脓毒症对血管内皮损伤的实验研究及中心静脉导管相关性血流感染的临床研究
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摘要
脓毒症(Sepsis)是由感染引起的全身性炎症反应综合征(systemic inflammatory response syndrome, SIRS),并证实有细菌存在或有高度可疑感染灶,是多器官功能障碍综合征(multiorgan dysfunction syndrome, MODS)的前兆。目前脓毒症和脓毒性休克仍然是世界重症医学所面临的难题,据统计,美国每年约有75万人发生脓毒性休克,病死率可达50%以上[1,2],深入探索脓毒症的病理生理和发生机制,寻找新的治疗脓毒症的方法,对指导临床治疗脓毒症,降低脓毒性休克的病死率具有重要价值。脓毒症时,内毒素等细菌成分作用于血管内皮,大量细胞因子释放,进一步引起促炎-抗炎系统失调和凝血功能紊乱,其中血管内皮细胞损伤在脓毒症凝血级联反应的发生发展过程中起着重要作用。本课题通过建立脓毒症模型,测定血浆血管性假性血友病因子(von Wilebrand factor, vWF)和内皮素(endothelin,ET)水平的变化,了解血管内皮损伤标志物的动态改变,并进一步研究脓毒症时肺组织vWF的表达,分析脓毒症时肺微循环内皮的损伤,为今后探明脓毒症的发病机制及寻求脓毒症治疗的新方法提供依据。
目的:通过检测脓毒症兔血浆vWF和ET水平的改变,研究脓毒症对血管内皮的损伤作用;并采用免疫组化技术进一步研究脓毒症时肺组织vWF的表达,探讨脓毒症对肺血管内皮的影响,为指导脓毒症的治疗提供新思路。
方法:新西兰白兔36只,随机分成3组:(1)正常对照组(n=12):通过兔耳缘静脉注射生理盐水;(2)脓毒症组(n=12):通过兔耳缘静脉注射大肠杆菌脂多糖(lipopolysaccharide, LPS)1mg·kg-1;(3)脓毒性休克组(n=12):通过兔耳缘静脉注射2mg·kg-1。各组动物均麻醉后分离出右侧颈总动脉及颈内静脉,经颈总动脉插管并连接压力换能器,监测平均动脉压、心率、呼吸频率。在静脉注射LPS后15min、30min、45min、60min、90min及120min时,经颈内静脉采血,然后分离血浆标本,进行vWF和ET的测定。vWF浓度采用酶联免疫吸附法(ELISA)测定, ET浓度采用非平衡放射免疫分析法测定。脓毒性休克组兔死亡后,立即开胸取肺标本,同期处死正常对照组及脓毒症组兔,取肺标本,应用免疫组化技术,检测肺组织vWF的表达。
结果:
1.脓毒症和脓毒性休克模型的建立实验动物静脉注射LPS 1mg/kg后,其血压无明显变化,而心率和呼吸频率逐渐升高,升高超过20%以上确立为脓毒症模型[3,4];实验动物静脉注射LPS 2mg/kg后,心率和呼吸频率升高超过20%以上,同时检测平均动脉压下降20%以上确立为脓毒性休克模型[3,4]。
2.脓毒症时血浆vWF和ET水平均升高,脓毒性休克组升高更明显实验动物静脉注射LPS后,血浆vWF和ET水平均有不同程度的升高,但早期升高幅度并不明显,在脓毒症出现之后,血浆vWF和ET水平升高明显,随着病程的进展,尤其当实验动物出现脓毒性休克时,血浆vWF和ET显著升高,差异有统计学意义(P<0.05)。
3.脓毒症兔肺组织vWF的表达增多,脓毒性休克组vWF表达增多更明显免疫组化检测结果显示,脓毒症组及脓毒性休克组兔肺组织vWF阳性染色面积分别占18.86±5.32%和35.58±5.45%,与对照组8.26±2.19%比较,均明显升高。
结论:
1.脓毒症早期就已出现血管内皮损伤,且损伤程度随着脓毒症的发展而加重。
2.脓毒症对肺血管内皮的损伤是脓毒症对全身血管内皮损伤在肺脏中的表现,并随着脓毒症的发展,肺血管内皮损伤逐渐加重。
3.血管内皮损伤逐渐加重引起组织微循环功能的障碍,可能在脓毒症及其引起的MODS中起着重要作用。
以上研究结果为今后探明脓毒症的病理生理学以及寻求脓毒症和MODS治疗的新思路提供实验依据。
中心静脉置管在临床上应用日趋广泛,各种中心静脉导管(Central venous catheter,CVC)用于血流动力学监测、给药、补液、胃肠外营养支持以及血液净化治疗等。随着穿刺工具、技术及导管材料的改进,长期应用的中心静脉通路变得安全、可靠,但插管后的感染时有发生。由置管引起的导管相关性脓毒症仍然是令临床医务人员感到棘手的严重并发症。在美国,每年院内血液感染约超过20万例,而这些感染中大多数与血管内装置的使用有关,其中90%与中心静脉导管有关,病死率为10%-20%;导管相关性血流感染在ICU院内感染中位居第三,病死率在ICU高达25%以上[1],中心静脉导管感染不仅增加医药费用,延长住院时间,而且对病人病情及生活质量产生不良影响。本课题通过对ICU中心静脉导管相关性血流感染(Central venous catheter-related bloodstream infection,CVC-RBI)病例进行研究,重点探讨CVC-RBI的菌群分布及药敏情况,明确引起CVC-RBI的相关易感因素,旨在为今后的临床应用提出建设性意见,更好地预防及处理CVC-RBI。
目的:探讨ICU内中心静脉导管相关性血流感染的病原学、易感因素及临床特点,以指导临床更好地预防感染,减少CVC-RBI的发生,正确地处理CVC-RBI,更好地使用CVC服务于临床。
方法:选取ICU中32例CVC-RBI确诊病例,患者皆为血流感染,分析其菌群分布及细菌耐药情况,并随机选择同期ICU收治的32例留置中心静脉导管但无相关性感染患者作为对照组,两组比较分析患者年龄、住院时间、血清白蛋白、格拉斯哥(Glasgow)评分、急性生理与慢性健康状况Ⅱ(APACHEⅡ)评分、肠内营养及气管切开等因素对CVC-RBI的影响。
结果:32例CVC-RBI病例中,共分离出菌株35株,其中革兰阳性菌14株,革兰阴性菌10株,真菌11株;置管7天后CVC-RBI发生率逐渐增高(占90.63%);与对照组比较,CVC-RBI组患者年龄较大(P<0.05),住院时间、导管留置时间较长(P<0.05),入科时APACHEⅡ评分较高(P<0.01),血清白蛋白和格拉斯哥(Glasgow)评分较低(P<0.05和P<0.01),给予肠内营养者较少(P<0.05),气管切开数较多(P<0.05)。
结论:对于住院时间较长、血清白蛋白低、病情危重度高、行肠外营养及高龄气管切开病人,尤其应注意CVC-RBI的发生;重视抗生素的合理应用,应根据已存在的危险因素采取相应措施。以上研究结果为今后指导临床使用CVC及寻求预防和治疗CVC-RBI新方法提供了重要依据。
Sepsis is the systemic inflammatory response to infection and premonition of multiple organ dysfunction syndrome. Nowadays, sepsis and septic shock are still the puzzle of critical care medicine in the world. Among about 750,000 patients with septic shock every year in the United States, the case fatality exceeds for 50 percent. To explore pathologic mechanism of sepsis and seek for approach to treating sepsis will have important value to instruct sepsis treating and decrease the mortality of septic shock. After blood vessel endothelium is injured by lipopolysaccharide(LPS) in sepsis, a great quantity cytokine released from endothelial cell causes the unbalance of inflammatory and anti-inflammatory system and coagulation functional disorder. In the study, sepsis model was established, and the change of blood plasma von Wilebrand factor(vWF) and endothelin(ET) were determined, and expression of vWF on lung was observed. Blood vessel endothelium injury was studied for investigating the mechanism of sepsis and seeking new approach of therapy.
Objective To explore blood vessel endothelium injury in sepsis by determining the change of plasma vWF and ET, and investigate pneumonic blood vessel endothelium injury in sepsis by observing expression of vWF on lung tissue.
Methods 36 New Zealand white rabbit were randomly divided into three groups(control group, sepsis group and septic shock group). 0.9% sodium chloride, LPS(1mg/kg) and LPS (2mg/kg) were injected into three groups through ear fringe vein respectively. After pressure transducer was connected with common carotid artery cannula,mean arterial pressure(MAP),heart rate(HR) and breathing frequency were monitored. In the time of 15 minutes, 30 minutes, 45 minutes, 60 minutes, 90 minutes and 120 minutes after injecting LPS, plasma vWF and ET were respectively determined by enzyme-linked immunosorbent assay and radio immunoassay. After the rabbit in the septic shock group died, lung preparation were taken and expressions of vWF on lung tissue were detected by immunohistochemical method.
Results
1 Sepsis and septic shock model were established.
After LPS(1mg/kg) was injected into experimental animal through ear fringe vein, MAP had no obvious change, HR and breathing frequency guadually increased over 20 pencent, sepsis model was established. After LPS(2mg/kg) was injected into experimental animal, HR and breathing frequency guadually increased over 20 pencent, and MAP decreased over 20 pencent, septic shock model was established.
2 Blood plasma vWF and ET increased in sepsis group and higher in septic shock group
Blood plasma vWF and ET increased remarkably after LPS was injected. Compared with control group, the extent of increasing was not clearly in the early time after injecting LPS. But when experimental animal developed septic shock, Blood plasma vWF and ET increased obviously(P<0.05).
3 Expressions of vWF on lung tissue increased in sepsis and more obviously in septic shock
Immunohistochemistry result displayed that positive staining of vWF was 18.86±5.32% in sepsis group and 35.58±5.45%in septic shock group, which increased obviously compared with 8.26±2.19% in control group.
Conclusions
1 Blood vessel endothelium injury happens in the early time of sepsis, and degree of injury aggravated along with the development of sepsis.
2 Pneumonic blood vessel endothelium injury is not only the pneumonic manifestation of systemic blood vessel endothelium injury but also aggravates along with the development of sepsis.
3 Blood vessel endothelium injury and dysfunction of microcirculation may play an important role in sepsis and multiorgan dysfunction syndrome(MODS).
All above mentioned research results may provide the experimental basis for exploring the pathophysiology of sepsis and finding the new methods about treating sepsis and MODS.
Central venous catheter is used in hemodynamic monitoring, administering fluid infusion, parenteral nutrition and blood purification. In spite of the improvement of puncturation and catheter materials, central venous catheter-related bloodstream infection(CVC-RBI) is still the severe formidable complication. In the United States of America, the number of nosocomial infection exceeds for 200,000 every year, 90 percent of which is related to central venous catheter. Catheter-related bloodstream infection, whose case fatality reaches up to 25 percent in ICU, ranks the third of nosocomial infection in ICU. CVC-RBI not only raises medical expenses, lengthens the time of hospitalization, but also is harmful to patient’s state and quality of life. In the present study, the cases of CVC-RBI in ICU are investigated. Etiology and predisposing factor of CVC-RBI are explored so as to prevent and handle CVC-RBI.
Objective To discuss the etiology, predisposing factor and clinic characteristic of CVC-RBI in ICU, for preventing infection and decreasing CVC-RBI, handle CVC-RBI, using CVC better in clinical work exactly.
Methods The common pathogens and the risk factors of CVC-RBI were analyzed in 32 cases of CVC-RBI chosen from ICU, which was compared with the control group on patient’s age, the time of hospitalization, serum albumin, Glasgow coma scales, APACHEⅡscore, enteral nutrition and incision of trachea.
Results Among 32 cases with CVC-RBI, 35 pathogens were isolated,including 14 gram-positive bacterium, 10 gram-negative bacterium and 11 fungi. The incidence of CVC-RBI increased gradually after the seventh day of the insertion of catheter(90.63%). Compared with the control, 32 cases with CVC-RBI were older(P<0.05), had more length of stay in hospital and insertion time of catheter(P<0.05), higher APACHEⅡscore(P<0.001), lower serum albumin level(P<0.05) and Glasgow coma scales (P<0.001), less enteral nutrition(P<0.05) and more incision of trachea(P<0.05).
Conclusions CVC-RBI should be paid attention to in older critical patients with hypoalbuminemia, incision of trachea or parenteral nutrition. Antibiotic should be used reasonably and adopt a corresponding measure according to risk factors.
All above-mentioned research results may provide the important basis for using CVC in clinic work and finding the new methods about preventing and treating CVC-RBI.
目的:通过检测脓毒症兔血浆vWF和ET水平的改变,研究脓毒症对血管内皮的损伤作用;并采用免疫组化技术进一步研究脓毒症时肺组织vWF的表达,探讨脓毒症对肺血管内皮的影响,为指导脓毒症的治疗提供新思路。
方法:新西兰白兔36只,随机分成3组:(1)正常对照组(n=12):通过兔耳缘静脉注射生理盐水;(2)脓毒症组(n=12):通过兔耳缘静脉注射大肠杆菌脂多糖(lipopolysaccharide, LPS)1mg·kg-1;(3)脓毒性休克组(n=12):通过兔耳缘静脉注射2mg·kg-1。各组动物均麻醉后分离出右侧颈总动脉及颈内静脉,经颈总动脉插管并连接压力换能器,监测平均动脉压、心率、呼吸频率。在静脉注射LPS后15min、30min、45min、60min、90min及120min时,经颈内静脉采血,然后分离血浆标本,进行vWF和ET的测定。vWF浓度采用酶联免疫吸附法(ELISA)测定, ET浓度采用非平衡放射免疫分析法测定。脓毒性休克组兔死亡后,立即开胸取肺标本,同期处死正常对照组及脓毒症组兔,取肺标本,应用免疫组化技术,检测肺组织vWF的表达。
结果:
1.脓毒症和脓毒性休克模型的建立实验动物静脉注射LPS 1mg/kg后,其血压无明显变化,而心率和呼吸频率逐渐升高,升高超过20%以上确立为脓毒症模型[3,4];实验动物静脉注射LPS 2mg/kg后,心率和呼吸频率升高超过20%以上,同时检测平均动脉压下降20%以上确立为脓毒性休克模型[3,4]。
2.脓毒症时血浆vWF和ET水平均升高,脓毒性休克组升高更明显实验动物静脉注射LPS后,血浆vWF和ET水平均有不同程度的升高,但早期升高幅度并不明显,在脓毒症出现之后,血浆vWF和ET水平升高明显,随着病程的进展,尤其当实验动物出现脓毒性休克时,血浆vWF和ET显著升高,差异有统计学意义(P<0.05)。
3.脓毒症兔肺组织vWF的表达增多,脓毒性休克组vWF表达增多更明显免疫组化检测结果显示,脓毒症组及脓毒性休克组兔肺组织vWF阳性染色面积分别占18.86±5.32%和35.58±5.45%,与对照组8.26±2.19%比较,均明显升高。
结论:
1.脓毒症早期就已出现血管内皮损伤,且损伤程度随着脓毒症的发展而加重。
2.脓毒症对肺血管内皮的损伤是脓毒症对全身血管内皮损伤在肺脏中的表现,并随着脓毒症的发展,肺血管内皮损伤逐渐加重。
3.血管内皮损伤逐渐加重引起组织微循环功能的障碍,可能在脓毒症及其引起的MODS中起着重要作用。
以上研究结果为今后探明脓毒症的病理生理学以及寻求脓毒症和MODS治疗的新思路提供实验依据。
中心静脉置管在临床上应用日趋广泛,各种中心静脉导管(Central venous catheter,CVC)用于血流动力学监测、给药、补液、胃肠外营养支持以及血液净化治疗等。随着穿刺工具、技术及导管材料的改进,长期应用的中心静脉通路变得安全、可靠,但插管后的感染时有发生。由置管引起的导管相关性脓毒症仍然是令临床医务人员感到棘手的严重并发症。在美国,每年院内血液感染约超过20万例,而这些感染中大多数与血管内装置的使用有关,其中90%与中心静脉导管有关,病死率为10%-20%;导管相关性血流感染在ICU院内感染中位居第三,病死率在ICU高达25%以上[1],中心静脉导管感染不仅增加医药费用,延长住院时间,而且对病人病情及生活质量产生不良影响。本课题通过对ICU中心静脉导管相关性血流感染(Central venous catheter-related bloodstream infection,CVC-RBI)病例进行研究,重点探讨CVC-RBI的菌群分布及药敏情况,明确引起CVC-RBI的相关易感因素,旨在为今后的临床应用提出建设性意见,更好地预防及处理CVC-RBI。
目的:探讨ICU内中心静脉导管相关性血流感染的病原学、易感因素及临床特点,以指导临床更好地预防感染,减少CVC-RBI的发生,正确地处理CVC-RBI,更好地使用CVC服务于临床。
方法:选取ICU中32例CVC-RBI确诊病例,患者皆为血流感染,分析其菌群分布及细菌耐药情况,并随机选择同期ICU收治的32例留置中心静脉导管但无相关性感染患者作为对照组,两组比较分析患者年龄、住院时间、血清白蛋白、格拉斯哥(Glasgow)评分、急性生理与慢性健康状况Ⅱ(APACHEⅡ)评分、肠内营养及气管切开等因素对CVC-RBI的影响。
结果:32例CVC-RBI病例中,共分离出菌株35株,其中革兰阳性菌14株,革兰阴性菌10株,真菌11株;置管7天后CVC-RBI发生率逐渐增高(占90.63%);与对照组比较,CVC-RBI组患者年龄较大(P<0.05),住院时间、导管留置时间较长(P<0.05),入科时APACHEⅡ评分较高(P<0.01),血清白蛋白和格拉斯哥(Glasgow)评分较低(P<0.05和P<0.01),给予肠内营养者较少(P<0.05),气管切开数较多(P<0.05)。
结论:对于住院时间较长、血清白蛋白低、病情危重度高、行肠外营养及高龄气管切开病人,尤其应注意CVC-RBI的发生;重视抗生素的合理应用,应根据已存在的危险因素采取相应措施。以上研究结果为今后指导临床使用CVC及寻求预防和治疗CVC-RBI新方法提供了重要依据。
Sepsis is the systemic inflammatory response to infection and premonition of multiple organ dysfunction syndrome. Nowadays, sepsis and septic shock are still the puzzle of critical care medicine in the world. Among about 750,000 patients with septic shock every year in the United States, the case fatality exceeds for 50 percent. To explore pathologic mechanism of sepsis and seek for approach to treating sepsis will have important value to instruct sepsis treating and decrease the mortality of septic shock. After blood vessel endothelium is injured by lipopolysaccharide(LPS) in sepsis, a great quantity cytokine released from endothelial cell causes the unbalance of inflammatory and anti-inflammatory system and coagulation functional disorder. In the study, sepsis model was established, and the change of blood plasma von Wilebrand factor(vWF) and endothelin(ET) were determined, and expression of vWF on lung was observed. Blood vessel endothelium injury was studied for investigating the mechanism of sepsis and seeking new approach of therapy.
Objective To explore blood vessel endothelium injury in sepsis by determining the change of plasma vWF and ET, and investigate pneumonic blood vessel endothelium injury in sepsis by observing expression of vWF on lung tissue.
Methods 36 New Zealand white rabbit were randomly divided into three groups(control group, sepsis group and septic shock group). 0.9% sodium chloride, LPS(1mg/kg) and LPS (2mg/kg) were injected into three groups through ear fringe vein respectively. After pressure transducer was connected with common carotid artery cannula,mean arterial pressure(MAP),heart rate(HR) and breathing frequency were monitored. In the time of 15 minutes, 30 minutes, 45 minutes, 60 minutes, 90 minutes and 120 minutes after injecting LPS, plasma vWF and ET were respectively determined by enzyme-linked immunosorbent assay and radio immunoassay. After the rabbit in the septic shock group died, lung preparation were taken and expressions of vWF on lung tissue were detected by immunohistochemical method.
Results
1 Sepsis and septic shock model were established.
After LPS(1mg/kg) was injected into experimental animal through ear fringe vein, MAP had no obvious change, HR and breathing frequency guadually increased over 20 pencent, sepsis model was established. After LPS(2mg/kg) was injected into experimental animal, HR and breathing frequency guadually increased over 20 pencent, and MAP decreased over 20 pencent, septic shock model was established.
2 Blood plasma vWF and ET increased in sepsis group and higher in septic shock group
Blood plasma vWF and ET increased remarkably after LPS was injected. Compared with control group, the extent of increasing was not clearly in the early time after injecting LPS. But when experimental animal developed septic shock, Blood plasma vWF and ET increased obviously(P<0.05).
3 Expressions of vWF on lung tissue increased in sepsis and more obviously in septic shock
Immunohistochemistry result displayed that positive staining of vWF was 18.86±5.32% in sepsis group and 35.58±5.45%in septic shock group, which increased obviously compared with 8.26±2.19% in control group.
Conclusions
1 Blood vessel endothelium injury happens in the early time of sepsis, and degree of injury aggravated along with the development of sepsis.
2 Pneumonic blood vessel endothelium injury is not only the pneumonic manifestation of systemic blood vessel endothelium injury but also aggravates along with the development of sepsis.
3 Blood vessel endothelium injury and dysfunction of microcirculation may play an important role in sepsis and multiorgan dysfunction syndrome(MODS).
All above mentioned research results may provide the experimental basis for exploring the pathophysiology of sepsis and finding the new methods about treating sepsis and MODS.
Central venous catheter is used in hemodynamic monitoring, administering fluid infusion, parenteral nutrition and blood purification. In spite of the improvement of puncturation and catheter materials, central venous catheter-related bloodstream infection(CVC-RBI) is still the severe formidable complication. In the United States of America, the number of nosocomial infection exceeds for 200,000 every year, 90 percent of which is related to central venous catheter. Catheter-related bloodstream infection, whose case fatality reaches up to 25 percent in ICU, ranks the third of nosocomial infection in ICU. CVC-RBI not only raises medical expenses, lengthens the time of hospitalization, but also is harmful to patient’s state and quality of life. In the present study, the cases of CVC-RBI in ICU are investigated. Etiology and predisposing factor of CVC-RBI are explored so as to prevent and handle CVC-RBI.
Objective To discuss the etiology, predisposing factor and clinic characteristic of CVC-RBI in ICU, for preventing infection and decreasing CVC-RBI, handle CVC-RBI, using CVC better in clinical work exactly.
Methods The common pathogens and the risk factors of CVC-RBI were analyzed in 32 cases of CVC-RBI chosen from ICU, which was compared with the control group on patient’s age, the time of hospitalization, serum albumin, Glasgow coma scales, APACHEⅡscore, enteral nutrition and incision of trachea.
Results Among 32 cases with CVC-RBI, 35 pathogens were isolated,including 14 gram-positive bacterium, 10 gram-negative bacterium and 11 fungi. The incidence of CVC-RBI increased gradually after the seventh day of the insertion of catheter(90.63%). Compared with the control, 32 cases with CVC-RBI were older(P<0.05), had more length of stay in hospital and insertion time of catheter(P<0.05), higher APACHEⅡscore(P<0.001), lower serum albumin level(P<0.05) and Glasgow coma scales (P<0.001), less enteral nutrition(P<0.05) and more incision of trachea(P<0.05).
Conclusions CVC-RBI should be paid attention to in older critical patients with hypoalbuminemia, incision of trachea or parenteral nutrition. Antibiotic should be used reasonably and adopt a corresponding measure according to risk factors.
All above-mentioned research results may provide the important basis for using CVC in clinic work and finding the new methods about preventing and treating CVC-RBI.
引文
1. Angus DC, Linde-Zwirble WT, Lidicker J, et al. Epidemiology of severe sepsis in the United States: analysis of incidence, outcome and associated costs of care[J]. Crit CareMed,2001,29(7):1303-10
2. Dellinger RP, Carlet JM, Masur H, et al. Surviving sepsis campaign guidelines for management of severe sepsis and septic shock[J]. Crit Care Med,2004,32(3):858-73
3. 朱雪琦,刘清泉,姚咏明.脓毒症动物模型制备方法的研究进展[J]. 中国危重病急救医学,2006,18(2):114-16
4. Parker SJ, Watkins PE. Experimental models of gram-negative sepsis[J].Br J Surg, 2001,88(1):22-30
5. American College of Chest Physician/Society for Critical Care medicine Consensus Conference:definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Crit Care Med,1992,20(6):864-74
6. Levy MM, Fink MP, Marshall JC, et al. 2001SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference. Crit Care Med, 2003,31(4):1250-56
7. Aird WC. The role of the endothelium in severe sepsis and multiple organ dysfunction syndrome[J]. Blood,2003,101(10):3765-77
8. 苗玉良,邓小明,李金宝,等.α-黑色素细胞刺激素对二次打击急性呼吸窘迫综合征大鼠肺血管内皮细胞凋亡的影响[J].中国危重病急救医学,2004,16(10):596-98
9. Boos CJ, Goon PK, Lip GY. The endothelium, inflammation, and coagulation in sepsis[J]. Clin Pharmacol Ther,2006,79(1):20-2
10. Levi M, ten Cate H, van der Poll T. Endothelium: interface between coagulation and inflammation[J]. Crit Care Med,2002,30(5 Suppl):S220-4
11. Riedemann NC, Guo RF, Ward PA. Novel strategies for the treatment of sepsis[J]. Nat Med, 2003,9(5):517-24
12. Kleinpell R. Advances in treating patients with severe sepsis.Role of drotrecogin alfa (activated) [J]. Crit Care Nurse. 2003,23(3):16-29
13. Haberichter SL, Jacobi P, Montgomery RR. Critical independent regions in the vWF propeptide and mature vWF that enable normal vWF storage[J]. Blood, 2003, 101(4): 1384-91
14. Rosnoblet C, Ribba AS, Wollheim CB, et al. Regulated von Willebrand factor (vWF) secretion is restored by pro-vWF expression in a transfectable endothelial cell line[J]. Biochim Biophys Acta, 2000,1495(1):112-19
15. Blann AD. Plasma von Willebrand factor, thrombosis, and the endothelium: the first 30 years[J]. Thromb Haemost,2006,95(1):49-55
16. 李锐,曹书华,王今达. 血管性假性血友病因子和细胞间黏附分子-1在急性呼吸窘 迫 综 合 征 中 的 动 态 变 化 及 早 期 诊 断 的 意 义 [J]. 中 华 急 诊 医 学 杂志,2004,13(4):251-53
17. Yanagisawa M, Kurhara H, Kimura S. et al. A novel potent vasoconstrlctior peptide produced by vascular endothelial cells[J].Nature,1988,332(6163):441-45
18. 孙书珍,李倩,汪翼,等. Ⅰ型糖尿病患儿血浆内皮素和血管性假血友病因子的检测及其与尿白蛋白的关系[J].中国实用儿科杂志,2006,21(8):590-92
19. Chignard M, Balloy V. Neutrophil recruitment and increased permeability during acute lung injury induced by lipopolysaccharide[J]. Am J Physiol Lung Cell Mol Physiol. 2000,279(6):1083-90
20. Remick DG, Ward PA. Evaluation of endotoxin models for the study of sepsis[J]. Shock, 2005,24(1Suppl):7-11
21. 胡森.MODS动物模型[M]//盛志勇,胡森.多器官功能障碍综合征.北京:科学出版社,1999:185-199
22. Ware LB, Eisner MD, Thompson BT, et al. Significance of von Willebrand factor in septic and nonseptic patients with acute lung injury[J].Am J Respir Crit Care Med, 2004,170(7):766-72
23. Moss M, Gillespie MK, Ackerson L, et al. Endothelial cell activity varies in patients at risk for the adult respiratory distress syndrome[J]. Crit Care Med, 1996,24(11):1782-86
24. Soop A, Albert J, Weitzberg E, Bengtsson A, et al. Complement activation, endothelin-1 and neuropeptide Y in relation to the cardiovascular response to endotoxin-induced systemic inflammation in healthy volunteers[J]. Acta Anaesthesiol Scand, 2004,48(1):74-81
25 Figueras-Aloy J, Gomez-Lopez L, Rodriguez-Miguelez JM, et al. Plasma endothelin-1 and clinical manifestations of neonatal sepsis[J]. J Perinat Med, 2004,32(6):522-26
26. Forni M, Mazzola S, Ribeiro LA, et al. Expression of endothelin-1 system in a pig model of endotoxic shock[J]. Regul Pept, 2005,131(1-3):89-96
27. Ishimaru S, Shichiri M, Mineshita S, et al. Role of endothelin-1/endothelin receptor system in endotoxic shock rats[J].Hypertens Res, 2001,24(2):119-26
28. Fein AM, Calalang-Colucci MG, Calalang-Colucci MG. Acute lung injury and acute respiratory distress syndrome in sepsis and septic shock[J]. Crit Care Clin, 2000,16(3):289-317
29. 谢艳萍,王建春,陈才平,等.LPS对鼠肺微血管内皮细胞水通道蛋白-1表达及其功能的影响[J].中国病理生理杂志,2005,21(1):104-7
30. Meduri G U. Clinical review: a paradigm shift: the directional effect of inflammation on bacterial growth. Clinical implications for patients with acute respiratory distress syndrome [J]. Crit Care,2002,6(1):24-9
31. Laterre PF, Wittebole X, Dhainaut JF. Anti-coagulant therapy in acute lung injury[J]. Crit Care Med, 2003,31(Suppl 4):S329-36
32. Tsokos M, Fehlauer F. Post-mortem markers of sepsis: an immuno histochemical study using VLA-4(CD49d/CD29) and ICAM-1(CD54) for the detection of sepsis-induced lung injury[J]. Int J Legal Med, 2001,114(4-5):291-94
1. Mermel LA, Farr BM, Sherertz RJ, et al. Guidelines for the management of intravascular catheter-related infections[J]. Clin Infect Dis,2001,32(9):1249-72
2. Memish ZA, Arabi Y, Cunningham G, et al. Comparison of US and non-US central venous catheter infection rates: evaluation of processes and indicators in infection control study[J]. Am J Infect Control,2003,31(4):237-42
3. 吴勤, 张继红, 吕润华.深静脉置管术在危重病人中的应用及并发症的防治[J]. 南方护理杂志.1997,4(6),21-23
4. David A, Risitano DC, Mazzeo G ,et al. Central venous catheters and infections[J]. Minerva Anestesiol,2005,71(9):561-64
5. 杜斌,陈德昌,刘大为.危重病患者中心静脉插管相关性感染的前瞻性研究[J].中华外科杂志,1997,35(7):398-401
6. Dobbins BM, Catton JA, Kite P, et al. Each lumen is a potential source of central venous catheter-related bloodstream infection[J]. Crit Care Med,2003,31(6):1688-90
7. Goetz AM, Wagener MM, Miller JM, et al. Risk of infection due to central venous catheters: effect of site of placement and catheter type[J].Infect Control Hosp Epidemiol,1998,19(11):842-45
8. Bong JJ, Kite P, Wilco MH, et al. Prevention of catheter related bloodstream infection by silver iontophoretic central venous catheters: a randomised controlled trial[J]. J Clin Pathol,2003,56(10):731-35
9. 夏欣华.ICU内中心静脉导管相关感染56例次分析[J].中国危重病急救医学,2002,14(12):735
10. Slaughter SE. Intravascular catheter-related infections. Strategies for combating this common foe[J]. Postgrad Med J,2004,116(5):59-66
11. 邹琳,俞森洋.导管相关感染的病原学及相关危险因素[J].中华医院感染学杂志,2005,15(4):405-407
12. 王锦权,陶晓根,承韶晖,等.重症监护病房医院获得性深部真菌感染的临床研究[J].中华内科杂志,2005,44(12):923-24
13. Deshpande KS, Hatem C, Ulrich HL, et al. The incidence of infectious complications of central venous catheters at the subclavian, internal jugular, and femoral sites in an intensive care unit population[J].Crit Care Med,2005,33(1):13-20
14. Plosker GL, Figgitt DP. Linezolid: a pharmacoeconomic review of its use in serious gram-positive infections[J].Pharmacoeconomics,2005,23(9):945-64
15. 曹孟淑,胡杰贵,徐元宏.114株下呼吸道铜绿假单胞菌的药敏分析及临床意义[J].安徽医科大学学报,2004,39(6):473-75
16. Viale P, Pagani L, Petrosillo N, et al. Antibiotic lock-technique for the treatment of catheter- related bloodstream infections[J]. J Chemother,2003,15(2):152-56
17. Giles Y, Aksoy M, Tezelman S. What really affects the incidence of central venous catheter-related infections for short-term catheterization[J]? Acta Chir Belg,2002,102(4):256-58
18. 张诗海,曾邦雄.85例中心静脉导管相关感染分析[J].中华医院感染学杂志,2002,12(2):89-90
19. Ferrett G, Mandala M, Cosimo SD, et al. Catheter-related blood stream infections, part II: specific pathogens and prevention [J]. Cancer Control,2003,10(1):79-91
20. 丁士芳,王可富,周炜,等.中心静脉导管相关性真菌败血症的临床分析[J].中国现代普通外科进展,2005,8(1):50-51
21. 邹琳,俞森洋.血管内导管相关的血行感染[J].解放军医学杂志,2005,30(1):82-84
22. 孙少川,李富彬.中心静脉导管相关感染的防治进展[J].医学综述,2002,8(1):51-52
23. Beghetto MG, Victorino J, Teixeira L, et al. Parenteral nutrition as a risk factor for central venous catheter–related infection[J]. JPEN J Parenter Enteral Nutr, 2005, 29(5):367-73
1. Angus DC, Linde-Zwirble WT, Lidicker J, et al. Epidemiology of severe sepsis in the United States: analysis of incidence, outcome and associated costs of care[J]. Crit Care Med,2001,29(7):1303-10
2. Dellinger RP, Carlet JM, Masur H, et al. Surviving sepsis campaign guidelines for management of severe sepsis and septic shock[J]. Crit Care Med, 2004, 32(10): 2169-70
3. 张雪静,黄秀兰,王伟. 土茯苓抑制白介素-1诱导的血管内皮细胞细胞间黏附分子-1的表达[J].中国医药学报,2004,19(6):344-46
4. Haberichter SL, Jacobi P, Montgomery RR. Critical independent regions in the vWF propeptide and mature vWF that enable normal vWF storage[J]. Blood, 2003, 101(4): 1384-91
5. Wu DM, Vanhoorelbeke K, Cauwenberghs N, et al. Inhibition of the von Willebrand (vWF)-collagen interaction by an antihuman vWF monoclonal antibody results in abolition of in vivo arterial platelet thrombus formation in baboons[J]. Blood, 2002, 99(10):3623-28
6. Moss M, Gillespie MK, Ackerson L, et al. Endothelial cell activity varies in patients at risk for the adult respiratory distress syndrome[J]. Crit Care Med, 1996, 24(11): 1782-86
7. Dhainaut JF, Yan SB, Cariou A, et al. Soluble thrombomodulin, plasma derived unactivated protein C, and recombinant human activated protein C in sepsis[J]. Crit Care Med,2002,30(5Suppl):S318-24
8. Yanagisawa M, Kurhara H, Kimura S. et al. A novel potent vasoconstrlctior peptide produced by vascular endothelial cells[J].Nature,1988,332(6163):441-45
9. Abraham E. Coagulation abnormalities in acute lung injury and sepsis[J]. Am J Respeir Cell Mol Biol, 2000,22(3):402-404
10. Figueras-Aloy J, Gomez-Lopez L, Rodriguez-Miguelez JM, et al. Plasma endothelin-1 and clinical manifestations of neonatal sepsis[J]. J Perinat Med,2004, 32(6): 522-26
11. 刘效华,王海滨,陈继玲.急性冠状动脉综合征血小板表面P-选择素的变化及意义[J].中国心血管病研究杂志,2004,2(8):649-50
12. Tobias PS, Soldau K, Ulevitch RJ. Isolation of a lipopolysaccharide-binding acute reactant from rabbit serum[J]. J Exp Med, 1986,164(3):777-93
13. Gluck T, Silver J, Epstein M, et al. Parameters influencing membrane CD14 expression and soluble CD14 levels in sepsis[J].Eur J Med Res,2001,6(8):351-58
14. Medzhitov R, Preston-Hurlburt P, Janeway CAJ. A human homologue of the drosophila Toll protein signals activation of adaptive immunity. Nature, 1997, 388 (6640):394-97
15. Beutler B, Poltorak A. Sepsis and evolution of the innate immune response[J]. Crit Care Med, 2001,29(7suppl):S2-6
16. Heumann D, Roger T. Initial responses to endotoxins and Gram-negative bacteria[J].Clin Chim Acta,2002,323(1-2):59-72
17. Nasraway SA. The problems and challenges of immunotherapy in sepsis[J]. Chest,2003,123(5Suppl): S451-59
18. Hotchkiss RS, Karl IE. The pathophysiology and treatment of sepsis[J].N Engl J Med 2003,348(2):138-50
19. 李红燕,张秀芳,庄逢源.白介素-1对人内皮细胞胞间粘附分子-1表达量的影响[J].解放军医学杂志,1999,24(3):179
20. 陶晓根,承韶辉,王锦权.糖皮质激素抵抗与脓毒血症[J].中国危重病急救医学,2001,13(5):307-309
21. Asadullah K, Sterry W, Volk HD. Interleukin-10 therapy review of a new approach[J]. Pharmacol Rev, 2003,55(2):241-69
22. 陈刚,傅志仁,王梁华,等.人白介素10对异种内皮细胞保护作用的研究[J].中国免疫学杂志,2004,20(6):410-12
23. Alloatti G, Penna C,Mariano F, et al. Role of NO and PAF in the impairment of skeletal muscle contractility induced by TNF- α [J].Am J Physiol Regulatory Integrative Comp Physiol,2000,279(6):R2156-63
24. Mayer K, Merfels M, Muhly-Reinholz M, et al. Omega-3 Fatty acids suppress monocyte adhesion to human endothelial cells: role of endothelial PAF generation[J].Am J Physiol Heart Circ Physiol,2002,283(2):H811-18
25. Schuster DP, Metzler M, Opal S, et al. Recombinant platelet-activating factor acetylhy-drolase to prevent acute respiratory distress syndrome and mortality in severe sepsis: Phase IIb, multicenter, randomized, placebo controlled, clinical trial[J]. Crit Care Med, 2003,31(6):1612-19
26. Hawiger J. Innate immunity and inflammation: a transcriptional paradigm[J]. Immunol Res, 2001,23(2-3):99-109
27. Petrache I, Verin AD, Crow MT, et al. Differential effect of MLC kinase in TNF-alpha-induced endothelial cell apoptosis and barrier dysfunction[J]. Am J Physiol Lung Cell Mol Physiol, 2001,280(6):L1168-78
1. Mermel LA, Farr BM, Sherertz RJ, et al. Guidelines for the management of intravascular catheter-related infection[J]. Clin Infect Dis,2001,32(9):1249-72
2. 杜斌,陈德昌,刘大为.危重病患者中心静脉插管相关性感染的前瞻性研究[J].中华外科杂志,1997,35(7):398-401
3. David A, Risitano DC, Mazzeo G, et al. Central venous catheters and infections[J]. Minerva Anestesiol,2005,71(9):561-64
4. 邹琳,俞森洋.导管相关感染的病原学及相关危险因素[J].中华医院感染学杂志,2005,15(4):405-407
5. 申捷,何岱昆,唐耀东.危重病人静脉导管相关性感染[J].中国医师进修杂志,2006,29(1):6-8
6. Dobbins BM, Catton JA, Kite P, et al. Each lumen is a potential source of central venous catheter-related bloodstream infection[J].Crit Care Med,2003,31(6): 1688-90
7. Goetz AM, Wagener MM, Miller JM, et al. Risk of infection due to central venous catheters: effect of site of placement and catheter type[J].Infect Control Hosp Epidemiol,1998,19(11):842-45
8. 郑立,李义贤,洪瑞乔,等.三种中心静脉置管导管相关性感染的对比研究[J].护士进修杂志,2006,21(9):783-85
9. 沃建华,黄韬,陆立平.中心静脉导管相关性脓毒症分析[J].中国实用外科杂志,2002,22(5):313
10. Ferrett G, Mandala M, Cosimo SD, et al. Catheter-related blood stream infections, part II: specific pathogens and prevention [J]. Cancer Control,2003, 10(1):79-91
11. Nouwen JL, Wielenga JJ, van Overhagen H, et al. Hickman catheter-related infections in neutropenic patients: insertion in the operating theater versus insertionin the radiology suite[J]. J Clin Oncol, 1999, 17(4):1304-10
12. Beghetto MG, Victorino J, Teixeira L,et al. Parenteral nutrition as a risk factor for central venous catheter–related infection[J]. JPEN J Parenter Enteral Nutr, 2005, 29(5):367-73
13. Deshpande KS, Hatem C, Ulrich HL, et al. The incidence of infectious complications of central venous catheters at the subclavian, internal jugular, and femoral sites in an intensive care unit population[J]. Crit Care Med, 2005, 33(1): 234-35
14. Eggimann P, Pittet D. Overview of catheter-relateel infections with special emphasis on prevention based on educational programs[J]. Clin Micro Infect, 2002, 8(5): 295- 309
15. O'Grady NP, Alexander M, Dellinger EP, et al. Guidelines for the prevention of intravascular catheter-related infections[J]. Infect Control Hosp Epidemiol.2002, 23(12):759-69
16. 丁士芳,王可富,周炜,等.中心静脉导管相关性真菌败血症的临床分析[J].中国现代普通外科进展,2005,8(1):50-51
17. 薛春华,花天放,吴鹏,等.中心静脉导管相关性感染[J].中国抗感染化疗杂志,2004,4(4):213-15
18. 夏欣华.ICU内中心静脉导管相关感染56例次分析[J].中国危重病急救医学2002,14(12):735
19. Viale P, Pagani L, Petrosillo N, et al. Antibiotic lock-technique for the treatment of catheter- related bloodstream infections[J]. J Chemother,2003,15(2):152-56
20. 孙 少 川 , 李 富 彬 . 中 心 静 脉 导 管 相 关 感 染 的 防 治 进 展 [J]. 医 学 综 述 , 2002,8(1):51-52
2. Dellinger RP, Carlet JM, Masur H, et al. Surviving sepsis campaign guidelines for management of severe sepsis and septic shock[J]. Crit Care Med,2004,32(3):858-73
3. 朱雪琦,刘清泉,姚咏明.脓毒症动物模型制备方法的研究进展[J]. 中国危重病急救医学,2006,18(2):114-16
4. Parker SJ, Watkins PE. Experimental models of gram-negative sepsis[J].Br J Surg, 2001,88(1):22-30
5. American College of Chest Physician/Society for Critical Care medicine Consensus Conference:definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Crit Care Med,1992,20(6):864-74
6. Levy MM, Fink MP, Marshall JC, et al. 2001SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference. Crit Care Med, 2003,31(4):1250-56
7. Aird WC. The role of the endothelium in severe sepsis and multiple organ dysfunction syndrome[J]. Blood,2003,101(10):3765-77
8. 苗玉良,邓小明,李金宝,等.α-黑色素细胞刺激素对二次打击急性呼吸窘迫综合征大鼠肺血管内皮细胞凋亡的影响[J].中国危重病急救医学,2004,16(10):596-98
9. Boos CJ, Goon PK, Lip GY. The endothelium, inflammation, and coagulation in sepsis[J]. Clin Pharmacol Ther,2006,79(1):20-2
10. Levi M, ten Cate H, van der Poll T. Endothelium: interface between coagulation and inflammation[J]. Crit Care Med,2002,30(5 Suppl):S220-4
11. Riedemann NC, Guo RF, Ward PA. Novel strategies for the treatment of sepsis[J]. Nat Med, 2003,9(5):517-24
12. Kleinpell R. Advances in treating patients with severe sepsis.Role of drotrecogin alfa (activated) [J]. Crit Care Nurse. 2003,23(3):16-29
13. Haberichter SL, Jacobi P, Montgomery RR. Critical independent regions in the vWF propeptide and mature vWF that enable normal vWF storage[J]. Blood, 2003, 101(4): 1384-91
14. Rosnoblet C, Ribba AS, Wollheim CB, et al. Regulated von Willebrand factor (vWF) secretion is restored by pro-vWF expression in a transfectable endothelial cell line[J]. Biochim Biophys Acta, 2000,1495(1):112-19
15. Blann AD. Plasma von Willebrand factor, thrombosis, and the endothelium: the first 30 years[J]. Thromb Haemost,2006,95(1):49-55
16. 李锐,曹书华,王今达. 血管性假性血友病因子和细胞间黏附分子-1在急性呼吸窘 迫 综 合 征 中 的 动 态 变 化 及 早 期 诊 断 的 意 义 [J]. 中 华 急 诊 医 学 杂志,2004,13(4):251-53
17. Yanagisawa M, Kurhara H, Kimura S. et al. A novel potent vasoconstrlctior peptide produced by vascular endothelial cells[J].Nature,1988,332(6163):441-45
18. 孙书珍,李倩,汪翼,等. Ⅰ型糖尿病患儿血浆内皮素和血管性假血友病因子的检测及其与尿白蛋白的关系[J].中国实用儿科杂志,2006,21(8):590-92
19. Chignard M, Balloy V. Neutrophil recruitment and increased permeability during acute lung injury induced by lipopolysaccharide[J]. Am J Physiol Lung Cell Mol Physiol. 2000,279(6):1083-90
20. Remick DG, Ward PA. Evaluation of endotoxin models for the study of sepsis[J]. Shock, 2005,24(1Suppl):7-11
21. 胡森.MODS动物模型[M]//盛志勇,胡森.多器官功能障碍综合征.北京:科学出版社,1999:185-199
22. Ware LB, Eisner MD, Thompson BT, et al. Significance of von Willebrand factor in septic and nonseptic patients with acute lung injury[J].Am J Respir Crit Care Med, 2004,170(7):766-72
23. Moss M, Gillespie MK, Ackerson L, et al. Endothelial cell activity varies in patients at risk for the adult respiratory distress syndrome[J]. Crit Care Med, 1996,24(11):1782-86
24. Soop A, Albert J, Weitzberg E, Bengtsson A, et al. Complement activation, endothelin-1 and neuropeptide Y in relation to the cardiovascular response to endotoxin-induced systemic inflammation in healthy volunteers[J]. Acta Anaesthesiol Scand, 2004,48(1):74-81
25 Figueras-Aloy J, Gomez-Lopez L, Rodriguez-Miguelez JM, et al. Plasma endothelin-1 and clinical manifestations of neonatal sepsis[J]. J Perinat Med, 2004,32(6):522-26
26. Forni M, Mazzola S, Ribeiro LA, et al. Expression of endothelin-1 system in a pig model of endotoxic shock[J]. Regul Pept, 2005,131(1-3):89-96
27. Ishimaru S, Shichiri M, Mineshita S, et al. Role of endothelin-1/endothelin receptor system in endotoxic shock rats[J].Hypertens Res, 2001,24(2):119-26
28. Fein AM, Calalang-Colucci MG, Calalang-Colucci MG. Acute lung injury and acute respiratory distress syndrome in sepsis and septic shock[J]. Crit Care Clin, 2000,16(3):289-317
29. 谢艳萍,王建春,陈才平,等.LPS对鼠肺微血管内皮细胞水通道蛋白-1表达及其功能的影响[J].中国病理生理杂志,2005,21(1):104-7
30. Meduri G U. Clinical review: a paradigm shift: the directional effect of inflammation on bacterial growth. Clinical implications for patients with acute respiratory distress syndrome [J]. Crit Care,2002,6(1):24-9
31. Laterre PF, Wittebole X, Dhainaut JF. Anti-coagulant therapy in acute lung injury[J]. Crit Care Med, 2003,31(Suppl 4):S329-36
32. Tsokos M, Fehlauer F. Post-mortem markers of sepsis: an immuno histochemical study using VLA-4(CD49d/CD29) and ICAM-1(CD54) for the detection of sepsis-induced lung injury[J]. Int J Legal Med, 2001,114(4-5):291-94
1. Mermel LA, Farr BM, Sherertz RJ, et al. Guidelines for the management of intravascular catheter-related infections[J]. Clin Infect Dis,2001,32(9):1249-72
2. Memish ZA, Arabi Y, Cunningham G, et al. Comparison of US and non-US central venous catheter infection rates: evaluation of processes and indicators in infection control study[J]. Am J Infect Control,2003,31(4):237-42
3. 吴勤, 张继红, 吕润华.深静脉置管术在危重病人中的应用及并发症的防治[J]. 南方护理杂志.1997,4(6),21-23
4. David A, Risitano DC, Mazzeo G ,et al. Central venous catheters and infections[J]. Minerva Anestesiol,2005,71(9):561-64
5. 杜斌,陈德昌,刘大为.危重病患者中心静脉插管相关性感染的前瞻性研究[J].中华外科杂志,1997,35(7):398-401
6. Dobbins BM, Catton JA, Kite P, et al. Each lumen is a potential source of central venous catheter-related bloodstream infection[J]. Crit Care Med,2003,31(6):1688-90
7. Goetz AM, Wagener MM, Miller JM, et al. Risk of infection due to central venous catheters: effect of site of placement and catheter type[J].Infect Control Hosp Epidemiol,1998,19(11):842-45
8. Bong JJ, Kite P, Wilco MH, et al. Prevention of catheter related bloodstream infection by silver iontophoretic central venous catheters: a randomised controlled trial[J]. J Clin Pathol,2003,56(10):731-35
9. 夏欣华.ICU内中心静脉导管相关感染56例次分析[J].中国危重病急救医学,2002,14(12):735
10. Slaughter SE. Intravascular catheter-related infections. Strategies for combating this common foe[J]. Postgrad Med J,2004,116(5):59-66
11. 邹琳,俞森洋.导管相关感染的病原学及相关危险因素[J].中华医院感染学杂志,2005,15(4):405-407
12. 王锦权,陶晓根,承韶晖,等.重症监护病房医院获得性深部真菌感染的临床研究[J].中华内科杂志,2005,44(12):923-24
13. Deshpande KS, Hatem C, Ulrich HL, et al. The incidence of infectious complications of central venous catheters at the subclavian, internal jugular, and femoral sites in an intensive care unit population[J].Crit Care Med,2005,33(1):13-20
14. Plosker GL, Figgitt DP. Linezolid: a pharmacoeconomic review of its use in serious gram-positive infections[J].Pharmacoeconomics,2005,23(9):945-64
15. 曹孟淑,胡杰贵,徐元宏.114株下呼吸道铜绿假单胞菌的药敏分析及临床意义[J].安徽医科大学学报,2004,39(6):473-75
16. Viale P, Pagani L, Petrosillo N, et al. Antibiotic lock-technique for the treatment of catheter- related bloodstream infections[J]. J Chemother,2003,15(2):152-56
17. Giles Y, Aksoy M, Tezelman S. What really affects the incidence of central venous catheter-related infections for short-term catheterization[J]? Acta Chir Belg,2002,102(4):256-58
18. 张诗海,曾邦雄.85例中心静脉导管相关感染分析[J].中华医院感染学杂志,2002,12(2):89-90
19. Ferrett G, Mandala M, Cosimo SD, et al. Catheter-related blood stream infections, part II: specific pathogens and prevention [J]. Cancer Control,2003,10(1):79-91
20. 丁士芳,王可富,周炜,等.中心静脉导管相关性真菌败血症的临床分析[J].中国现代普通外科进展,2005,8(1):50-51
21. 邹琳,俞森洋.血管内导管相关的血行感染[J].解放军医学杂志,2005,30(1):82-84
22. 孙少川,李富彬.中心静脉导管相关感染的防治进展[J].医学综述,2002,8(1):51-52
23. Beghetto MG, Victorino J, Teixeira L, et al. Parenteral nutrition as a risk factor for central venous catheter–related infection[J]. JPEN J Parenter Enteral Nutr, 2005, 29(5):367-73
1. Angus DC, Linde-Zwirble WT, Lidicker J, et al. Epidemiology of severe sepsis in the United States: analysis of incidence, outcome and associated costs of care[J]. Crit Care Med,2001,29(7):1303-10
2. Dellinger RP, Carlet JM, Masur H, et al. Surviving sepsis campaign guidelines for management of severe sepsis and septic shock[J]. Crit Care Med, 2004, 32(10): 2169-70
3. 张雪静,黄秀兰,王伟. 土茯苓抑制白介素-1诱导的血管内皮细胞细胞间黏附分子-1的表达[J].中国医药学报,2004,19(6):344-46
4. Haberichter SL, Jacobi P, Montgomery RR. Critical independent regions in the vWF propeptide and mature vWF that enable normal vWF storage[J]. Blood, 2003, 101(4): 1384-91
5. Wu DM, Vanhoorelbeke K, Cauwenberghs N, et al. Inhibition of the von Willebrand (vWF)-collagen interaction by an antihuman vWF monoclonal antibody results in abolition of in vivo arterial platelet thrombus formation in baboons[J]. Blood, 2002, 99(10):3623-28
6. Moss M, Gillespie MK, Ackerson L, et al. Endothelial cell activity varies in patients at risk for the adult respiratory distress syndrome[J]. Crit Care Med, 1996, 24(11): 1782-86
7. Dhainaut JF, Yan SB, Cariou A, et al. Soluble thrombomodulin, plasma derived unactivated protein C, and recombinant human activated protein C in sepsis[J]. Crit Care Med,2002,30(5Suppl):S318-24
8. Yanagisawa M, Kurhara H, Kimura S. et al. A novel potent vasoconstrlctior peptide produced by vascular endothelial cells[J].Nature,1988,332(6163):441-45
9. Abraham E. Coagulation abnormalities in acute lung injury and sepsis[J]. Am J Respeir Cell Mol Biol, 2000,22(3):402-404
10. Figueras-Aloy J, Gomez-Lopez L, Rodriguez-Miguelez JM, et al. Plasma endothelin-1 and clinical manifestations of neonatal sepsis[J]. J Perinat Med,2004, 32(6): 522-26
11. 刘效华,王海滨,陈继玲.急性冠状动脉综合征血小板表面P-选择素的变化及意义[J].中国心血管病研究杂志,2004,2(8):649-50
12. Tobias PS, Soldau K, Ulevitch RJ. Isolation of a lipopolysaccharide-binding acute reactant from rabbit serum[J]. J Exp Med, 1986,164(3):777-93
13. Gluck T, Silver J, Epstein M, et al. Parameters influencing membrane CD14 expression and soluble CD14 levels in sepsis[J].Eur J Med Res,2001,6(8):351-58
14. Medzhitov R, Preston-Hurlburt P, Janeway CAJ. A human homologue of the drosophila Toll protein signals activation of adaptive immunity. Nature, 1997, 388 (6640):394-97
15. Beutler B, Poltorak A. Sepsis and evolution of the innate immune response[J]. Crit Care Med, 2001,29(7suppl):S2-6
16. Heumann D, Roger T. Initial responses to endotoxins and Gram-negative bacteria[J].Clin Chim Acta,2002,323(1-2):59-72
17. Nasraway SA. The problems and challenges of immunotherapy in sepsis[J]. Chest,2003,123(5Suppl): S451-59
18. Hotchkiss RS, Karl IE. The pathophysiology and treatment of sepsis[J].N Engl J Med 2003,348(2):138-50
19. 李红燕,张秀芳,庄逢源.白介素-1对人内皮细胞胞间粘附分子-1表达量的影响[J].解放军医学杂志,1999,24(3):179
20. 陶晓根,承韶辉,王锦权.糖皮质激素抵抗与脓毒血症[J].中国危重病急救医学,2001,13(5):307-309
21. Asadullah K, Sterry W, Volk HD. Interleukin-10 therapy review of a new approach[J]. Pharmacol Rev, 2003,55(2):241-69
22. 陈刚,傅志仁,王梁华,等.人白介素10对异种内皮细胞保护作用的研究[J].中国免疫学杂志,2004,20(6):410-12
23. Alloatti G, Penna C,Mariano F, et al. Role of NO and PAF in the impairment of skeletal muscle contractility induced by TNF- α [J].Am J Physiol Regulatory Integrative Comp Physiol,2000,279(6):R2156-63
24. Mayer K, Merfels M, Muhly-Reinholz M, et al. Omega-3 Fatty acids suppress monocyte adhesion to human endothelial cells: role of endothelial PAF generation[J].Am J Physiol Heart Circ Physiol,2002,283(2):H811-18
25. Schuster DP, Metzler M, Opal S, et al. Recombinant platelet-activating factor acetylhy-drolase to prevent acute respiratory distress syndrome and mortality in severe sepsis: Phase IIb, multicenter, randomized, placebo controlled, clinical trial[J]. Crit Care Med, 2003,31(6):1612-19
26. Hawiger J. Innate immunity and inflammation: a transcriptional paradigm[J]. Immunol Res, 2001,23(2-3):99-109
27. Petrache I, Verin AD, Crow MT, et al. Differential effect of MLC kinase in TNF-alpha-induced endothelial cell apoptosis and barrier dysfunction[J]. Am J Physiol Lung Cell Mol Physiol, 2001,280(6):L1168-78
1. Mermel LA, Farr BM, Sherertz RJ, et al. Guidelines for the management of intravascular catheter-related infection[J]. Clin Infect Dis,2001,32(9):1249-72
2. 杜斌,陈德昌,刘大为.危重病患者中心静脉插管相关性感染的前瞻性研究[J].中华外科杂志,1997,35(7):398-401
3. David A, Risitano DC, Mazzeo G, et al. Central venous catheters and infections[J]. Minerva Anestesiol,2005,71(9):561-64
4. 邹琳,俞森洋.导管相关感染的病原学及相关危险因素[J].中华医院感染学杂志,2005,15(4):405-407
5. 申捷,何岱昆,唐耀东.危重病人静脉导管相关性感染[J].中国医师进修杂志,2006,29(1):6-8
6. Dobbins BM, Catton JA, Kite P, et al. Each lumen is a potential source of central venous catheter-related bloodstream infection[J].Crit Care Med,2003,31(6): 1688-90
7. Goetz AM, Wagener MM, Miller JM, et al. Risk of infection due to central venous catheters: effect of site of placement and catheter type[J].Infect Control Hosp Epidemiol,1998,19(11):842-45
8. 郑立,李义贤,洪瑞乔,等.三种中心静脉置管导管相关性感染的对比研究[J].护士进修杂志,2006,21(9):783-85
9. 沃建华,黄韬,陆立平.中心静脉导管相关性脓毒症分析[J].中国实用外科杂志,2002,22(5):313
10. Ferrett G, Mandala M, Cosimo SD, et al. Catheter-related blood stream infections, part II: specific pathogens and prevention [J]. Cancer Control,2003, 10(1):79-91
11. Nouwen JL, Wielenga JJ, van Overhagen H, et al. Hickman catheter-related infections in neutropenic patients: insertion in the operating theater versus insertionin the radiology suite[J]. J Clin Oncol, 1999, 17(4):1304-10
12. Beghetto MG, Victorino J, Teixeira L,et al. Parenteral nutrition as a risk factor for central venous catheter–related infection[J]. JPEN J Parenter Enteral Nutr, 2005, 29(5):367-73
13. Deshpande KS, Hatem C, Ulrich HL, et al. The incidence of infectious complications of central venous catheters at the subclavian, internal jugular, and femoral sites in an intensive care unit population[J]. Crit Care Med, 2005, 33(1): 234-35
14. Eggimann P, Pittet D. Overview of catheter-relateel infections with special emphasis on prevention based on educational programs[J]. Clin Micro Infect, 2002, 8(5): 295- 309
15. O'Grady NP, Alexander M, Dellinger EP, et al. Guidelines for the prevention of intravascular catheter-related infections[J]. Infect Control Hosp Epidemiol.2002, 23(12):759-69
16. 丁士芳,王可富,周炜,等.中心静脉导管相关性真菌败血症的临床分析[J].中国现代普通外科进展,2005,8(1):50-51
17. 薛春华,花天放,吴鹏,等.中心静脉导管相关性感染[J].中国抗感染化疗杂志,2004,4(4):213-15
18. 夏欣华.ICU内中心静脉导管相关感染56例次分析[J].中国危重病急救医学2002,14(12):735
19. Viale P, Pagani L, Petrosillo N, et al. Antibiotic lock-technique for the treatment of catheter- related bloodstream infections[J]. J Chemother,2003,15(2):152-56
20. 孙 少 川 , 李 富 彬 . 中 心 静 脉 导 管 相 关 感 染 的 防 治 进 展 [J]. 医 学 综 述 , 2002,8(1):51-52