liebeskind DS, Sung G, et al. Predictors of good clinical outcomes,mortality, and successful revascularization in patients with acute ischemic strokeundergoing thrombectomy: pooled analysis of the Mechanical Embolus Removal inCerebral Ischemia (MERCI) and Multi MERCI Trials. Stroke,2009,40:3777-3783.
[30] Josephson SA, Saver JL, Smith WS; Merci and Multi Merci Investigators.Comparisonof mechanical embolectomy and intraarterial thrombolysis in acute ischemic strokewithin the MCA: MERCI and Multi MERCI compared to PROACT II. NeurocritCare,2009,10:43-49.
[31] Gobin YP, Starkman S, Duckwiler GR, et al. MERCI1: a phase1study ofmechanical embolus removal in cerebral ischemia.Stroke,2004,35:2848-2854.
[32] Shi ZS, Loh Y, Walker G, et al. Clinical outcomes in middle cerebral artery trunkocclusions versus secondary division occlusions after mechanical thrombectomy:pooled analysis of the Mechanical Embolus Removal in Cerebral Ischemia (MERCI)and Multi MERCI trials. Stroke,2010,41:953-960.
[33] Flint AC, Duckwiler GR, Budzik RF, et al. Mechanical thrombectomy of intracranialinternal carotid occlusion: pooled results of the MERCI and Multi MERCI Part I trials.Stroke,2007,38:1274-1280.
[34] Penumbra Pivotal Stroke Trial Investigators Investigators. The penumbra pivotalstroke trial：safety and effectiveness of a new generation of mechanical devices forclot removal in intracranial large vessel occlusive disease. Stroke,2009,40:2761-2768.
[35] Hussain SI, Zaidat OO, Fitzsimmons BF. The Penumbra system for mechanicalthrombectomy in endovascular acute ischemic stroke therapy. Neurology,2012,25,S135-41.
[36] Tarr R, Hsu D, Kulcsar Z, et al. The POST trial: initial post-market experience of thePenumbra system: revascularization of large vessel occlusion in acute ischemic strokein the United States and Europe. J Neurointerv Surg,2010,2:341-344.
[37] Kelly ME, Furlan AJ, Fiorella D. Recanalization of an acute middle cerebral arteryocclusion using a self-expanding, reconstrainable, intracranial microstent as atemporary endovascular bypass. Stroke,2008,39:1770-1773.
[38] Machi P, Costalat V, Lobotesis K, et a1. Solitaire FR thrembectomy system:immediate resuhs in56consecutive acute ischemic stroke patients. J Neurointerv Surg,2012,4:62-66.
[39] Almekhtafi MA, Menon BK, Freiheit EA, et a1. A meta-analysis of observationalintra-arterial stroke therapy studies using the MERCI device，Penumbra system，andretrievable stents. Am J Neuroradiol,2013,34:140-145.
[40] Mokin M, Kass-Hout T, Levy EI. Solitaire FR-a promising new device for acuteischemie stroke treatment. World Neumsurg,2012,78:557-558.
[41] Nogueira RG, Latsep HL, Gupta R, et a1. TREVO versus MERCI retrievers forthrombectomy revascularisation of large vessel occlusions in acute ischaemic stroke(TREVO2)：a randomised trial. Lancet,2012,380:1231-1240.
[42] Nogueira RG, Levy EI, Gounis M, et a1. The Trevo device：preclinical data of a novelstroke thrombectomy device in two different animal models of arterialthrombo-occlusive disease. J Neurointerv Surg,2011,4:295-300.
[43] Jaharl R. Solitaire flow-restoration device for treatment of acute ischemic stroke：safety and recanalization efficacy studv in a swine vessel oclusinn model. AJNR,2010,31:1938-1943.
[44] Kim TK, Rhim JK, Lee CJ, et a1. The limitations of thmmbectomy with solitaire ABas first-line treatment in acute ischemic stroke: a single center experience. JCerebrovasc Endovasc Neurosurg,2012,14:203-209．
[45] Liebeskind DS. Collateral therapeutics for cerebral ischemia. Expert Rev Neurother,2004,4:255-265.
[46]刘振生，王苇，李澄，等.急性脑梗死FLAIR序列血管高信号形成机制探讨.临床放射学杂志，2011,30::618-620.
[47] Liebeskind DS. Aortic occlusion for cerebral ischemia: from theory to practice. CurrCardiol Rep,2008,10:31-36.
[48] Stokland O, Miller MM, Ilebekk A, et al. Mechanism of hemodynamic responses toocclusion of the descending thoracic aorta. Am J Physiol,1980,238:H423-H429.
[49] Saether OD, Juul R, Aadahl P, et al. Cerebral haemodynamics during thoracic-andthoracoabdominal aortic aneurysm repair. Eur J Vasc Endovasc Surg,1996,12:81-85.
[50] Hammer M, Jovin T, Wahr JA, et al. Partial occlusion of the descending aortaincreases cerebral blood flow in a nonstroke porcine model. Cerebrovasc Dis,2009,28:406-410.
[51] Noor R, Wang CX, Todd K, et al. Partial Intra-Aortic Occlusion Improves PerfusionDeficits and Infarct Size Following Focal Cerebral Ischemia. J Neuroimaging,2010,20:272-276.
[52] Hussain MS, Bhagat YA, Liu S, et al. DWI Lesion Volume Reduction FollowingAcute Stroke Treatment with Transient Partial Aortic Obstruction. J Neuroimaging,2010,20:379-381.
[53] Shuaib A, Bornstein NM, Diener HC, et al. Partial aortic occlusion for cerebralperfusion augmentation: safety and efficacy of NeuroFlo in Acute Ischemic Stroketrial. Stroke,2011,42:1680-90.
[54] Lutsep HL, Altafullah IM, Roberts R, et al. Neurologic safety event rates in theSENTIS trial control population. Acta Neurol Scand,2013,127:e5-7.
[55] Leker RR, Molina C, Cockroft K, et al. Effects of age on outcome in the SENTIS trial:better outcomes in elderly patients. Cerebrovasc Dis,2012,34:263-271.
[56] Shuaib A, Schwab S, Rutledge JN, et al. Importance of proper patient selection andendpoint selection in evaluation of new therapies in acute stroke: further analysis ofthe SENTIS trial. J Neurointerv Surg,2013,5Suppl1:121-124.
[57] Hammer MD, Schwamm L, Starkman S, et al. Safety and feasibility of NeuroFlo usein eight-to24-hour ischemic stroke patients. Int J Stroke,2012,7:655-661.
[58] Saqqur M, Ibrahim M, Butcher K, et al. Transcranial Doppler and CerebralAugmentation in Acute Ischemic Stroke. J Neuroimaging,2013,23:460-465.
[59] Emery DJ, Schellinger PD, Selchen D, et al. Safety and feasibility of collateral bloodflow augmentation after intravenous thrombolysis. Stroke,2011,42:1135-1137.
[60] Schellinger PD, Shuaib A, K hrmann M, et al. Reduced Mortality and SevereDisability Rates in the SENTIS Trial. AJNR Am J Neuroradiol,2013,34:2312-2316.
[61] Schellinger PD, K hrmann M, Liu S, et al. Favorable vascular profile is anindependent predictor of outcome: a post hoc analysis of the safety and efficacy ofNeuroFlo Technology in Ischemic Stroke trial. Stroke,2013,44:1606-1608.
[62]李凌鑫,樊小农,石学敏.大脑中动脉阻塞法建立局灶性脑缺血模型的研究进展.中华神经科杂志,2009,42:208-210.
[63]全冠民,袁涛,刘怀军,等.自体血栓栓塞性兔大脑中动脉脑梗死影像学模型的建立.临床放射学杂志,2008,27:1266-1269.
[64] Murphy BD, Chen X, Lee TY. Serial changes in CT cerebral blood volume and flowafter4hours of middle cerebral occlusion in an animal model of embolic cerebralischemia. AJNR,2007,28:743-749.
[65] Benes V, Zabramski JM, Boston M, et al. Effect of intra-arterial tissue plasminogenactivator and urokinase on autologous arterial emboli in the cerebral circulation ofrabbits. Stroke,1990,21:1594-1599.
[66] Brown AT, Skinner RD, Flores R, et al. Stroke location and brain function in anembolic rabbit stroke model. J Vasc Interv Radiol,2010,21:903-909.
[67] Culp BC, Brown AT, Erdem E, et al. Selective intracranial magnification angiographyof the rabbit: Basic techniques and anatomy. JVIR,2007,18:187-192.
[68]冯雷,潘力,冯光,等.介入技术制作兔大脑中动脉闭塞模型的研究.重庆医学,2011,40:535-538.
[69]李世德,杨丹,王永亮,等.兔低位腹主动脉阻断后血流动力学的变化.广西医科大学学报2012,29:17-18.
[70]武钢,王赞智,张弛,等.体外腹主动脉末端阻断动物犬模型的建立及意义.创伤外科杂志,2011,13:159-162.
[71]张永飞.腹主动脉阻断术的临床应用研究.中华创伤杂志,2002,18:464-466.
[1] Culp BC, Brown AT, Erdem E, Lowery J, Culp WC. Selective intracranialmagnification angiography of the rabbit: Basic techniques and anatomy. JVIR,2007,18:187-192.
[2] Murphy BD, Chen X, Lee TY. Serial changes in CT cerebral blood volume and flowafter4hours of middle cerebral occlusion in an animal model of embolic cerebralischemia. AJNR,2007,28:743-749.
[3] Hennings LJ, Flores R, Roberson PK, et al. Persistent penumbra in a rabbit strokemodel: incidence and histologic characteristics. Stroke Res Treat,2011:76-83.
[4] Kelly ME, Schültke E, Fiedler S, et al. Synchrotron-based intravenous cerebralangiography in a small animal model. Phys Med Biol,2007,52:1001-1012.
[5] Musella R. Anatomy of the normal carotid circulation and effects of the bilateralligature of various branches of the common carotid artery bifurcation. Arteriographicstudy in rabbits. Boll Soc Ital Biol Sper,1964,40:417-418.
[6] Hillman B, Rumbaugh C. One-catheter technique for magnification carotid andvertebral angiography in the rabbit. Invest Radiol.1977,12:373-375.
[7] Klimek E, Fournier D, Montanera W, et al. Selective transfemoral cerebralangiography of the rabbit. Technique and applications. J Neuroradiol,1990,17:20-25.
[8] Harder DR, Schulte ML, Clough AV, et al. An angiographic method for in vivo studyof arteries of the circle of Willis in small animals. Am J Physiol,1992,263(5Pt2):H1616-622.
[9] Culp WC, Woods SD, Brown AT, et al. Three variations in rabbit angiographic strokemodels. J Neurosci Methods,2013,212:322-328.
[10] Chen W, Qi J, Zhang J, Huang W, et al. Dynamic changes of the CT perfusionparameters in the embolic model of cerebral ischemia. J Huazhong Univ SciTechnolog Med Sci,2004,24:615-617.
[11] Yenari MA, de Crespigny A, Palmer JT, et al. Improved perfusion with rt-PA andhirulog in a rabbit model of embolic stroke. J Cereb Blood Flow Metab,1997,17:401-411.
[12] Caldwell B, Flores R, Lowery J, et al. Variations in the circle of Willis in the NewZealand white rabbit. JVIR,2011,22:1188-1192.
[13] Kapoor K, Kak VK, Singh B. Morphology and comparative anatomy of circulusarteriosus cerebri in mammals.Anat Histol Embryol,2003,32:347-355.
[14]闫峰,吉训明,宣芸,等.新西兰家兔大脑中动脉闭塞脑缺血模型建立的经验.首都医科大学学报,2010,31:79-83.
[15]林燕,杨佩钢,余琦,等.自体血栓性家兔局部脑缺血性梗死模型的建立.南方医科大学学报,2009,29:2291-2294.
[16]孔令琦,谢敬霞,韩鸿宾,等.提高线栓法大脑中动脉闭塞性兔脑缺血模型稳定性和可重复性的研究.中国医学影像技术,2004,20:209-212.
[17]全冠民,袁涛,刘怀军,等.自体血栓栓塞性兔大脑中动脉脑梗死影像学模型的建立.临床放射学杂志,2008,27:1266-1269.
[18]陈丽,戴炯,严国锋,等.血管内介入技术制作兔局灶性脑缺血模型.海交通大学学报（医学版）,2012,32:585-588.
[19]李凌鑫，樊小农，石学敏.大脑中动脉阻塞法建立局灶性脑缺血模型的研究进展[J].中华神经科杂志，2009，42（42）：208-210.
[20] Brown AT, Skinner RD, Flores R, et al. Stroke location and brain function in anembolic rabbit stroke model. JVIR,2010,21:903-909.
[21] Kirchhof K, Welzel T, Zoubaa S, et al. New method of embolus preparation forstandardized embolic stroke in rabbits. Stroke,2002,33:2329-2333.
[22] Lee JS, Hamilton MG, Zabramski JM．Variations in the anatomy of the rabbit cervicalcarotid artery. Stroke,1994,25:501-503.
[23] Jaban R, Stewart D, Vinters HV, et a1. Middle cerebral artery occlusion in the rabbitusing selective angiography: application for assessment of thrombolysis. Stroke,2008,39:1613-1615．
[24]杨飞,姜建威,王鹏,等.新西兰大白兔脑血管造影：脑底动脉环的解剖与变异.介入放射学杂志,2013,22:216-218.
[25] Brown A, Woods S, Skinner R, et al. Neurological Assessment Scores in RabbitEmbolic Stroke Models. Open Neurol J,2013,31:38-43.
[26] Huisa BN, Chen Y, Meyer BC, et al. Incremental treatments with laser therapyaugments good behavioral outcome in the rabbit small clot embolic stroke model.Lasers Med Sci,2013,28:1085-1089.
[1]李凌鑫,樊小农,石学敏.大脑中动脉阻塞法建立局灶性脑缺血模型的研究进展.中华神经科杂志,2009,42:208-210.
[2]孔令琦,谢敬霞,韩鸿宾,等.提高线栓法大脑中动脉闭塞性兔脑缺血模型稳定性和可重复性的研究.中国医学影像技术,2004,20:209-212.
[3]全冠民,袁涛,刘怀军,等.自体血栓栓塞性兔大脑中动脉脑梗死影像学模型的建立.临床放射学杂志,2008,27:1266-1269.
[4] Murphy BD, Chen X, Lee TY. Serial changes in CT cerebral blood volume and flowafter4hours of middle cerebral occlusion in an animal model of embolic cerebralischemia. AJNR,2007,28:743-749.
[5] Benes V, Zabramski JM, Boston M, et al. Effect of intra-arterial tissue plasminogenactivator and urokinase on autologous arterial emboli in the cerebral circulation ofrabbits. Stroke,1990,21:1594-1599.
[6] Brown AT, Skinner RD, Flores R, et al. Stroke location and brain function in anembolic rabbit stroke model. J Vasc Interv Radiol,2010,21:903-909.
[7] Culp BC, Brown AT, Erdem E, et al. Selective intracranial magnification angiographyof the rabbit: Basic techniques and anatomy. JVIR,2007,18:187-192.
[8] Caldwell B, Flores R, Lowery J, et al. Variations in the circle of Willis in the NewZealand white rabbit. JVIR,2011,22:1188-1192.
[9]冯雷,潘力,冯光,等.介入技术制作兔大脑中动脉闭塞模型的研究.重庆医学,2011,40:535-538.
[10] Hennings LJ, Flores R, Roberson PK, et al. Persistent penumbra in a rabbit strokemodel: incidence and histologic characteristics. Stroke Res Treat,2011,2011:76-83.
[11] Burgess A, Huang Y, Waspe AC, et al. High-intensity focused ultrasound (HIFU) fordissolution of clots in a rabbit model of embolic stroke. PLoS One,2012,7:e42311.
[12] Lapchak PA, Doyan S, Fan X, et al. Synergistic Effect of AJW200, a von WillebrandFactor Neutralizing Antibody with Low Dose (0.9mg/mg) Thrombolytic TherapyFollowing Embolic Stroke in Rabbits. J Neurol Neurophysiol,2013,4(2). doi:10.4172/2155-9562.1000146.
[13] Culp WC, Woods SD, Skinner RD, et al. Dodecafluoropentane emulsion decreasesinfarct volume in a rabbit ischemic stroke model. J Vasc Interv Radiol,2012,23:116-121.
[14] Brown A, Woods S, Skinner R, et al. Neurological Assessment Scores in RabbitEmbolic Stroke Models. Open Neurol J,2013,31:38-43.
[15] Huisa BN, Chen Y, Meyer BC, et al. Incremental treatments with laser therapyaugments good behavioral outcome in the rabbit small clot embolic stroke model.Lasers Med Sci,2013,28:1085-1089.
[16] Meyer DM, Compton P, Eastwood JA, et al. Antiplatelet loading improves behavioraloutcome in a rabbit model of stroke. Stroke,2013,44:3246-3248.
[17] Woods SD, Skinner RD, Ricca AM, et al. Progress in dodecafluoropentane emulsionas a neuroprotective agent in a rabbit stroke model. Mol Neurobiol,2013,48:363-367.
[1] Reinhard M, Wihler C, Roth M, et al. Cerebral autoregulation dynamics in acuteischemic stroke after rtPA thrombolysis. Cerebrovasc Dis,2008,26:147-155.
[2] Strandgaard S, Paulson OB. Cerebral auto-regulation. Stroke,1984,15:413-416.
[3] Adams HP, del Zoppo G, Alberts MJ, et al. Guidelines for the early management ofadults with ischemic stroke. Stroke,2007,38:1655-1711.
[4] Ogoh S, Brothers RM, Barnes Q, et al. The effect of changes in cardiac output onmiddle cerebral artery mean blood velocity at rest and during exer-cise. J Physiol,2005,569:697-704.
[5] Liebeskind DS. Aortic occlusion for cerebral ischemia: from theory to practice. CurrCardiol Rep,2008,10:31-36.
[6] Stokland O, Miller MM, Ilebekk A, et al. Mechanism of hemodynamic responses toocclusion of the descending thoracic aorta. Am J Physiol,1980,238:H423-H429.
[7] Saether OD, Juul R, Aadahl P, et al. Cerebral haemodynamics during thoracic-andthoracoabdominal aortic aneurysm repair. Eur J Vasc Endovasc Surg,1996,12:81-85.
[8] Stromholm T, Dale LG, Saether OD, et al. Selective carotid angiography duringcross-clamping of the descending thoracic aorta in pigs. Int Angiol,1996,15:263-267.
[9] Nussbaum ES, Heros RC, Solien EE, et al. Intra-aortic balloon counterpulsationaugments cerebral blood flow in a canine model of subarachnoid hemorrhage-inducedcerebral vasospasm. Neurosurgery,1995,36:879-884.
[10] Gelman S, Rabbani S, Bradley EL Jr. Inferior and superior vena caval blood flowsduring cross-clamping of the thoracic aorta in pigs. J Thorac Cardiovasc Surg,1988,96:387-392.
[11] Hammer M, Jovin T, Wahr JA, et al. Partial occlusion of the descending aortaincreases cerebral blood flow in a nonstroke porcine model. Cerebrovasc Dis,2009,28:406-410.
[12] Lylyk P, Vila JF, Miranda C, et al. Partial aortic obstruction improves cerebralperfusion and clinical symptoms in patients with symptomatic vasospasm. Neurol Res,2005,27:Suppl1:S129-135.
[13] Noor R, Wang CX, Todd K, et al. Partial Intra-Aortic Occlusion Improves PerfusionDeficits and Infarct Size Following Focal Cerebral Ischemia. J Neuroimaging,2010,20:272-276.
[14] Campbell MS, Grotta JC, Gomez CR, et al. Perfusion augmentation in stroke usingcontrolled aortic obstruction: pilot study results. Stroke,2004,35:291.
[15] Hussain MS, Bhagat YA, Liu S, et al. DWI Lesion Volume Reduction FollowingAcute Stroke Treatment with Transient Partial Aortic Obstruction. J Neuroimaging,2010,20:379-381.
[16] Shuaib A, Bornstein NM, Diener HC, et al. Partial aortic occlusion for cerebralperfusion augmentation: safety and efficacy of NeuroFlo in Acute Ischemic Stroketrial. Stroke,2011,42:1680-90.
[17] Lutsep HL, Altafullah IM, Roberts R, et al. Neurologic safety event rates in theSENTIS trial control population. Acta Neurol Scand,2013,127:e5-7.
[18] Leker RR, Molina C, Cockroft K, et al. Effects of age on outcome in the SENTIS trial:better outcomes in elderly patients. Cerebrovasc Dis,2012,34:263-271.
[19] Shuaib A, Schwab S, Rutledge JN, et al. Importance of proper patient selection andendpoint selection in evaluation of new therapies in acute stroke: further analysis ofthe SENTIS trial. J Neurointerv Surg,2013,5Suppl1:i21-4.
[20] Hammer MD, Schwamm L, Starkman S, et al. Safety and feasibility of NeuroFlo usein eight-to24-hour ischemic stroke patients. Int J Stroke,2012,7:655-661.
[21] Saqqur M, Ibrahim M, Butcher K, et al. Transcranial Doppler and CerebralAugmentation in Acute Ischemic Stroke. J Neuroimaging,2013,23:460-465.
[22] Emery DJ, Schellinger PD, Selchen D, et al. Safety and feasibility of collateral bloodflow augmentation after intravenous thrombolysis. Stroke,2011,42:1135-1137.
[23] Schellinger PD, Shuaib A, K hrmann M, et al. Reduced Mortality and SevereDisability Rates in the SENTIS Trial. AJNR Am J Neuroradiol.2013,34:2312-2316.
[24] Schellinger PD, K hrmann M, Liu S, et al. Favorable vascular profile is anindependent predictor of outcome: a post hoc analysis of the safety and efficacy ofNeuroFlo Technology in Ischemic Stroke trial. Stroke,2013,44:1606-1608.
[1]黄斌,赵纪春,马玉奎,等.低位腹主动脉内球囊阻断技术在骨盆和骶骨肿瘤切除术中的应用.中国普外基础与临床杂志,2011,18:635-638.
[2]徐懋,张耕,韦峰,等.球囊阻断低位腹主动脉在腰骶骨肿瘤手术中的应用.中国微创外科杂志,2010,10:147-149.
[3]李世德,詹新立,韦玮,等.暂时低位腹主动脉阻断用于骨盆、骶骨肿瘤切除术的安全性探讨.中华骨科杂志,2009,29:1038-1042.
[4]张晓庆,刘健慧,朱颖霞,等.低位腹主动脉球囊阻断技术在复杂骨盆和盆腔部位手术中的应用.临床麻醉学杂志,2008,24:17-19.
[5] Martinelli T, Thony F, Decléty P, et al. Intra-aortic balloon occlusion to salvagepatients with life-threatening hemorrhagic shocks from pelvic fractures. J Trauma,2010,68:942-948.
[6] Usman N, Noblet J, Low D, Thangaratinam S. Intra-aortic balloon occlusion withoutfluoroscopy for severe postpartum haemorrhage secondary to placenta percreta. Int JObstet Anesth.2014,23:91-93.
[7] S vik E, Stokkeland P, Storm BS, et al. The use of aortic occlusion balloon catheterwithout fluoroscopy for life-threatening post-partum haemorrhage. Acta AnaesthesiolScand,2012,56:388-393.
[8] Abu-Zidan FM. Should intra-aortic balloon occlusion be used to stop bleeding fromsevere pelvic fractures? J Trauma,2010,69:1005-1006.
[9] Liebeskind DS. Aortic occlusion for cerebral ischemia: from theory to practice. CurrCardiol Rep,2008,10:31-36.
[10] Hammer M, Jovin T, Wahr JA, et al. Partial occlusion of the descending aortaincreases cerebral blood flow in a nonstroke porcine model. Cerebrovasc Dis,2009,28:406-410.
[11] Lylyk P, Vila JF, Miranda C, et al. Partial aortic obstruction improves cerebralperfusion and clinical symptoms in patients with symptomatic vasospasm. Neurol Res,2005,27:Suppl1:S129-135.
[12] Noor R, Wang CX, Todd K, et al. Partial Intra-Aortic Occlusion Improves PerfusionDeficits and Infarct Size Following Focal Cerebral Ischemia. J Neuroimaging,2010,20:272-276.
[13] Campbell MS, Grotta JC, Gomez CR, et al. Perfusion augmentation in stroke usingcontrolled aortic obstruction: pilot study results. Stroke,2004,35:291.
[14] Hussain MS, Bhagat YA, Liu S, et al. DWI Lesion Volume Reduction FollowingAcute Stroke Treatment with Transient Partial Aortic Obstruction. J Neuroimaging,2010,20:379-381.
[15] Uflacker R, Sch nholz C, Papamitisakis N. Interim report of the SENTIS trial:cerebral perfusion augmentation via partial aortic occlusion in acute ischemic stroke. JCardiovasc Surg,2008,49:715-721.
[16] Shuaib A, Bornstein NM, Diener HC, et al. Partial aortic occlusion for cerebralperfusion augmentation: safety and efficacy of NeuroFlo in Acute Ischemic Stroketrial. Stroke,2011,42(6):1680-1690.
[17] Lutsep HL, Altafullah IM, Roberts R, et al. Neurologic safety event rates in theSENTIS trial control population. Acta Neurol Scand,2013,127:e5-7.
[18] Leker RR, Molina C, Cockroft K, et al. Effects of age on outcome in the SENTIS trial:better outcomes in elderly patients. Cerebrovasc Dis,2012,34:263-271.
[19] Shuaib A, Schwab S, Rutledge JN, et al. Importance of proper patient selection andendpoint selection in evaluation of new therapies in acute stroke: further analysis ofthe SENTIS trial. J Neurointerv Surg,2013,5Suppl1:i21-4.
[20] Hammer MD, Schwamm L, Starkman S, et al. Safety and feasibility of NeuroFlo usein eight-to24-hour ischemic stroke patients. Int J Stroke,2012,7:655-661.
[21] Saqqur M, Ibrahim M, Butcher K, et al. Transcranial Doppler and CerebralAugmentation in Acute Ischemic Stroke. J Neuroimaging,2013,23:460-465.
[22] Emery DJ, Schellinger PD, Selchen D, et al. Safety and feasibility of collateral bloodflow augmentation after intravenous thrombolysis. Stroke,2011,42:1135-1137.
[23] Schellinger PD, Shuaib A, K hrmann M, et al. Reduced Mortality and SevereDisability Rates in the SENTIS Trial. AJNR Am J Neuroradiol.2013,34:2312-2316.
[24] Schellinger PD, K hrmann M, Liu S, et al. Favorable vascular profile is anindependent predictor of outcome: a post hoc analysis of the safety and efficacy ofNeuroFlo Technology in Ischemic Stroke trial. Stroke,2013,44:1606-1608.
[25] Shuaib A, Butcher K, Mohammad AA, et al. Collateral blood vessels in acuteischaemic stroke: a potential therapeutic target. Lancet Neurol,2011,10:909-921.
[26] Liebeskind DS. Reperfusion for acute ischemic stroke: arterial revascularization andcollateral therapeutics. Curr Opin Neurol.2010,23:36-45.
[27] Hennerici MG, Kern R, Szabo K. Non-pharmacological strategies for the treatment ofacute ischaemic stroke. Lancet Neurol,2013,12:572-584.
[28] Winship IR, Armitage GA, Ramakrishnan G, et al. Augmenting collateral blood flowduring ischemic stroke via transient aortic occlusion. J Cereb Blood Flow Metab,2014,34:61-71.
[29]曲度,曲强,张弦,等.腹主动脉阻断术临床原理及其上中下段安全时限探讨.海南医学,2009,20:1-13.
[30] Storkland O, Miller MM, Ilebekk A, et al. Mechanism of hemodynamic responses toocclusion of the descending thoracic aorta. Am J Physiol,1980,238:H42-H429.
[31] Hammer M, Jovin T, Wahr JA, et al. Partial occlusion of the descending aortaincreases cerebral blood flow in a nonstroke porcine model. Cerebrovasc Dis,2009,28:406-410.
[32]李世德,杨丹,王永亮,等.兔低位腹主动脉阻断后血流动力学的变化.广西医科大学学报2012,29:17-18.
[33]武钢,王赞智,张弛,等.体外腹主动脉末端阻断动物犬模型的建立及意义.创伤外科杂志,2011,13:159-162.
[34]张永飞.腹主动脉阻断术的临床应用研究.中华创伤杂志,2002,18:464-466.
[35]曲度,张弦.腹主动脉阻断后及撒钳后综合征的发生机制.杭州医学高等专科学校学报,200l,22:44-48.
[1]阮志兵.急性脑梗死CT脑灌注成像研究进展.实用放射学杂志,2012,28:1961-1963.
[2] Nabavi DG, Cenic A, Dool J, et al. Quantitative assessment of cerebralhemodynamics using CT: stability, accuracy, and precision studies in dogs. J ComputAssist Tomogr,1999,23:506-515.
[3] Cenic A, Nabavi DG, Craen RA, et al. Dynamic CT measurement of cerebral bloodflow: a validation study. AJNR Am J Neuroradiol1999,20:63-73.
[4] Derdeyn CP, Videen TO, Yundt KD, et al. Variability of cerebral blood volume andoxygen extraction: stages of cerebral haemodynamic impairment revisited. Brain2002,125:595-607
[5] Murphy BD, Chen X, Lee TY. Serial changes in CT cerebral blood volume and flowafter4hours of middle cerebral occlusion in an animal model of embolic cerebralischemia. AJNR Am J Neuroradiol.2007,28:743-749.
[6] Sette G, Baron JC, Mazoyer B, et al. Local brain haemodynamics and oxygenmetabolismin cerebrovascular disease.Positron emission tomography. Brain,1989,112:931-951.
[7] Liebeskind DS. Aortic occlusion for cerebral ischemia: from theory to practice. CurrCardiol Rep,2008,10:31-36.
[8] Stokland O, Miller MM, Ilebekk A, et al. Mechanism of hemodynamic responses toocclusion of the descending thoracic aorta. Am J Physiol,1980,238:H423-H429.
[9] Saether OD, Juul R, Aadahl P, et al. Cerebral haemodynamics during thoracic-andthoracoabdominal aortic aneurysm repair. Eur J Vasc Endovasc Surg,1996,12:81-85.
[10] Stromholm T, Dale LG, Saether OD, et al. Selective carotid angiography duringcross-clamping of the descending thoracic aorta in pigs. Int Angiol,1996,15:263-267.
[11] Hammer M, Jovin T, Wahr JA, et al. Partial occlusion of the descending aortaincreases cerebral blood flow in a nonstroke porcine model. Cerebrovasc Dis,2009,28:406-410.
[12] Campbell MS, Grotta JC, Gomez CR, et al. Perfusion augmentation in stroke usingcontrolled aortic obstruction: pilot study results. Stroke,2004,35:291.
[13] Saether OD, Juul R, Aadahl P, et al. Cerebral haemodynamics during thoracic-andthoracoabdominal aortic aneurysm repair. Eur J Vasc Endovasc Surg,1996,12:81-85.
[14] Nussbaum ES, Heros RC, Solien EE, et al. Intra-aortic balloon counterpulsationaugments cerebral blood flow in a canine model of subarachnoid hemorrhage-inducedcerebral vasospasm. Neurosurgery,1995,36:879-884.
[15] Gelman S, Rabbani S, Bradley EL Jr. Inferior and superior vena caval blood flowsduring cross-clamping of the thoracic aorta in pigs. J Thorac Cardiovasc Surg,1988,96:387-392.
[16] Pranevicius O, Pranevicius M, Liebeskind DS. Partial aortic occlusion and cerebralvenous steal: venous effects of arterial manipulation in acute stroke. Stroke,2011,42:1478-1481.
[17] Pranevicius O, Pranevicius M, Pranevicius H, et al. Transition to collateral flow afterarterial occlusion predisposes to cerebral venous steal. Stroke.2012,43:575-579.
[18] Hatashita S, Hoff JT. Cortical tissue pressure gradients in early ischemic brain edema.J Cereb Blood Flow Metab,1986,6:1-7.
[19] Iannotti F, Hoff JT, Schielke GP. Brain tissue pressure in focal cerebral ischemia. JNeurosurg,1985,62:83-89.
[20] Pranevicius M, Pranevicius O. Cerebral venous steal: blood low diversion withincreased tissue pressure. Neurosurgery,2002,51:1267-1273.
[21] Ames A III, Wright RL, Kowada M, et al. Cerebral ischemia. II. The no-reflowphenomenon. Am J Pathol,1968,52:437-453.
[22] Alexandrov AV, Hall CE, Labiche LA, et al. Ischemic stunning of the brain: earlyrecanalization without immediate clinical improvement in acute ischemic stroke.Stroke,2004,35:449-452.
[23] Noor R, Wang CX, Todd K, et al. Partial Intra-Aortic Occlusion Improves PerfusionDeficits and Infarct Size Following Focal Cerebral Ischemia. J Neuroimaging,2010,20:272-276.
[24] Hussain MS, Bhagat YA, Liu S, et al. DWI Lesion Volume Reduction FollowingAcute Stroke Treatment with Transient Partial Aortic Obstruction. J Neuroimaging,2010,20:379-381.
[25] Shuaib A, Bornstein NM, Diener HC, et al. Partial aortic occlusion for cerebralperfusion augmentation: safety and efficacy of NeuroFlo in Acute Ischemic Stroketrial. Stroke,2011,42:1680-90.
[26] Lutsep HL, Altafullah IM, Roberts R, et al. Neurologic safety event rates in theSENTIS trial control population. Acta Neurol Scand,2013,127:e5-7.
[27] Leker RR, Molina C, Cockroft K, et al. Effects of age on outcome in the SENTIS trial:better outcomes in elderly patients. Cerebrovasc Dis,2012,34:263-271.
[28] Shuaib A, Schwab S, Rutledge JN, et al. Importance of proper patient selection andendpoint selection in evaluation of new therapies in acute stroke: further analysis ofthe SENTIS trial. J Neurointerv Surg,2013,5Suppl1:i21-4.
[29] Hammer MD, Schwamm L, Starkman S, et al. Safety and feasibility of NeuroFlo usein eight-to24-hour ischemic stroke patients. Int J Stroke,2012,7:655-661.
[30] Saqqur M, Ibrahim M, Butcher K, et al. Transcranial Doppler and CerebralAugmentation in Acute Ischemic Stroke. J Neuroimaging,2013,23:460-465.
[31] Emery DJ, Schellinger PD, Selchen D, et al. Safety and feasibility of collateral bloodflow augmentation after intravenous thrombolysis. Stroke,2011,42:1135-1137.
[32] Schellinger PD, Shuaib A, K hrmann M, et al. Reduced Mortality and SevereDisability Rates in the SENTIS Trial. AJNR Am J Neuroradiol,2013,34:2312-2316.
[33] Schellinger PD, K hrmann M, Liu S, et al. Favorable vascular profile is anindependent predictor of outcome: a post hoc analysis of the safety and efficacy ofNeuroFlo Technology in Ischemic Stroke trial. Stroke,2013,44:1606-1608.
[1] Nogueira RG, Yoo AJ, Buonanno FS, et al. Endovascular approaches to acute stroke,part2: a comprehensive review of studies and trials. AJNR,2009,30:859-875.
[2] Okahara M, Kiyosue H, Mori H, et al. Anatomic variations of the cerebral arteries andtheir embrayology: A pictorial review. Eur Radiol,2002,12:2548-2561.
[3] Liebeskind DS. Collateral circulation. Stroke,2003,34:2279-2284.
[4] Wei L，Erinjeri JP，Rovainen CM，et a1. Collateral growth and angiogenesis aroundcortical stroke. Stroke,200l,32:2179-2184．
[5] Kuroda S, Houkin K. Moyamoya disease: current concepts and future perspectives.Lancet Neurol.2008,7:1056-1066.
[6] Orosz L, Hoksbergen AW, Molnár C, et al. Clinical applicability of a mathematicalmodel in assessing the functional ability of the communicating arteries of the circle ofWillis. J Neurol Sci,2009,15:278:94-99.
[7] Liebeskind DS, Cotsonic GA, Saver JL, et al. Collateral circulation in symptomaticintracranial atherosclerosis. J Cereb Blood Flow Metab,2010,31:1293-1301.
[8] Henderson RD, Eliasziw M, Fox AJ, et al. Angiographically defined collateralcirculation and risk of stroke in patients with severe carotid artery stenosis. NorthAmerican Symptomatic Carotid Endarterectomy Trial (NASCET) Group. Stroke,2000,31:128-132.
[9] Kitagawa K, Yagita Y, Sasaki T, et al. Chronic mild reduction of cerebral perfusionpressure induces ischemic tolerance in focal cerebral ischemia. Stroke,2005,36:2270-2274.
[10] Brozici M, van der Zwan A, Hillen B. Anatomy and Functionality of LeptomeningealAnastomoses: A Review. Stroke,2003,34:2750-2762.
[11] Lima FO, Furie KL, Silva GS, et al. The pattern of leptomeningeal collaterals on CTangiography is a strong predictor of long-term functional outcome in stroke patientswith large vessel intracranial occlusion. Stroke,2010,41:2316-2322.
[12] Ovbiagele B, Saver JL, Starkman S, et al. Statin enhancement of collateralization inacute. Neurology,2007,68:2129-2131.
[13] van Weel V, de Vries M, Voshol PJ, et al. Hypercholesterolemia reduces collateralartery growth more dominantly than hyperglycemia or insulin resistance in mice.Arterioscler Thromb Vasc Biol,2006,26:1383-1390.
[14] Liebeskind DS. Imaging the future of stroke: I ischemia. Ann Neurol,2009,66:575-590.
[15] Bang OY, Saver JL, Buck BH, et al. Impact of collateral flow on tissue fate in acuteischemic stroke. J Neurol Neurosurg Psychiatry,2007,79:625-629.
[16] Bozzao L, Fantozzi LM, Bastianello S, et al. Early collateral blood supply and lateparenchymal brain damage in the patients with middle cerebral artery occlusion.Stroke,1989,20:735-740.
[17] Higashida RT, Furlan AT, Roberts H, et al. Trial design and reporting standards forintra-arterial thrombolysis for acute ischemic stroke. Stroke,2003;34:e109-137.
[18] Kaufmann TJ, Huston J3rd, Mandrekar JN, et al. Complications of diagnosticcerebral angiography: evaluation of19,826consecutive patients. Radiology,2007,243:812-819.
[19] van Laar PJ, van der Grond J, Bremmer JP, et al. Assessment of the contribution ofthe external carotid artery to brain perfusion in patients with internal carotid arteryocclusion. Stroke,2008,39:3003-3008.
[20] Miteff F, Levi CR, Bateman GA, et al. The independent predictive utility of computedtomography angiographic collateral status in acute ischaemic stroke. Brain,2009,132:2231-2238.
[21] Maas MB, Lev MH, Ay H, et al. Collateral vessels on CT angiography predictoutcome in acute ischemic stroke. Stroke,2009,40:3001-3005.
[22] Choi JY, Kim EJ, Hong JM, et al. Conventional enhancement CT: a valuable tool forevaluating pial collateral flow in acute ischemic stroke. Cerebrovasc Dis,2011,31:346-352.
[23] Jung SL, Lee YJ, Ahn KJ, et al. Assessment of collateral flow with multi-phasic CT:correlation with diffusion weighted MRI in MCA occlusion. J Neuroimaging,2011,21:225-228.
[24] Gasparotti R, Grassi M, Mardighian D, et al. Perfusion CT in patients with acuteischemic stroke treated with intra-arterial thrombolysis: predictive value of infarctcore size on clinical outcome. AJNR Am J Neuroradiol,2009,30:722-727.
[25] Hoksbergen AW, Fülesdi B, Legemate DA, et al. Collateral configuration of thecircle of Willis: transcranial color-coded duplex ultrasonography and comparison withpostmortem anatomy. Stroke,2000,31:1346-1351.
[26] Sanossian N, Saver JL, Alger JR, et al. Angiography reveals that fluid-attenuatedinversion recovery vascular hyperintensities are due to slow flow, not thrombus.AJNR,2009,30:564-568.
[27] Cheng B, Ebinger M, Kufner A, et al. Hyperintense vessels on acute strokefluid-attenuated inversion recovery imaging: associations with clinical and other MRIfindings. Stroke,2012,43:2957-2961.
[28] Liu W, Xu G, Yue X, et al. Hyperintense vessels on FLAIR: a useful non-invasivemethod for assessing intracerebral collaterals. Eur J Radiol,2011,80:786-791.
[29] Liu W, Yin Q, Yao L, et al. Decreased hyperintense vessels on FLAIR images afterendovascular recanalization of symptomatic internal carotid artery occlusion. Eur JRadiol,2012,81:1595-1600.
[30] Haussen DC, Koch S, Saraf-Lavi E, et al. FLAIR Distal Hyperintense Vessels as aMarker of Perfusion-Diffusion Mismatch in Acute Stroke. J Neuroimaging,2013,23:397-400.
[31] Pérez de la Ossa N, Hernández-Pérez M, Domènech S, et al. Hyperintensity ofdistal vessels on FLAIR is associated with slow progression of the infarction in acuteischemic stroke. Cerebrovasc Dis,2012,34:376-384.
[32] Lee KY, Latour LL, Luby M, et al. Distal hyperintense vessels on FLAIR: an MRImarker for collateral circulation in acute stroke? Neurology,2009,72:1134-1139.
[33] Liebeskind DS, Cotsonis GA, Saver JL, et al. Collateral circulation in symptomaticintracranial atherosclerosis. J Cereb Blood Flow Metab,2011,31:1293-1301.
[34] Yamauchi H, Kudoh T, Sugimoto K, et al. Pattern of collaterals, type of infarcts, andhaemodynamic impairment in carotid artery occlusion. J Neurol Neurosurg Psychiatry,2004,75:1697-1701.
[35] Liebeskind DS, Cotsonis GA, Saver JL, et al. Collaterals dramatically alter stroke riskin intracranial atherosclerosis. Ann Neurol.2011,69:963-974.
[36] Romero JR, Pikula A, Nguyen TN, et al. Cerebral collateral circulation in carotidartery disease. Curr Cardiol Rev,2009,5:279-288.
[37] Liu XT, Wang W, Wang LJ, et al. Correlation of collateral circulation and prognosisin patients with acute cerebral infarction. Zhonghua Yi Xue Za Zhi,2011,22:766-768.
[38] Bang OY, Saver JL, Buck BH, et al. Impact of collateral flow on tissue fate in acuteischaemic stroke. J Neurol Neurosurg Psychiatry,2008,79:625-629.
[39] Liebeskind DS, Kim D, Starkman S, et al. Collateral failure? Late mechanicalthrombectomy after failed intravenous thrombolysis. J Neuroimaging,2010,20:78-82.
[40] Christoforidis GA, Mohammad Y, Kehagias D, et al. Angiographic assessment of pialcollaterals as a prognostic indicator following intra-arterial thrombolysis for acuteischemic stroke. AJNR Am J Neuroradiol,2005,26:1789-1797.
[41] Kucinski T, Koch C, Eckert B, et al. Collateral circulation is an independentradiological predictor of outcome after thrombolysis in acute ischaemic stroke.Neuroradiology,2003,45:11-18.
[42] Yasargil MG, Krayenbuhl HA, Jacobson JH. Microneurosurgical arterialreconstruction. Surgery,1970,67:221-233.
[43] Hofmeijer J, Klijn CJM, Kappelle LJ, et al. Collateral circulation via the ophthalmicartery or leptomeningeal vessels is associated with impaired cerebral vasoreactivity inpatients with symptomatic carotid artery occlusion. Cerebrovasc Dis,2002,14:22-26.
[44] The EC/IC bypass study group. Failure of extracranial-intracranial arterial bypass toreduce the risk of ischemic stroke. Results of an international randomized trial. NEngl J Med,1985,313:1191-1200.
[45] Grubb RL, Derdeyn CP, Fritsch SM, et al. Importance of hemody namic factors in theprognosis of symptomatic carotid occlusion. JAMA,1998,280:1055-1060
[46] Derdeyn CP, Gage BF, Grubb RL, et al. Cost-effectiveness analysis of therapy forsymptomatic carotid occlusion:PET screening before selective extracranial-to-intracranial bypass versus medical treatment. J Nucl Med,2000,41:800-807.
[47] Powers WJ, Clarke WR, Grubb RL, et al. Extracranial-intracranial bypass surgery forstroke prevention in hemodynamic cerebral ischemia:The carotid occlusion surgerystudy randomized trial. JAMA,2011,306:1983-1992.
[48]黄家星，林文华，刘丽萍，等.缺血性卒中侧支循环评估与干预中国专家共识.中国卒中杂志,2013,8:285-293.
[49] Adams HP, del Zoppo G, Alberts MJ, et al. Guidelines for the early management ofadults with ischemic stroke. Stroke,2007,38:1655-1711.
[50] Hsu CY, Norris JW, Hogan EL, et al. Propentofylline in non-hemorrhagic stroke: arandomized placebo-controlled double-blinded controlled trial. Stroke,1988,19:716-722.
[51] Chan YW, Kay CS. Pentoxifylline in the treatment of acute ischaemic stroke: areappraisal in Chinese stroke patients. Clin Exp Neurol,1993,13:526-530.
[52] Eames PJ, Blake MJ, Dawson SL, et al. Dynamic cerebral autoregulation and beat tobeat blood pressure control are impaired in acute ischaemic stroke. J NeurolNeurosurg Psychiatry,2002,72:467-472.
[53] Smith HA, Thompson-Dobkin J, Yonas H, et al. Correlation of xenon-enhancedcomputed tomography-defned cerebral blood fow reactivity and collateral fowpatterns. Stroke,1994,25:1784-1787.
[54] Schwarz S, Georgiadis D, Aschoff A, et al. Effects of induced hyper tension onintracranial pressure and flow velocities of the middle cerebral arteries in patientswith large hemispheric stroke. Stroke,2002,33:998-1004.
[54] Hillis AE, Ulatowski JA, Barker PB, et al. A pilot randomized trial of induced bloodpressure elevation:Effects on function and focal perfusion in acute and subacutestroke. Cerebrovasc Dis,2003,16:236-246.
[56] Rordorf G, Cramer SC, Efird JT, et al. Pharmacological elevation of blood pressure inacute stroke. Clinical effects and safety. Stroke,1997,28:2133-2138.
[57] Rordorf G, Cramer SC, E? rd JT, et al. Pharmacological elevation of blood pressurein acute stroke: clinical e? ects and safety. Stroke,1997,28:2133-2138.
[58] Wityk RJ, Restrepo L. Hypoperfusion and its augmentation in patients with brainischemia. Curr Treat Options Cardiovasc Med,2003,5:193-199.
[59] Amin-Hanjani S, Barker FG, Charbel FT, et al. Extracranial-intracranial bypass forstroke-is this the end of the line or a bump in the road?. Neurosurgery,2012,71:557-561.
[60] Zheng ZS, Li TM, Kambic H, et al. Sequential external counterpulsation(SECP) inChina. Trans Am Soc Artif Intern Organs,1983,29:599-603.
[61] Werner D, Schneider M, Weise M, et al. Pneumatic external counterpulsation:A newnoninvasive method to improve organ perfusion. Am J Cardiol,1999,84:950-952.
[62] Arora RR, Chou TM, Jain D, et al. The multicenter study of enhanced externalcounterpulsation(MUST-EECP):Ef fect of EECP on exercise-induced myocardialischemia and anginal episodes. J Am Coll Cardiol,1999,33:1833-1840.
[63] Lin W, Xiong L, Han J, et al. External counterpulsation augments blood pressure andcerebral flow velocities in ischemic stroke patients with cerebral int racranial largeartery occlusive disease. Stroke,2012,43:3007-3011.
[64] Masuda D, Nohara R, Hirai T, et al. Enhanced external counterpulsation improvedmyocardial perfusion and coronary fow reserve in patients with chronic stableangina:evaluation by(13)n-ammonia positron emission tomography. Eur Heart J,2001,22:1451-1458.
[65] Lin W, Xiong L, Han J, et al. External counterpulsation augments blood pressure andcerebral flow velocities in ischemic stroke patients with cerebral intracranial largeartery occlusive disease. Stroke,2012,43:3007-3011.
[66] Han JH, Leung TW, Lain WW. Preliminary findings of external counterpulsation forischemic stroke patient with large artery occlusive disease. Stroke,2008,39:1340-1343.
[67] Liebeskind DS. Aortic occlusion for cerebral ischemia: from theory to practice. CurrCardiol Rep,2008,10:31-36.
[68] Stokland O, Miller MM, Ilebekk A, et al. Mechanism of hemodynamic responses toocclusion of the descending thoracic aorta. Am J Physiol,1980,238:H423-H429.
[69] Saether OD, Juul R, Aadahl P, et al. Cerebral haemodynamics during thoracic-andthoracoabdominal aortic aneurysm repair. Eur J Vasc Endovasc Surg,1996,12:81-85.
[70] Stromholm T, Dale LG, Saether OD, et al. Selective carotid angiography duringcross-clamping of the descending thoracic aorta in pigs. Int Angiol,1996,15:263-267.
[71] Nussbaum ES, Heros RC, Solien EE, et al. Intra-aortic balloon counterpulsationaugments cerebral blood flow in a canine model of subarachnoid hemorrhage-inducedcerebral vasospasm. Neurosurgery,1995,36:879-884.
[72] Gelman S, Rabbani S, Bradley EL Jr. Inferior and superior vena caval blood flowsduring cross-clamping of the thoracic aorta in pigs. J Thorac Cardiovasc Surg,1988,96:387-392.
[73] Hatashita S, Hoff JT. Cortical tissue pressure gradients in early ischemic brain edema.J Cereb Blood Flow Metab,1986,6:1-7.
[74] Iannotti F, Hoff JT, Schielke GP. Brain tissue pressure in focal cerebral ischemia. JNeurosurg,1985,62:83-89.
[75] Pranevicius M, Pranevicius O. Cerebral venous steal: blood low diversion withincreased tissue pressure. Neurosurgery,2002,51:1267-1273.
[76] Ames A III, Wright RL, Kowada M, et al. Cerebral ischemia. II. The no-reflowphenomenon. Am J Pathol,1968,52:437-453.
[77] Alexandrov AV, Hall CE, Labiche LA, et al. Ischemic stunning of the brain: earlyrecanalization without immediate clinical improvement in acute ischemic stroke.Stroke,2004,35:449-452.
[78] Pranevicius O, Pranevicius M, Liebeskind DS. Partial aortic occlusion and cerebralvenous steal: venous effects of arterial manipulation in acute stroke. Stroke,2011,42:1478-1481.
[79] Pranevicius O, Pranevicius M, Pranevicius H, et al. Transition to collateral flow afterarterial occlusion predisposes to cerebral venous steal. Stroke,2012,43,575-579.
[80] Hammer M, Jovin T, Wahr JA, et al. Partial occlusion of the descending aortaincreases cerebral blood flow in a nonstroke porcine model. Cerebrovasc Dis,2009,28:406-410.
[81] Lylyk P, Vila JF, Miranda C, et al. Partial aortic obstruction improves cerebralperfusion and clinical symptoms in patients with symptomatic vasospasm. Neurol Res,2005,27:Suppl1:S129-135.
[82] Noor R, Wang CX, Todd K, et al. Partial Intra-Aortic Occlusion Improves PerfusionDeficits and Infarct Size Following Focal Cerebral Ischemia. J Neuroimaging,2010,20:272-276.
[83] Campbell MS, Grotta JC, Gomez CR, et al. Perfusion augmentation in stroke usingcontrolled aortic obstruction: pilot study results. Stroke,2004,35:291.
[84] Hussain MS, Bhagat YA, Liu S, et al. DWI Lesion Volume Reduction FollowingAcute Stroke Treatment with Transient Partial Aortic Obstruction. J Neuroimaging,2010,20:379-381.
[85] Uflacker R, Sch nholz C, Papamitisakis N. Interim report of the SENTIS trial:cerebral perfusion augmentation via partial aortic occlusion in acute ischemic stroke. JCardiovasc Surg,2008,49:715-721.
[86] Shuaib A, Bornstein NM, Diener HC, et al. Partial aortic occlusion for cerebralperfusion augmentation: safety and efficacy of NeuroFlo in Acute Ischemic Stroketrial. Stroke,2011,42:1680-1690.
[87] Lutsep HL, Altafullah IM, Roberts R, et al. Neurologic safety event rates in theSENTIS trial control population. Acta Neurol Scand,2013,127:e5-7.
[88] Leker RR, Molina C, Cockroft K, et al. Effects of age on outcome in the SENTIS trial:better outcomes in elderly patients. Cerebrovasc Dis,2012,34:263-271.
[89] Shuaib A, Schwab S, Rutledge JN, et al. Importance of proper patient selection andendpoint selection in evaluation of new therapies in acute stroke: further analysis ofthe SENTIS trial. J Neurointerv Surg,2013,5Suppl1:i21-4.
[90] Hammer MD, Schwamm L, Starkman S, et al. Safety and feasibility of NeuroFlo usein eight-to24-hour ischemic stroke patients. Int J Stroke,2012,7:655-661.
[91] Saqqur M, Ibrahim M, Butcher K, et al. Transcranial Doppler and CerebralAugmentation in Acute Ischemic Stroke. J Neuroimaging,2013,23:460-465.
[92] Emery DJ, Schellinger PD, Selchen D, et al. Safety and feasibility of collateral bloodflow augmentation after intravenous thrombolysis. Stroke,2011,42:1135-1137.
[93] Schellinger PD, Shuaib A, K hrmann M, et al. Reduced Mortality and SevereDisability Rates in the SENTIS Trial. AJNR Am J Neuroradiol,2013,34:2312-2316.
[94] Schellinger PD, K hrmann M, Liu S, et al. Favorable vascular profile is anindependent predictor of outcome: a post hoc analysis of the safety and efficacy ofNeuroFlo Technology in Ischemic Stroke trial. Stroke,2013,44:1606-1608.
[95] Shuaib A, Butcher K, Mohammad AA, et al. Collateral blood vessels in acuteischaemic stroke: a potential therapeutic target. Lancet Neurol,2011,10:909-921.
[96] Liebeskind DS. Reperfusion for acute ischemic stroke: arterial revascularization andcollateral therapeutics. Curr Opin Neurol,2010,23:36-45.
[97] Hennerici MG, Kern R, Szabo K. Non-pharmacological strategies for the treatment ofacute ischaemic stroke. Lancet Neurol,2013,12:572-584.
[2] Mitka M. Rapid stroke treatment an elusive goal. JAMA,2008,299:1653-1654.
[3] Wang Y, Liao X, Zhao X, et a1. Using recombinant tissue plasminogen activator lotreal acute ischemic stroke in China：analysis of the results from the chinese nationalstroke registry(CNSR). Stroke,2011,42:1658-1664.
[4] Hacke W, Kaste M, Bluhmki E, et a1. Thmmbolysis with alteplase3to4.5hours afteracute ischemic stroke. N Engl J Med,2008,359:1317-1329.
[5] Furlan A, Higashida R, Wechsler L, et al. Intra-arterial prourokinase for acuteischemic stroke, the PROACT II study: a randomized controlled trial-Prolyse in AcuteCerebral Thromboembolism. JAMA,1999,282:2003-2011.
[6] Del Zoppo GJ, Higashida RT, Furlan AJ, et al. PROACT: a phase II randomized trialof recombinant pro-urokinase by direct arterial delivery in acute middlecerebral.artery stroke. Stroke,1998,29:4-11.
[7] Nogueira RG, Schwamm LH, Hirsch JA. Endovascular approaches to acute stroke,part1: Drugs, devices, and data. AJNR Am J Neuroradiol,2009,30:649-661.
[8] Nogueira RG, Yoo AJ, Buonanno FS, et al. Endovascular approaches to acute stroke,part2: a comprehensive review of studies and trials. AJNR Am J Neuroradiol,2009,30:859-875.
[9] Arnold M, Schroth G, Nedeltchev K, et al. Intra-arterial thrombolysis in100patientswith acute stroke due to middle cerebral artery occlusion. Stroke,2002,33:1828-1833.
[10] Eckert B, Kucinski T, Pfeiffer G, et al. Endovascular therapy of acute vertebrobasilarocclusion: early treatment onset as the most important factor. Cerebrovasc Dis,2002,14:42-50.
[11] IMS Study Investigators. Combined intravenous and intra-arterial recanalization foracute ischemic stroke: the Interventional Management of Stroke Study. Stroke,2004,35:904-911.
[12] Jauch EC, Saver JL, Adams HP Jr, et al. Guidelines for the early management ofpatients with acute ischemic stroke: a guideline for healthcare professionals from theAmerican Heart Association/American Stroke Association. Stroke,2013,44:870-947.
[13] Sorimachi T, Fujii Y, Tsuchiya N, et al. Recanalization by mechanical embolusdisruption during intra-arterial thrombolysis in the carotid territory. Am J Neuroradiol,2004,25:1391-1402.
[14] Kim DJ, Kim DI, Byun JS, et al. Simple microwire and microcatheter mechanicalthrombolysis with adjuvant intraarterial urokinase for treatment of hyperacuteischemic stroke patients. Acta Radiol,2008,49:351-357.
[15] Yoon W, Park MS, Cho KH. Low-dose intra-arterial urokinase and aggressivemechanical clot disruption for acute ischemic stroke after failure of intravenousthrombolysis. AJNR Am J Neuroradiol,2010,31:161-164.
[16] Qureshi AI, Siddiqui AM, Suri MF, et al. Aggressive mechanical clot disruption andlow-dose intra-arterial third-generation thrombolytic agent for ischemic stroke: aprospective study. Neurosurgery,2002,51:1319-1327.
[17] Ikushima I, Ohta H, Hirai T, et al. Balloon catheter disruption of middle cerebralartery thrombus in conjunction with thrombolysis for the treatment of acute middlecerebral artery embolism. AJNR Am J Neuroradiol,2007,28:513-517.
[18] Nogueira RG, Schwamm LH, Buonanno FS, et al. Low-pressure balloon angioplastywith adjuvant pharmacological therapy in patients with acute ischemic stroke causedby intracranial arterial occlusions. Neuroradiology,2008,50:331-340.
[19]刘振生,王苇,张新江,等.球囊碎栓辅助动脉溶栓治疗急性大脑中动脉闭塞.介入放射学杂志,2009,18:84-86.
[20] Hitchcock KE，Holland CK. Ultrasound-assisted thrombolysis for stroke therapy:better thrombus break-up with bubbles. Stroke,2010,41(10Suppl):50-53.
[21] Tomsick T, Broderick J, Carrozella J, et a1. Revascularization results in theInterventional Management of Stroke II trial. AJNR Am J Neuroradiol,2008,29:582-587.
[22] Smith WS, Sung G, Sawer J, et a1. Mechanical thrombectomy for acute ischemicstroke：final results of the Multi MERCI trial.Stroke,2008,39:1205-1212.
[23] Nogueira RG, Smith WS; MERCI and Multi MERCI Writing Committee. Safety andefficacy of endovascular thrombectomy in patients with abnormal hemostasis: pooledanalysis of the MERCI and multi MERCI trials. Stroke,2009,40:516-522.
[24] Alshekhlee A, Pandya DJ, English J, et al. Merci mechanical thrombectomy retrieverfor acute ischemic stroke therapy: literature review. Neurology,2012,25:79(13Suppl1):S126-34.
[25] Almekhlafi MA, Menon BK, Freiheit EA, et al. A meta-analysis of observationalintra-arterial stroke therapy studies using the Merci device, Penumbra system, andretrievable stents. AJNR Am J Neuroradiol,2013,34:140-145.
[26] Tenser MS, Amar AP, Mack WJ. Mechanical thrombectomy for acute ischemic strokeusing the MERCI retriever and penumbra aspiration systems. World Neurosurg,2011,76(6Suppl):S16-23.
[27] Fields JD, Lutsep HL, Smith WS; MERCI Multi MERCI Investigators. Higherdegrees of recanalization after mechanical thrombectomy for acute stroke areassociated with improved outcome and decreased mortality: pooled analysis of theMERCI and Multi MERCI trials. AJNR Am J Neuroradiol,2011,32:2170-2174.
[28] Nogueira RG, Smith WS, Sung G, et al. Effect of time to reperfusion on clinicaloutcome of anterior circulation strokes treated with thrombectomy: pooled analysis ofthe MERCI and Multi MERCI trials. Stroke,2011,42:3144-3149.
[29] Nogueira RG, Liebeskind DS, Sung G, et al. Predictors of good clinical outcomes,mortality, and successful revascularization in patients with acute ischemic strokeundergoing thrombectomy: pooled analysis of the Mechanical Embolus Removal inCerebral Ischemia (MERCI) and Multi MERCI Trials. Stroke,2009,40:3777-3783.
[30] Josephson SA, Saver JL, Smith WS; Merci and Multi Merci Investigators.Comparisonof mechanical embolectomy and intraarterial thrombolysis in acute ischemic strokewithin the MCA: MERCI and Multi MERCI compared to PROACT II. NeurocritCare,2009,10:43-49.
[31] Gobin YP, Starkman S, Duckwiler GR, et al. MERCI1: a phase1study ofmechanical embolus removal in cerebral ischemia.Stroke,2004,35:2848-2854.
[32] Shi ZS, Loh Y, Walker G, et al. Clinical outcomes in middle cerebral artery trunkocclusions versus secondary division occlusions after mechanical thrombectomy:pooled analysis of the Mechanical Embolus Removal in Cerebral Ischemia (MERCI)and Multi MERCI trials. Stroke,2010,41:953-960.
[33] Flint AC, Duckwiler GR, Budzik RF, et al. Mechanical thrombectomy of intracranialinternal carotid occlusion: pooled results of the MERCI and Multi MERCI Part I trials.Stroke,2007,38:1274-1280.
[34] Penumbra Pivotal Stroke Trial Investigators Investigators. The penumbra pivotalstroke trial：safety and effectiveness of a new generation of mechanical devices forclot removal in intracranial large vessel occlusive disease. Stroke,2009,40:2761-2768.
[35] Hussain SI, Zaidat OO, Fitzsimmons BF. The Penumbra system for mechanicalthrombectomy in endovascular acute ischemic stroke therapy. Neurology,2012,25,S135-41.
[36] Tarr R, Hsu D, Kulcsar Z, et al. The POST trial: initial post-market experience of thePenumbra system: revascularization of large vessel occlusion in acute ischemic strokein the United States and Europe. J Neurointerv Surg,2010,2:341-344.
[37] Kelly ME, Furlan AJ, Fiorella D. Recanalization of an acute middle cerebral arteryocclusion using a self-expanding, reconstrainable, intracranial microstent as atemporary endovascular bypass. Stroke,2008,39:1770-1773.
[38] Machi P, Costalat V, Lobotesis K, et a1. Solitaire FR thrembectomy system:immediate resuhs in56consecutive acute ischemic stroke patients. J Neurointerv Surg,2012,4:62-66.
[39] Almekhtafi MA, Menon BK, Freiheit EA, et a1. A meta-analysis of observationalintra-arterial stroke therapy studies using the MERCI device，Penumbra system，andretrievable stents. Am J Neuroradiol,2013,34:140-145.
[40] Mokin M, Kass-Hout T, Levy EI. Solitaire FR-a promising new device for acuteischemie stroke treatment. World Neumsurg,2012,78:557-558.
[41] Nogueira RG, Latsep HL, Gupta R, et a1. TREVO versus MERCI retrievers forthrombectomy revascularisation of large vessel occlusions in acute ischaemic stroke(TREVO2)：a randomised trial. Lancet,2012,380:1231-1240.
[42] Nogueira RG, Levy EI, Gounis M, et a1. The Trevo device：preclinical data of a novelstroke thrombectomy device in two different animal models of arterialthrombo-occlusive disease. J Neurointerv Surg,2011,4:295-300.
[43] Jaharl R. Solitaire flow-restoration device for treatment of acute ischemic stroke：safety and recanalization efficacy studv in a swine vessel oclusinn model. AJNR,2010,31:1938-1943.
[44] Kim TK, Rhim JK, Lee CJ, et a1. The limitations of thmmbectomy with solitaire ABas first-line treatment in acute ischemic stroke: a single center experience. JCerebrovasc Endovasc Neurosurg,2012,14:203-209．
[45] Liebeskind DS. Collateral therapeutics for cerebral ischemia. Expert Rev Neurother,2004,4:255-265.
[46]刘振生，王苇，李澄，等.急性脑梗死FLAIR序列血管高信号形成机制探讨.临床放射学杂志，2011,30::618-620.
[47] Liebeskind DS. Aortic occlusion for cerebral ischemia: from theory to practice. CurrCardiol Rep,2008,10:31-36.
[48] Stokland O, Miller MM, Ilebekk A, et al. Mechanism of hemodynamic responses toocclusion of the descending thoracic aorta. Am J Physiol,1980,238:H423-H429.
[49] Saether OD, Juul R, Aadahl P, et al. Cerebral haemodynamics during thoracic-andthoracoabdominal aortic aneurysm repair. Eur J Vasc Endovasc Surg,1996,12:81-85.
[50] Hammer M, Jovin T, Wahr JA, et al. Partial occlusion of the descending aortaincreases cerebral blood flow in a nonstroke porcine model. Cerebrovasc Dis,2009,28:406-410.
[51] Noor R, Wang CX, Todd K, et al. Partial Intra-Aortic Occlusion Improves PerfusionDeficits and Infarct Size Following Focal Cerebral Ischemia. J Neuroimaging,2010,20:272-276.
[52] Hussain MS, Bhagat YA, Liu S, et al. DWI Lesion Volume Reduction FollowingAcute Stroke Treatment with Transient Partial Aortic Obstruction. J Neuroimaging,2010,20:379-381.
[53] Shuaib A, Bornstein NM, Diener HC, et al. Partial aortic occlusion for cerebralperfusion augmentation: safety and efficacy of NeuroFlo in Acute Ischemic Stroketrial. Stroke,2011,42:1680-90.
[54] Lutsep HL, Altafullah IM, Roberts R, et al. Neurologic safety event rates in theSENTIS trial control population. Acta Neurol Scand,2013,127:e5-7.
[55] Leker RR, Molina C, Cockroft K, et al. Effects of age on outcome in the SENTIS trial:better outcomes in elderly patients. Cerebrovasc Dis,2012,34:263-271.
[56] Shuaib A, Schwab S, Rutledge JN, et al. Importance of proper patient selection andendpoint selection in evaluation of new therapies in acute stroke: further analysis ofthe SENTIS trial. J Neurointerv Surg,2013,5Suppl1:121-124.
[57] Hammer MD, Schwamm L, Starkman S, et al. Safety and feasibility of NeuroFlo usein eight-to24-hour ischemic stroke patients. Int J Stroke,2012,7:655-661.
[58] Saqqur M, Ibrahim M, Butcher K, et al. Transcranial Doppler and CerebralAugmentation in Acute Ischemic Stroke. J Neuroimaging,2013,23:460-465.
[59] Emery DJ, Schellinger PD, Selchen D, et al. Safety and feasibility of collateral bloodflow augmentation after intravenous thrombolysis. Stroke,2011,42:1135-1137.
[60] Schellinger PD, Shuaib A, K hrmann M, et al. Reduced Mortality and SevereDisability Rates in the SENTIS Trial. AJNR Am J Neuroradiol,2013,34:2312-2316.
[61] Schellinger PD, K hrmann M, Liu S, et al. Favorable vascular profile is anindependent predictor of outcome: a post hoc analysis of the safety and efficacy ofNeuroFlo Technology in Ischemic Stroke trial. Stroke,2013,44:1606-1608.
[62]李凌鑫,樊小农,石学敏.大脑中动脉阻塞法建立局灶性脑缺血模型的研究进展.中华神经科杂志,2009,42:208-210.
[63]全冠民,袁涛,刘怀军,等.自体血栓栓塞性兔大脑中动脉脑梗死影像学模型的建立.临床放射学杂志,2008,27:1266-1269.
[64] Murphy BD, Chen X, Lee TY. Serial changes in CT cerebral blood volume and flowafter4hours of middle cerebral occlusion in an animal model of embolic cerebralischemia. AJNR,2007,28:743-749.
[65] Benes V, Zabramski JM, Boston M, et al. Effect of intra-arterial tissue plasminogenactivator and urokinase on autologous arterial emboli in the cerebral circulation ofrabbits. Stroke,1990,21:1594-1599.
[66] Brown AT, Skinner RD, Flores R, et al. Stroke location and brain function in anembolic rabbit stroke model. J Vasc Interv Radiol,2010,21:903-909.
[67] Culp BC, Brown AT, Erdem E, et al. Selective intracranial magnification angiographyof the rabbit: Basic techniques and anatomy. JVIR,2007,18:187-192.
[68]冯雷,潘力,冯光,等.介入技术制作兔大脑中动脉闭塞模型的研究.重庆医学,2011,40:535-538.
[69]李世德,杨丹,王永亮,等.兔低位腹主动脉阻断后血流动力学的变化.广西医科大学学报2012,29:17-18.
[70]武钢,王赞智,张弛,等.体外腹主动脉末端阻断动物犬模型的建立及意义.创伤外科杂志,2011,13:159-162.
[71]张永飞.腹主动脉阻断术的临床应用研究.中华创伤杂志,2002,18:464-466.
[1] Culp BC, Brown AT, Erdem E, Lowery J, Culp WC. Selective intracranialmagnification angiography of the rabbit: Basic techniques and anatomy. JVIR,2007,18:187-192.
[2] Murphy BD, Chen X, Lee TY. Serial changes in CT cerebral blood volume and flowafter4hours of middle cerebral occlusion in an animal model of embolic cerebralischemia. AJNR,2007,28:743-749.
[3] Hennings LJ, Flores R, Roberson PK, et al. Persistent penumbra in a rabbit strokemodel: incidence and histologic characteristics. Stroke Res Treat,2011:76-83.
[4] Kelly ME, Schültke E, Fiedler S, et al. Synchrotron-based intravenous cerebralangiography in a small animal model. Phys Med Biol,2007,52:1001-1012.
[5] Musella R. Anatomy of the normal carotid circulation and effects of the bilateralligature of various branches of the common carotid artery bifurcation. Arteriographicstudy in rabbits. Boll Soc Ital Biol Sper,1964,40:417-418.
[6] Hillman B, Rumbaugh C. One-catheter technique for magnification carotid andvertebral angiography in the rabbit. Invest Radiol.1977,12:373-375.
[7] Klimek E, Fournier D, Montanera W, et al. Selective transfemoral cerebralangiography of the rabbit. Technique and applications. J Neuroradiol,1990,17:20-25.
[8] Harder DR, Schulte ML, Clough AV, et al. An angiographic method for in vivo studyof arteries of the circle of Willis in small animals. Am J Physiol,1992,263(5Pt2):H1616-622.
[9] Culp WC, Woods SD, Brown AT, et al. Three variations in rabbit angiographic strokemodels. J Neurosci Methods,2013,212:322-328.
[10] Chen W, Qi J, Zhang J, Huang W, et al. Dynamic changes of the CT perfusionparameters in the embolic model of cerebral ischemia. J Huazhong Univ SciTechnolog Med Sci,2004,24:615-617.
[11] Yenari MA, de Crespigny A, Palmer JT, et al. Improved perfusion with rt-PA andhirulog in a rabbit model of embolic stroke. J Cereb Blood Flow Metab,1997,17:401-411.
[12] Caldwell B, Flores R, Lowery J, et al. Variations in the circle of Willis in the NewZealand white rabbit. JVIR,2011,22:1188-1192.
[13] Kapoor K, Kak VK, Singh B. Morphology and comparative anatomy of circulusarteriosus cerebri in mammals.Anat Histol Embryol,2003,32:347-355.
[14]闫峰,吉训明,宣芸,等.新西兰家兔大脑中动脉闭塞脑缺血模型建立的经验.首都医科大学学报,2010,31:79-83.
[15]林燕,杨佩钢,余琦,等.自体血栓性家兔局部脑缺血性梗死模型的建立.南方医科大学学报,2009,29:2291-2294.
[16]孔令琦,谢敬霞,韩鸿宾,等.提高线栓法大脑中动脉闭塞性兔脑缺血模型稳定性和可重复性的研究.中国医学影像技术,2004,20:209-212.
[17]全冠民,袁涛,刘怀军,等.自体血栓栓塞性兔大脑中动脉脑梗死影像学模型的建立.临床放射学杂志,2008,27:1266-1269.
[18]陈丽,戴炯,严国锋,等.血管内介入技术制作兔局灶性脑缺血模型.海交通大学学报（医学版）,2012,32:585-588.
[19]李凌鑫，樊小农，石学敏.大脑中动脉阻塞法建立局灶性脑缺血模型的研究进展[J].中华神经科杂志，2009，42（42）：208-210.
[20] Brown AT, Skinner RD, Flores R, et al. Stroke location and brain function in anembolic rabbit stroke model. JVIR,2010,21:903-909.
[21] Kirchhof K, Welzel T, Zoubaa S, et al. New method of embolus preparation forstandardized embolic stroke in rabbits. Stroke,2002,33:2329-2333.
[22] Lee JS, Hamilton MG, Zabramski JM．Variations in the anatomy of the rabbit cervicalcarotid artery. Stroke,1994,25:501-503.
[23] Jaban R, Stewart D, Vinters HV, et a1. Middle cerebral artery occlusion in the rabbitusing selective angiography: application for assessment of thrombolysis. Stroke,2008,39:1613-1615．
[24]杨飞,姜建威,王鹏,等.新西兰大白兔脑血管造影：脑底动脉环的解剖与变异.介入放射学杂志,2013,22:216-218.
[25] Brown A, Woods S, Skinner R, et al. Neurological Assessment Scores in RabbitEmbolic Stroke Models. Open Neurol J,2013,31:38-43.
[26] Huisa BN, Chen Y, Meyer BC, et al. Incremental treatments with laser therapyaugments good behavioral outcome in the rabbit small clot embolic stroke model.Lasers Med Sci,2013,28:1085-1089.
[1]李凌鑫,樊小农,石学敏.大脑中动脉阻塞法建立局灶性脑缺血模型的研究进展.中华神经科杂志,2009,42:208-210.
[2]孔令琦,谢敬霞,韩鸿宾,等.提高线栓法大脑中动脉闭塞性兔脑缺血模型稳定性和可重复性的研究.中国医学影像技术,2004,20:209-212.
[3]全冠民,袁涛,刘怀军,等.自体血栓栓塞性兔大脑中动脉脑梗死影像学模型的建立.临床放射学杂志,2008,27:1266-1269.
[4] Murphy BD, Chen X, Lee TY. Serial changes in CT cerebral blood volume and flowafter4hours of middle cerebral occlusion in an animal model of embolic cerebralischemia. AJNR,2007,28:743-749.
[5] Benes V, Zabramski JM, Boston M, et al. Effect of intra-arterial tissue plasminogenactivator and urokinase on autologous arterial emboli in the cerebral circulation ofrabbits. Stroke,1990,21:1594-1599.
[6] Brown AT, Skinner RD, Flores R, et al. Stroke location and brain function in anembolic rabbit stroke model. J Vasc Interv Radiol,2010,21:903-909.
[7] Culp BC, Brown AT, Erdem E, et al. Selective intracranial magnification angiographyof the rabbit: Basic techniques and anatomy. JVIR,2007,18:187-192.
[8] Caldwell B, Flores R, Lowery J, et al. Variations in the circle of Willis in the NewZealand white rabbit. JVIR,2011,22:1188-1192.
[9]冯雷,潘力,冯光,等.介入技术制作兔大脑中动脉闭塞模型的研究.重庆医学,2011,40:535-538.
[10] Hennings LJ, Flores R, Roberson PK, et al. Persistent penumbra in a rabbit strokemodel: incidence and histologic characteristics. Stroke Res Treat,2011,2011:76-83.
[11] Burgess A, Huang Y, Waspe AC, et al. High-intensity focused ultrasound (HIFU) fordissolution of clots in a rabbit model of embolic stroke. PLoS One,2012,7:e42311.
[12] Lapchak PA, Doyan S, Fan X, et al. Synergistic Effect of AJW200, a von WillebrandFactor Neutralizing Antibody with Low Dose (0.9mg/mg) Thrombolytic TherapyFollowing Embolic Stroke in Rabbits. J Neurol Neurophysiol,2013,4(2). doi:10.4172/2155-9562.1000146.
[13] Culp WC, Woods SD, Skinner RD, et al. Dodecafluoropentane emulsion decreasesinfarct volume in a rabbit ischemic stroke model. J Vasc Interv Radiol,2012,23:116-121.
[14] Brown A, Woods S, Skinner R, et al. Neurological Assessment Scores in RabbitEmbolic Stroke Models. Open Neurol J,2013,31:38-43.
[15] Huisa BN, Chen Y, Meyer BC, et al. Incremental treatments with laser therapyaugments good behavioral outcome in the rabbit small clot embolic stroke model.Lasers Med Sci,2013,28:1085-1089.
[16] Meyer DM, Compton P, Eastwood JA, et al. Antiplatelet loading improves behavioraloutcome in a rabbit model of stroke. Stroke,2013,44:3246-3248.
[17] Woods SD, Skinner RD, Ricca AM, et al. Progress in dodecafluoropentane emulsionas a neuroprotective agent in a rabbit stroke model. Mol Neurobiol,2013,48:363-367.
[1] Reinhard M, Wihler C, Roth M, et al. Cerebral autoregulation dynamics in acuteischemic stroke after rtPA thrombolysis. Cerebrovasc Dis,2008,26:147-155.
[2] Strandgaard S, Paulson OB. Cerebral auto-regulation. Stroke,1984,15:413-416.
[3] Adams HP, del Zoppo G, Alberts MJ, et al. Guidelines for the early management ofadults with ischemic stroke. Stroke,2007,38:1655-1711.
[4] Ogoh S, Brothers RM, Barnes Q, et al. The effect of changes in cardiac output onmiddle cerebral artery mean blood velocity at rest and during exer-cise. J Physiol,2005,569:697-704.
[5] Liebeskind DS. Aortic occlusion for cerebral ischemia: from theory to practice. CurrCardiol Rep,2008,10:31-36.
[6] Stokland O, Miller MM, Ilebekk A, et al. Mechanism of hemodynamic responses toocclusion of the descending thoracic aorta. Am J Physiol,1980,238:H423-H429.
[7] Saether OD, Juul R, Aadahl P, et al. Cerebral haemodynamics during thoracic-andthoracoabdominal aortic aneurysm repair. Eur J Vasc Endovasc Surg,1996,12:81-85.
[8] Stromholm T, Dale LG, Saether OD, et al. Selective carotid angiography duringcross-clamping of the descending thoracic aorta in pigs. Int Angiol,1996,15:263-267.
[9] Nussbaum ES, Heros RC, Solien EE, et al. Intra-aortic balloon counterpulsationaugments cerebral blood flow in a canine model of subarachnoid hemorrhage-inducedcerebral vasospasm. Neurosurgery,1995,36:879-884.
[10] Gelman S, Rabbani S, Bradley EL Jr. Inferior and superior vena caval blood flowsduring cross-clamping of the thoracic aorta in pigs. J Thorac Cardiovasc Surg,1988,96:387-392.
[11] Hammer M, Jovin T, Wahr JA, et al. Partial occlusion of the descending aortaincreases cerebral blood flow in a nonstroke porcine model. Cerebrovasc Dis,2009,28:406-410.
[12] Lylyk P, Vila JF, Miranda C, et al. Partial aortic obstruction improves cerebralperfusion and clinical symptoms in patients with symptomatic vasospasm. Neurol Res,2005,27:Suppl1:S129-135.
[13] Noor R, Wang CX, Todd K, et al. Partial Intra-Aortic Occlusion Improves PerfusionDeficits and Infarct Size Following Focal Cerebral Ischemia. J Neuroimaging,2010,20:272-276.
[14] Campbell MS, Grotta JC, Gomez CR, et al. Perfusion augmentation in stroke usingcontrolled aortic obstruction: pilot study results. Stroke,2004,35:291.
[15] Hussain MS, Bhagat YA, Liu S, et al. DWI Lesion Volume Reduction FollowingAcute Stroke Treatment with Transient Partial Aortic Obstruction. J Neuroimaging,2010,20:379-381.
[16] Shuaib A, Bornstein NM, Diener HC, et al. Partial aortic occlusion for cerebralperfusion augmentation: safety and efficacy of NeuroFlo in Acute Ischemic Stroketrial. Stroke,2011,42:1680-90.
[17] Lutsep HL, Altafullah IM, Roberts R, et al. Neurologic safety event rates in theSENTIS trial control population. Acta Neurol Scand,2013,127:e5-7.
[18] Leker RR, Molina C, Cockroft K, et al. Effects of age on outcome in the SENTIS trial:better outcomes in elderly patients. Cerebrovasc Dis,2012,34:263-271.
[19] Shuaib A, Schwab S, Rutledge JN, et al. Importance of proper patient selection andendpoint selection in evaluation of new therapies in acute stroke: further analysis ofthe SENTIS trial. J Neurointerv Surg,2013,5Suppl1:i21-4.
[20] Hammer MD, Schwamm L, Starkman S, et al. Safety and feasibility of NeuroFlo usein eight-to24-hour ischemic stroke patients. Int J Stroke,2012,7:655-661.
[21] Saqqur M, Ibrahim M, Butcher K, et al. Transcranial Doppler and CerebralAugmentation in Acute Ischemic Stroke. J Neuroimaging,2013,23:460-465.
[22] Emery DJ, Schellinger PD, Selchen D, et al. Safety and feasibility of collateral bloodflow augmentation after intravenous thrombolysis. Stroke,2011,42:1135-1137.
[23] Schellinger PD, Shuaib A, K hrmann M, et al. Reduced Mortality and SevereDisability Rates in the SENTIS Trial. AJNR Am J Neuroradiol.2013,34:2312-2316.
[24] Schellinger PD, K hrmann M, Liu S, et al. Favorable vascular profile is anindependent predictor of outcome: a post hoc analysis of the safety and efficacy ofNeuroFlo Technology in Ischemic Stroke trial. Stroke,2013,44:1606-1608.
[1]黄斌,赵纪春,马玉奎,等.低位腹主动脉内球囊阻断技术在骨盆和骶骨肿瘤切除术中的应用.中国普外基础与临床杂志,2011,18:635-638.
[2]徐懋,张耕,韦峰,等.球囊阻断低位腹主动脉在腰骶骨肿瘤手术中的应用.中国微创外科杂志,2010,10:147-149.
[3]李世德,詹新立,韦玮,等.暂时低位腹主动脉阻断用于骨盆、骶骨肿瘤切除术的安全性探讨.中华骨科杂志,2009,29:1038-1042.
[4]张晓庆,刘健慧,朱颖霞,等.低位腹主动脉球囊阻断技术在复杂骨盆和盆腔部位手术中的应用.临床麻醉学杂志,2008,24:17-19.
[5] Martinelli T, Thony F, Decléty P, et al. Intra-aortic balloon occlusion to salvagepatients with life-threatening hemorrhagic shocks from pelvic fractures. J Trauma,2010,68:942-948.
[6] Usman N, Noblet J, Low D, Thangaratinam S. Intra-aortic balloon occlusion withoutfluoroscopy for severe postpartum haemorrhage secondary to placenta percreta. Int JObstet Anesth.2014,23:91-93.
[7] S vik E, Stokkeland P, Storm BS, et al. The use of aortic occlusion balloon catheterwithout fluoroscopy for life-threatening post-partum haemorrhage. Acta AnaesthesiolScand,2012,56:388-393.
[8] Abu-Zidan FM. Should intra-aortic balloon occlusion be used to stop bleeding fromsevere pelvic fractures? J Trauma,2010,69:1005-1006.
[9] Liebeskind DS. Aortic occlusion for cerebral ischemia: from theory to practice. CurrCardiol Rep,2008,10:31-36.
[10] Hammer M, Jovin T, Wahr JA, et al. Partial occlusion of the descending aortaincreases cerebral blood flow in a nonstroke porcine model. Cerebrovasc Dis,2009,28:406-410.
[11] Lylyk P, Vila JF, Miranda C, et al. Partial aortic obstruction improves cerebralperfusion and clinical symptoms in patients with symptomatic vasospasm. Neurol Res,2005,27:Suppl1:S129-135.
[12] Noor R, Wang CX, Todd K, et al. Partial Intra-Aortic Occlusion Improves PerfusionDeficits and Infarct Size Following Focal Cerebral Ischemia. J Neuroimaging,2010,20:272-276.
[13] Campbell MS, Grotta JC, Gomez CR, et al. Perfusion augmentation in stroke usingcontrolled aortic obstruction: pilot study results. Stroke,2004,35:291.
[14] Hussain MS, Bhagat YA, Liu S, et al. DWI Lesion Volume Reduction FollowingAcute Stroke Treatment with Transient Partial Aortic Obstruction. J Neuroimaging,2010,20:379-381.
[15] Uflacker R, Sch nholz C, Papamitisakis N. Interim report of the SENTIS trial:cerebral perfusion augmentation via partial aortic occlusion in acute ischemic stroke. JCardiovasc Surg,2008,49:715-721.
[16] Shuaib A, Bornstein NM, Diener HC, et al. Partial aortic occlusion for cerebralperfusion augmentation: safety and efficacy of NeuroFlo in Acute Ischemic Stroketrial. Stroke,2011,42(6):1680-1690.
[17] Lutsep HL, Altafullah IM, Roberts R, et al. Neurologic safety event rates in theSENTIS trial control population. Acta Neurol Scand,2013,127:e5-7.
[18] Leker RR, Molina C, Cockroft K, et al. Effects of age on outcome in the SENTIS trial:better outcomes in elderly patients. Cerebrovasc Dis,2012,34:263-271.
[19] Shuaib A, Schwab S, Rutledge JN, et al. Importance of proper patient selection andendpoint selection in evaluation of new therapies in acute stroke: further analysis ofthe SENTIS trial. J Neurointerv Surg,2013,5Suppl1:i21-4.
[20] Hammer MD, Schwamm L, Starkman S, et al. Safety and feasibility of NeuroFlo usein eight-to24-hour ischemic stroke patients. Int J Stroke,2012,7:655-661.
[21] Saqqur M, Ibrahim M, Butcher K, et al. Transcranial Doppler and CerebralAugmentation in Acute Ischemic Stroke. J Neuroimaging,2013,23:460-465.
[22] Emery DJ, Schellinger PD, Selchen D, et al. Safety and feasibility of collateral bloodflow augmentation after intravenous thrombolysis. Stroke,2011,42:1135-1137.
[23] Schellinger PD, Shuaib A, K hrmann M, et al. Reduced Mortality and SevereDisability Rates in the SENTIS Trial. AJNR Am J Neuroradiol.2013,34:2312-2316.
[24] Schellinger PD, K hrmann M, Liu S, et al. Favorable vascular profile is anindependent predictor of outcome: a post hoc analysis of the safety and efficacy ofNeuroFlo Technology in Ischemic Stroke trial. Stroke,2013,44:1606-1608.
[25] Shuaib A, Butcher K, Mohammad AA, et al. Collateral blood vessels in acuteischaemic stroke: a potential therapeutic target. Lancet Neurol,2011,10:909-921.
[26] Liebeskind DS. Reperfusion for acute ischemic stroke: arterial revascularization andcollateral therapeutics. Curr Opin Neurol.2010,23:36-45.
[27] Hennerici MG, Kern R, Szabo K. Non-pharmacological strategies for the treatment ofacute ischaemic stroke. Lancet Neurol,2013,12:572-584.
[28] Winship IR, Armitage GA, Ramakrishnan G, et al. Augmenting collateral blood flowduring ischemic stroke via transient aortic occlusion. J Cereb Blood Flow Metab,2014,34:61-71.
[29]曲度,曲强,张弦,等.腹主动脉阻断术临床原理及其上中下段安全时限探讨.海南医学,2009,20:1-13.
[30] Storkland O, Miller MM, Ilebekk A, et al. Mechanism of hemodynamic responses toocclusion of the descending thoracic aorta. Am J Physiol,1980,238:H42-H429.
[31] Hammer M, Jovin T, Wahr JA, et al. Partial occlusion of the descending aortaincreases cerebral blood flow in a nonstroke porcine model. Cerebrovasc Dis,2009,28:406-410.
[32]李世德,杨丹,王永亮,等.兔低位腹主动脉阻断后血流动力学的变化.广西医科大学学报2012,29:17-18.
[33]武钢,王赞智,张弛,等.体外腹主动脉末端阻断动物犬模型的建立及意义.创伤外科杂志,2011,13:159-162.
[34]张永飞.腹主动脉阻断术的临床应用研究.中华创伤杂志,2002,18:464-466.
[35]曲度,张弦.腹主动脉阻断后及撒钳后综合征的发生机制.杭州医学高等专科学校学报,200l,22:44-48.
[1]阮志兵.急性脑梗死CT脑灌注成像研究进展.实用放射学杂志,2012,28:1961-1963.
[2] Nabavi DG, Cenic A, Dool J, et al. Quantitative assessment of cerebralhemodynamics using CT: stability, accuracy, and precision studies in dogs. J ComputAssist Tomogr,1999,23:506-515.
[3] Cenic A, Nabavi DG, Craen RA, et al. Dynamic CT measurement of cerebral bloodflow: a validation study. AJNR Am J Neuroradiol1999,20:63-73.
[4] Derdeyn CP, Videen TO, Yundt KD, et al. Variability of cerebral blood volume andoxygen extraction: stages of cerebral haemodynamic impairment revisited. Brain2002,125:595-607
[5] Murphy BD, Chen X, Lee TY. Serial changes in CT cerebral blood volume and flowafter4hours of middle cerebral occlusion in an animal model of embolic cerebralischemia. AJNR Am J Neuroradiol.2007,28:743-749.
[6] Sette G, Baron JC, Mazoyer B, et al. Local brain haemodynamics and oxygenmetabolismin cerebrovascular disease.Positron emission tomography. Brain,1989,112:931-951.
[7] Liebeskind DS. Aortic occlusion for cerebral ischemia: from theory to practice. CurrCardiol Rep,2008,10:31-36.
[8] Stokland O, Miller MM, Ilebekk A, et al. Mechanism of hemodynamic responses toocclusion of the descending thoracic aorta. Am J Physiol,1980,238:H423-H429.
[9] Saether OD, Juul R, Aadahl P, et al. Cerebral haemodynamics during thoracic-andthoracoabdominal aortic aneurysm repair. Eur J Vasc Endovasc Surg,1996,12:81-85.
[10] Stromholm T, Dale LG, Saether OD, et al. Selective carotid angiography duringcross-clamping of the descending thoracic aorta in pigs. Int Angiol,1996,15:263-267.
[11] Hammer M, Jovin T, Wahr JA, et al. Partial occlusion of the descending aortaincreases cerebral blood flow in a nonstroke porcine model. Cerebrovasc Dis,2009,28:406-410.
[12] Campbell MS, Grotta JC, Gomez CR, et al. Perfusion augmentation in stroke usingcontrolled aortic obstruction: pilot study results. Stroke,2004,35:291.
[13] Saether OD, Juul R, Aadahl P, et al. Cerebral haemodynamics during thoracic-andthoracoabdominal aortic aneurysm repair. Eur J Vasc Endovasc Surg,1996,12:81-85.
[14] Nussbaum ES, Heros RC, Solien EE, et al. Intra-aortic balloon counterpulsationaugments cerebral blood flow in a canine model of subarachnoid hemorrhage-inducedcerebral vasospasm. Neurosurgery,1995,36:879-884.
[15] Gelman S, Rabbani S, Bradley EL Jr. Inferior and superior vena caval blood flowsduring cross-clamping of the thoracic aorta in pigs. J Thorac Cardiovasc Surg,1988,96:387-392.
[16] Pranevicius O, Pranevicius M, Liebeskind DS. Partial aortic occlusion and cerebralvenous steal: venous effects of arterial manipulation in acute stroke. Stroke,2011,42:1478-1481.
[17] Pranevicius O, Pranevicius M, Pranevicius H, et al. Transition to collateral flow afterarterial occlusion predisposes to cerebral venous steal. Stroke.2012,43:575-579.
[18] Hatashita S, Hoff JT. Cortical tissue pressure gradients in early ischemic brain edema.J Cereb Blood Flow Metab,1986,6:1-7.
[19] Iannotti F, Hoff JT, Schielke GP. Brain tissue pressure in focal cerebral ischemia. JNeurosurg,1985,62:83-89.
[20] Pranevicius M, Pranevicius O. Cerebral venous steal: blood low diversion withincreased tissue pressure. Neurosurgery,2002,51:1267-1273.
[21] Ames A III, Wright RL, Kowada M, et al. Cerebral ischemia. II. The no-reflowphenomenon. Am J Pathol,1968,52:437-453.
[22] Alexandrov AV, Hall CE, Labiche LA, et al. Ischemic stunning of the brain: earlyrecanalization without immediate clinical improvement in acute ischemic stroke.Stroke,2004,35:449-452.
[23] Noor R, Wang CX, Todd K, et al. Partial Intra-Aortic Occlusion Improves PerfusionDeficits and Infarct Size Following Focal Cerebral Ischemia. J Neuroimaging,2010,20:272-276.
[24] Hussain MS, Bhagat YA, Liu S, et al. DWI Lesion Volume Reduction FollowingAcute Stroke Treatment with Transient Partial Aortic Obstruction. J Neuroimaging,2010,20:379-381.
[25] Shuaib A, Bornstein NM, Diener HC, et al. Partial aortic occlusion for cerebralperfusion augmentation: safety and efficacy of NeuroFlo in Acute Ischemic Stroketrial. Stroke,2011,42:1680-90.
[26] Lutsep HL, Altafullah IM, Roberts R, et al. Neurologic safety event rates in theSENTIS trial control population. Acta Neurol Scand,2013,127:e5-7.
[27] Leker RR, Molina C, Cockroft K, et al. Effects of age on outcome in the SENTIS trial:better outcomes in elderly patients. Cerebrovasc Dis,2012,34:263-271.
[28] Shuaib A, Schwab S, Rutledge JN, et al. Importance of proper patient selection andendpoint selection in evaluation of new therapies in acute stroke: further analysis ofthe SENTIS trial. J Neurointerv Surg,2013,5Suppl1:i21-4.
[29] Hammer MD, Schwamm L, Starkman S, et al. Safety and feasibility of NeuroFlo usein eight-to24-hour ischemic stroke patients. Int J Stroke,2012,7:655-661.
[30] Saqqur M, Ibrahim M, Butcher K, et al. Transcranial Doppler and CerebralAugmentation in Acute Ischemic Stroke. J Neuroimaging,2013,23:460-465.
[31] Emery DJ, Schellinger PD, Selchen D, et al. Safety and feasibility of collateral bloodflow augmentation after intravenous thrombolysis. Stroke,2011,42:1135-1137.
[32] Schellinger PD, Shuaib A, K hrmann M, et al. Reduced Mortality and SevereDisability Rates in the SENTIS Trial. AJNR Am J Neuroradiol,2013,34:2312-2316.
[33] Schellinger PD, K hrmann M, Liu S, et al. Favorable vascular profile is anindependent predictor of outcome: a post hoc analysis of the safety and efficacy ofNeuroFlo Technology in Ischemic Stroke trial. Stroke,2013,44:1606-1608.
[1] Nogueira RG, Yoo AJ, Buonanno FS, et al. Endovascular approaches to acute stroke,part2: a comprehensive review of studies and trials. AJNR,2009,30:859-875.
[2] Okahara M, Kiyosue H, Mori H, et al. Anatomic variations of the cerebral arteries andtheir embrayology: A pictorial review. Eur Radiol,2002,12:2548-2561.
[3] Liebeskind DS. Collateral circulation. Stroke,2003,34:2279-2284.
[4] Wei L，Erinjeri JP，Rovainen CM，et a1. Collateral growth and angiogenesis aroundcortical stroke. Stroke,200l,32:2179-2184．
[5] Kuroda S, Houkin K. Moyamoya disease: current concepts and future perspectives.Lancet Neurol.2008,7:1056-1066.
[6] Orosz L, Hoksbergen AW, Molnár C, et al. Clinical applicability of a mathematicalmodel in assessing the functional ability of the communicating arteries of the circle ofWillis. J Neurol Sci,2009,15:278:94-99.
[7] Liebeskind DS, Cotsonic GA, Saver JL, et al. Collateral circulation in symptomaticintracranial atherosclerosis. J Cereb Blood Flow Metab,2010,31:1293-1301.
[8] Henderson RD, Eliasziw M, Fox AJ, et al. Angiographically defined collateralcirculation and risk of stroke in patients with severe carotid artery stenosis. NorthAmerican Symptomatic Carotid Endarterectomy Trial (NASCET) Group. Stroke,2000,31:128-132.
[9] Kitagawa K, Yagita Y, Sasaki T, et al. Chronic mild reduction of cerebral perfusionpressure induces ischemic tolerance in focal cerebral ischemia. Stroke,2005,36:2270-2274.
[10] Brozici M, van der Zwan A, Hillen B. Anatomy and Functionality of LeptomeningealAnastomoses: A Review. Stroke,2003,34:2750-2762.
[11] Lima FO, Furie KL, Silva GS, et al. The pattern of leptomeningeal collaterals on CTangiography is a strong predictor of long-term functional outcome in stroke patientswith large vessel intracranial occlusion. Stroke,2010,41:2316-2322.
[12] Ovbiagele B, Saver JL, Starkman S, et al. Statin enhancement of collateralization inacute. Neurology,2007,68:2129-2131.
[13] van Weel V, de Vries M, Voshol PJ, et al. Hypercholesterolemia reduces collateralartery growth more dominantly than hyperglycemia or insulin resistance in mice.Arterioscler Thromb Vasc Biol,2006,26:1383-1390.
[14] Liebeskind DS. Imaging the future of stroke: I ischemia. Ann Neurol,2009,66:575-590.
[15] Bang OY, Saver JL, Buck BH, et al. Impact of collateral flow on tissue fate in acuteischemic stroke. J Neurol Neurosurg Psychiatry,2007,79:625-629.
[16] Bozzao L, Fantozzi LM, Bastianello S, et al. Early collateral blood supply and lateparenchymal brain damage in the patients with middle cerebral artery occlusion.Stroke,1989,20:735-740.
[17] Higashida RT, Furlan AT, Roberts H, et al. Trial design and reporting standards forintra-arterial thrombolysis for acute ischemic stroke. Stroke,2003;34:e109-137.
[18] Kaufmann TJ, Huston J3rd, Mandrekar JN, et al. Complications of diagnosticcerebral angiography: evaluation of19,826consecutive patients. Radiology,2007,243:812-819.
[19] van Laar PJ, van der Grond J, Bremmer JP, et al. Assessment of the contribution ofthe external carotid artery to brain perfusion in patients with internal carotid arteryocclusion. Stroke,2008,39:3003-3008.
[20] Miteff F, Levi CR, Bateman GA, et al. The independent predictive utility of computedtomography angiographic collateral status in acute ischaemic stroke. Brain,2009,132:2231-2238.
[21] Maas MB, Lev MH, Ay H, et al. Collateral vessels on CT angiography predictoutcome in acute ischemic stroke. Stroke,2009,40:3001-3005.
[22] Choi JY, Kim EJ, Hong JM, et al. Conventional enhancement CT: a valuable tool forevaluating pial collateral flow in acute ischemic stroke. Cerebrovasc Dis,2011,31:346-352.
[23] Jung SL, Lee YJ, Ahn KJ, et al. Assessment of collateral flow with multi-phasic CT:correlation with diffusion weighted MRI in MCA occlusion. J Neuroimaging,2011,21:225-228.
[24] Gasparotti R, Grassi M, Mardighian D, et al. Perfusion CT in patients with acuteischemic stroke treated with intra-arterial thrombolysis: predictive value of infarctcore size on clinical outcome. AJNR Am J Neuroradiol,2009,30:722-727.
[25] Hoksbergen AW, Fülesdi B, Legemate DA, et al. Collateral configuration of thecircle of Willis: transcranial color-coded duplex ultrasonography and comparison withpostmortem anatomy. Stroke,2000,31:1346-1351.
[26] Sanossian N, Saver JL, Alger JR, et al. Angiography reveals that fluid-attenuatedinversion recovery vascular hyperintensities are due to slow flow, not thrombus.AJNR,2009,30:564-568.
[27] Cheng B, Ebinger M, Kufner A, et al. Hyperintense vessels on acute strokefluid-attenuated inversion recovery imaging: associations with clinical and other MRIfindings. Stroke,2012,43:2957-2961.
[28] Liu W, Xu G, Yue X, et al. Hyperintense vessels on FLAIR: a useful non-invasivemethod for assessing intracerebral collaterals. Eur J Radiol,2011,80:786-791.
[29] Liu W, Yin Q, Yao L, et al. Decreased hyperintense vessels on FLAIR images afterendovascular recanalization of symptomatic internal carotid artery occlusion. Eur JRadiol,2012,81:1595-1600.
[30] Haussen DC, Koch S, Saraf-Lavi E, et al. FLAIR Distal Hyperintense Vessels as aMarker of Perfusion-Diffusion Mismatch in Acute Stroke. J Neuroimaging,2013,23:397-400.
[31] Pérez de la Ossa N, Hernández-Pérez M, Domènech S, et al. Hyperintensity ofdistal vessels on FLAIR is associated with slow progression of the infarction in acuteischemic stroke. Cerebrovasc Dis,2012,34:376-384.
[32] Lee KY, Latour LL, Luby M, et al. Distal hyperintense vessels on FLAIR: an MRImarker for collateral circulation in acute stroke? Neurology,2009,72:1134-1139.
[33] Liebeskind DS, Cotsonis GA, Saver JL, et al. Collateral circulation in symptomaticintracranial atherosclerosis. J Cereb Blood Flow Metab,2011,31:1293-1301.
[34] Yamauchi H, Kudoh T, Sugimoto K, et al. Pattern of collaterals, type of infarcts, andhaemodynamic impairment in carotid artery occlusion. J Neurol Neurosurg Psychiatry,2004,75:1697-1701.
[35] Liebeskind DS, Cotsonis GA, Saver JL, et al. Collaterals dramatically alter stroke riskin intracranial atherosclerosis. Ann Neurol.2011,69:963-974.
[36] Romero JR, Pikula A, Nguyen TN, et al. Cerebral collateral circulation in carotidartery disease. Curr Cardiol Rev,2009,5:279-288.
[37] Liu XT, Wang W, Wang LJ, et al. Correlation of collateral circulation and prognosisin patients with acute cerebral infarction. Zhonghua Yi Xue Za Zhi,2011,22:766-768.
[38] Bang OY, Saver JL, Buck BH, et al. Impact of collateral flow on tissue fate in acuteischaemic stroke. J Neurol Neurosurg Psychiatry,2008,79:625-629.
[39] Liebeskind DS, Kim D, Starkman S, et al. Collateral failure? Late mechanicalthrombectomy after failed intravenous thrombolysis. J Neuroimaging,2010,20:78-82.
[40] Christoforidis GA, Mohammad Y, Kehagias D, et al. Angiographic assessment of pialcollaterals as a prognostic indicator following intra-arterial thrombolysis for acuteischemic stroke. AJNR Am J Neuroradiol,2005,26:1789-1797.
[41] Kucinski T, Koch C, Eckert B, et al. Collateral circulation is an independentradiological predictor of outcome after thrombolysis in acute ischaemic stroke.Neuroradiology,2003,45:11-18.
[42] Yasargil MG, Krayenbuhl HA, Jacobson JH. Microneurosurgical arterialreconstruction. Surgery,1970,67:221-233.
[43] Hofmeijer J, Klijn CJM, Kappelle LJ, et al. Collateral circulation via the ophthalmicartery or leptomeningeal vessels is associated with impaired cerebral vasoreactivity inpatients with symptomatic carotid artery occlusion. Cerebrovasc Dis,2002,14:22-26.
[44] The EC/IC bypass study group. Failure of extracranial-intracranial arterial bypass toreduce the risk of ischemic stroke. Results of an international randomized trial. NEngl J Med,1985,313:1191-1200.
[45] Grubb RL, Derdeyn CP, Fritsch SM, et al. Importance of hemody namic factors in theprognosis of symptomatic carotid occlusion. JAMA,1998,280:1055-1060
[46] Derdeyn CP, Gage BF, Grubb RL, et al. Cost-effectiveness analysis of therapy forsymptomatic carotid occlusion:PET screening before selective extracranial-to-intracranial bypass versus medical treatment. J Nucl Med,2000,41:800-807.
[47] Powers WJ, Clarke WR, Grubb RL, et al. Extracranial-intracranial bypass surgery forstroke prevention in hemodynamic cerebral ischemia:The carotid occlusion surgerystudy randomized trial. JAMA,2011,306:1983-1992.
[48]黄家星，林文华，刘丽萍，等.缺血性卒中侧支循环评估与干预中国专家共识.中国卒中杂志,2013,8:285-293.
[49] Adams HP, del Zoppo G, Alberts MJ, et al. Guidelines for the early management ofadults with ischemic stroke. Stroke,2007,38:1655-1711.
[50] Hsu CY, Norris JW, Hogan EL, et al. Propentofylline in non-hemorrhagic stroke: arandomized placebo-controlled double-blinded controlled trial. Stroke,1988,19:716-722.
[51] Chan YW, Kay CS. Pentoxifylline in the treatment of acute ischaemic stroke: areappraisal in Chinese stroke patients. Clin Exp Neurol,1993,13:526-530.
[52] Eames PJ, Blake MJ, Dawson SL, et al. Dynamic cerebral autoregulation and beat tobeat blood pressure control are impaired in acute ischaemic stroke. J NeurolNeurosurg Psychiatry,2002,72:467-472.
[53] Smith HA, Thompson-Dobkin J, Yonas H, et al. Correlation of xenon-enhancedcomputed tomography-defned cerebral blood fow reactivity and collateral fowpatterns. Stroke,1994,25:1784-1787.
[54] Schwarz S, Georgiadis D, Aschoff A, et al. Effects of induced hyper tension onintracranial pressure and flow velocities of the middle cerebral arteries in patientswith large hemispheric stroke. Stroke,2002,33:998-1004.
[54] Hillis AE, Ulatowski JA, Barker PB, et al. A pilot randomized trial of induced bloodpressure elevation:Effects on function and focal perfusion in acute and subacutestroke. Cerebrovasc Dis,2003,16:236-246.
[56] Rordorf G, Cramer SC, Efird JT, et al. Pharmacological elevation of blood pressure inacute stroke. Clinical effects and safety. Stroke,1997,28:2133-2138.
[57] Rordorf G, Cramer SC, E? rd JT, et al. Pharmacological elevation of blood pressurein acute stroke: clinical e? ects and safety. Stroke,1997,28:2133-2138.
[58] Wityk RJ, Restrepo L. Hypoperfusion and its augmentation in patients with brainischemia. Curr Treat Options Cardiovasc Med,2003,5:193-199.
[59] Amin-Hanjani S, Barker FG, Charbel FT, et al. Extracranial-intracranial bypass forstroke-is this the end of the line or a bump in the road?. Neurosurgery,2012,71:557-561.
[60] Zheng ZS, Li TM, Kambic H, et al. Sequential external counterpulsation(SECP) inChina. Trans Am Soc Artif Intern Organs,1983,29:599-603.
[61] Werner D, Schneider M, Weise M, et al. Pneumatic external counterpulsation:A newnoninvasive method to improve organ perfusion. Am J Cardiol,1999,84:950-952.
[62] Arora RR, Chou TM, Jain D, et al. The multicenter study of enhanced externalcounterpulsation(MUST-EECP):Ef fect of EECP on exercise-induced myocardialischemia and anginal episodes. J Am Coll Cardiol,1999,33:1833-1840.
[63] Lin W, Xiong L, Han J, et al. External counterpulsation augments blood pressure andcerebral flow velocities in ischemic stroke patients with cerebral int racranial largeartery occlusive disease. Stroke,2012,43:3007-3011.
[64] Masuda D, Nohara R, Hirai T, et al. Enhanced external counterpulsation improvedmyocardial perfusion and coronary fow reserve in patients with chronic stableangina:evaluation by(13)n-ammonia positron emission tomography. Eur Heart J,2001,22:1451-1458.
[65] Lin W, Xiong L, Han J, et al. External counterpulsation augments blood pressure andcerebral flow velocities in ischemic stroke patients with cerebral intracranial largeartery occlusive disease. Stroke,2012,43:3007-3011.
[66] Han JH, Leung TW, Lain WW. Preliminary findings of external counterpulsation forischemic stroke patient with large artery occlusive disease. Stroke,2008,39:1340-1343.
[67] Liebeskind DS. Aortic occlusion for cerebral ischemia: from theory to practice. CurrCardiol Rep,2008,10:31-36.
[68] Stokland O, Miller MM, Ilebekk A, et al. Mechanism of hemodynamic responses toocclusion of the descending thoracic aorta. Am J Physiol,1980,238:H423-H429.
[69] Saether OD, Juul R, Aadahl P, et al. Cerebral haemodynamics during thoracic-andthoracoabdominal aortic aneurysm repair. Eur J Vasc Endovasc Surg,1996,12:81-85.
[70] Stromholm T, Dale LG, Saether OD, et al. Selective carotid angiography duringcross-clamping of the descending thoracic aorta in pigs. Int Angiol,1996,15:263-267.
[71] Nussbaum ES, Heros RC, Solien EE, et al. Intra-aortic balloon counterpulsationaugments cerebral blood flow in a canine model of subarachnoid hemorrhage-inducedcerebral vasospasm. Neurosurgery,1995,36:879-884.
[72] Gelman S, Rabbani S, Bradley EL Jr. Inferior and superior vena caval blood flowsduring cross-clamping of the thoracic aorta in pigs. J Thorac Cardiovasc Surg,1988,96:387-392.
[73] Hatashita S, Hoff JT. Cortical tissue pressure gradients in early ischemic brain edema.J Cereb Blood Flow Metab,1986,6:1-7.
[74] Iannotti F, Hoff JT, Schielke GP. Brain tissue pressure in focal cerebral ischemia. JNeurosurg,1985,62:83-89.
[75] Pranevicius M, Pranevicius O. Cerebral venous steal: blood low diversion withincreased tissue pressure. Neurosurgery,2002,51:1267-1273.
[76] Ames A III, Wright RL, Kowada M, et al. Cerebral ischemia. II. The no-reflowphenomenon. Am J Pathol,1968,52:437-453.
[77] Alexandrov AV, Hall CE, Labiche LA, et al. Ischemic stunning of the brain: earlyrecanalization without immediate clinical improvement in acute ischemic stroke.Stroke,2004,35:449-452.
[78] Pranevicius O, Pranevicius M, Liebeskind DS. Partial aortic occlusion and cerebralvenous steal: venous effects of arterial manipulation in acute stroke. Stroke,2011,42:1478-1481.
[79] Pranevicius O, Pranevicius M, Pranevicius H, et al. Transition to collateral flow afterarterial occlusion predisposes to cerebral venous steal. Stroke,2012,43,575-579.
[80] Hammer M, Jovin T, Wahr JA, et al. Partial occlusion of the descending aortaincreases cerebral blood flow in a nonstroke porcine model. Cerebrovasc Dis,2009,28:406-410.
[81] Lylyk P, Vila JF, Miranda C, et al. Partial aortic obstruction improves cerebralperfusion and clinical symptoms in patients with symptomatic vasospasm. Neurol Res,2005,27:Suppl1:S129-135.
[82] Noor R, Wang CX, Todd K, et al. Partial Intra-Aortic Occlusion Improves PerfusionDeficits and Infarct Size Following Focal Cerebral Ischemia. J Neuroimaging,2010,20:272-276.
[83] Campbell MS, Grotta JC, Gomez CR, et al. Perfusion augmentation in stroke usingcontrolled aortic obstruction: pilot study results. Stroke,2004,35:291.
[84] Hussain MS, Bhagat YA, Liu S, et al. DWI Lesion Volume Reduction FollowingAcute Stroke Treatment with Transient Partial Aortic Obstruction. J Neuroimaging,2010,20:379-381.
[85] Uflacker R, Sch nholz C, Papamitisakis N. Interim report of the SENTIS trial:cerebral perfusion augmentation via partial aortic occlusion in acute ischemic stroke. JCardiovasc Surg,2008,49:715-721.
[86] Shuaib A, Bornstein NM, Diener HC, et al. Partial aortic occlusion for cerebralperfusion augmentation: safety and efficacy of NeuroFlo in Acute Ischemic Stroketrial. Stroke,2011,42:1680-1690.
[87] Lutsep HL, Altafullah IM, Roberts R, et al. Neurologic safety event rates in theSENTIS trial control population. Acta Neurol Scand,2013,127:e5-7.
[88] Leker RR, Molina C, Cockroft K, et al. Effects of age on outcome in the SENTIS trial:better outcomes in elderly patients. Cerebrovasc Dis,2012,34:263-271.
[89] Shuaib A, Schwab S, Rutledge JN, et al. Importance of proper patient selection andendpoint selection in evaluation of new therapies in acute stroke: further analysis ofthe SENTIS trial. J Neurointerv Surg,2013,5Suppl1:i21-4.
[90] Hammer MD, Schwamm L, Starkman S, et al. Safety and feasibility of NeuroFlo usein eight-to24-hour ischemic stroke patients. Int J Stroke,2012,7:655-661.
[91] Saqqur M, Ibrahim M, Butcher K, et al. Transcranial Doppler and CerebralAugmentation in Acute Ischemic Stroke. J Neuroimaging,2013,23:460-465.
[92] Emery DJ, Schellinger PD, Selchen D, et al. Safety and feasibility of collateral bloodflow augmentation after intravenous thrombolysis. Stroke,2011,42:1135-1137.
[93] Schellinger PD, Shuaib A, K hrmann M, et al. Reduced Mortality and SevereDisability Rates in the SENTIS Trial. AJNR Am J Neuroradiol,2013,34:2312-2316.
[94] Schellinger PD, K hrmann M, Liu S, et al. Favorable vascular profile is anindependent predictor of outcome: a post hoc analysis of the safety and efficacy ofNeuroFlo Technology in Ischemic Stroke trial. Stroke,2013,44:1606-1608.
[95] Shuaib A, Butcher K, Mohammad AA, et al. Collateral blood vessels in acuteischaemic stroke: a potential therapeutic target. Lancet Neurol,2011,10:909-921.
[96] Liebeskind DS. Reperfusion for acute ischemic stroke: arterial revascularization andcollateral therapeutics. Curr Opin Neurol,2010,23:36-45.
[97] Hennerici MG, Kern R, Szabo K. Non-pharmacological strategies for the treatment ofacute ischaemic stroke. Lancet Neurol,2013,12:572-584.