腰池连续引流结合药物治疗蛛网膜下腔出血与单纯脑脊液置换疗效对比分析研究
摘要
目的：蛛网膜下腔出血(subarachnoid hemorrhage，SAH)是神经内科常见急危重症之一，致死、致残率高，除了急性期急性脑脊液循环梗阻、脑积水、高颅压等早期病理因素外，迟发性脑血管痉挛(delayed cerebral vessels spasm，DCVS)是SAH的常见并发症，其发生率可高达30％—60％[1]，是SAH患者致死、致残的主要原因。内科保守治疗SAH愈后较差，采用腰穿脑脊液置换术能加快蛛网膜下腔积血的清除速度，减少并发症、降低致死、致残率，是临床上常用的治疗方法之一，但此方法引流脑脊液的数量有限，且反复腰穿易造成病人紧张。腰池置管脑脊液连续外引流术遵循脑脊液循环的生理机制，每天引流脑脊液量大，积血的清除速度快，联合椎管注入尿激酶(Urokinase，UK)及地塞米松可最大限度的溶解积血，降低颅内压及减少血性脑脊液的刺激，能更有效的减少脑血管痉挛发生，国内外仅有少量报道[2，3，4]。本文以单纯腰穿脑脊液置换术为对照，研究脑脊液连续引流结合椎管内注入UK及地塞米松对SAH的治疗作用，同时应用经颅多普勒(TCD)检测观察脑脊液连续引流结合椎管内注入UK及地塞米松治疗(联合治疗组)对DCVS的预防作用，为临床上采取更有效的治疗SAH和预防DCVS的方法提供试验依据。
方法：将我院2003年6月致2006年6月入院的符合1996年全国脑血管病学术会议制订的SAH诊断标准[5]的SAH患者随机分为单纯脑脊液置换组和联合治疗组。患者入院后均作Hunt分级，常规应用脱水剂、止血剂和钙离子拮抗剂等。在无腰穿禁忌症的情况下，脑脊液置换术组：常规腰穿，分次放出脑脊液20ml，注入等量生理盐水置换，入院前4d每同脑脊液置换一次，以后改为隔天一次或三天一次。联合治疗组于入院后4～6 h内应用腰池置管脑脊液持续外引流术，测初压后，置入硬膜外麻醉导管，控制引流速度为每24 h引流150～300ml，以后的3天内，每引流24 h椎管内注射尿激酶(UK)2万U，12 h后椎管内注射地塞米松10mg，每次注药后闭管2h。两组均以头颅CT显示蛛网膜下腔积血消失或脑脊液变清亮、压力正常为结束脑脊液置换和引流指标。观察并记录两组病例头痛缓解时间、脑脊液压力恢复正常时间、意识清醒时间，并于引流后第1、2、4、7、10、15 d作CT检查记录蛛网膜下腔积血的清除时间；所有患者手术后每天应用TCD探测颅内各血管的血流速度(流速>140cm／s视为存在血管痉挛)发现血管痉挛的病例，比较两组DCVS的发生率。
结果：共收集SAH患者74人，脑脊液置换术组35例，联合治疗组39例。两组患者在性别，年龄，疾病构成上无显著性差异。治疗前Hunt分级两组间也无显著性差异，联合治疗组在头痛缓解时间、蛛网膜下腔积血清除时间、脑脊液压力正常时间、脑脊液常规、生化恢复正常时间、意识清醒时间、DCVS的发生率等方面均少于脑脊液置换术组(p＜0.05)。
结论：1．腰池连续引流联合椎管注入尿激酶(uK)和地塞米松治疗蛛网膜下腔出血方法安全，临床综合效果优于常规脑脊液置换法，DCVS发生率低。2．脑脊液连续引流联合椎管内注入尿激酶和地塞米松治疗SAH的方法，简单易操作，治疗效果好，适合临床使用。
Obejective: subarachnoid hemorrhage (SAH) is one of the emergencies in neurology department, delayed cerebral vessels spasm (DCVS)is its common complication with high incidence rate about 30%-60%. DCVS is the most important death cause of SAIl patients. It is difficult to cure these patients with only medical treatment. Replacement of the cerebrospinal fluid by lumbar puncture can clean up haematocele in subarachnoid space quickly and decrease the incidence of mutilation and death and now it is widely used to treat SAH patients. But with this method the cerebrospinal fluid being drained is limited and patients are easy to be nervous. Persistent cerebrospinal fluid draining by putting a canal in lunar subarachnoid space, which abide by the physiological mechanisms of cerebrospinal fluid circulation and more cerebrospinal fluid could be replaced, more hematocele could be cleared. Combined treatment with Urokinase(UK) and dexamethasone can dissolve most of the hematocele, lower the intracranial pressure, palliate the blood irritation and decrease the incidence of cerebral vessel spasm. Some research have been done in overseas, we did not find any research about this field in china. In this research we investigate the curative effect of persistent cerebrospinal fluid draining by lumbosubarachnoid cannula combining with UK and dexamethasone intradural injection to SAH patients, compared with the common method of replacing the cerebrospinal fluid by lumbar puncture. We also investigate its preservation effect to DCVS diagnosed by TCD.
Method: Divide the SAH patients in our hospital from 2003.6 to 2006.6 into treatment group and control group. All these patients were diagnosed by the SAIl diagnostic criteria established by the chinese cerebrovascular disease metting 1996, and confirmed by computed tomography(CT). Hunt level were scored every patient.All of them were treated with dehydrater, haemostat, and calcium channel blocker. Patients in the control group received lumbar puncture and replacement of the cerebrospinal fluid,as 20ml cerebrospinal fluid was released and equal volume of normal saline was injected. In the first 4days once replacement every day, in the after days once every 2 or 3 days.Patients in the treatment group were dealt with persistent cerebrospinal fluid draining by lumbosubarachnoid cannula combining with Urokinase(UK) and dexamethasone intradural injection. Patients received normal lunar puncture. After measuring the intracranial pressure, a 16 code segmental eqidural catheter was put into the cephalad subarachnoid space. A tubing and an asepsis drainage pack were connected to the end of the catheter, controlling the drainage rate to 150～300ml/24h.In.the following 3 days, 20 thousand units UK was injected intradural and the catheter was clipped for 2h after 24h drainage. 12h after UK was injected, 10mg dexamethasone was injected intradural and the catheter was clipped for 2h again. In both group, when the routine and biochemistry examination of the cerebrospinal fluid was completely normal, the replacement or drainage ended. Record the time when the headache was relieved, the cerebrospinal fluid pressure was normal and the patients woke up,respectively. CT scans was done at 1, 2, 4, 7, 10 and 15 days after the drainage ended to record the time when the haematocele was cleared up. All these patients received TCD every day after the operation, to detect the blood flow rate of all intracranial vassels DCVS was diagnosed if the blood flow rate was beyond 140cm/s and identified by MRA. Compared the incidence of DCVS between these two groups.
Result: There were 39 patients in the treatment group and 35 patients in the control group. There were e in sex age and disease composition and the hunt level between these two groups,.There were significant differences in time of headache relief, haematocele disappearing, cerebrospinal fluid pressure becoming normal and patients waking up between these two groups. The incidence of DCVS was significant different between these two groups, too. Conclusion: Treating SAH patients with persistent cerebrospinal fluid draining by lumbosubarachnoid cannula combining with UK and dexamethasone intradural injection is safe and effective, which have a better curative effect and a lower incidence of DCVS.than the common method of replacing the cerebrospinal fluid by lumbar puncture
方法：将我院2003年6月致2006年6月入院的符合1996年全国脑血管病学术会议制订的SAH诊断标准[5]的SAH患者随机分为单纯脑脊液置换组和联合治疗组。患者入院后均作Hunt分级，常规应用脱水剂、止血剂和钙离子拮抗剂等。在无腰穿禁忌症的情况下，脑脊液置换术组：常规腰穿，分次放出脑脊液20ml，注入等量生理盐水置换，入院前4d每同脑脊液置换一次，以后改为隔天一次或三天一次。联合治疗组于入院后4～6 h内应用腰池置管脑脊液持续外引流术，测初压后，置入硬膜外麻醉导管，控制引流速度为每24 h引流150～300ml，以后的3天内，每引流24 h椎管内注射尿激酶(UK)2万U，12 h后椎管内注射地塞米松10mg，每次注药后闭管2h。两组均以头颅CT显示蛛网膜下腔积血消失或脑脊液变清亮、压力正常为结束脑脊液置换和引流指标。观察并记录两组病例头痛缓解时间、脑脊液压力恢复正常时间、意识清醒时间，并于引流后第1、2、4、7、10、15 d作CT检查记录蛛网膜下腔积血的清除时间；所有患者手术后每天应用TCD探测颅内各血管的血流速度(流速>140cm／s视为存在血管痉挛)发现血管痉挛的病例，比较两组DCVS的发生率。
结果：共收集SAH患者74人，脑脊液置换术组35例，联合治疗组39例。两组患者在性别，年龄，疾病构成上无显著性差异。治疗前Hunt分级两组间也无显著性差异，联合治疗组在头痛缓解时间、蛛网膜下腔积血清除时间、脑脊液压力正常时间、脑脊液常规、生化恢复正常时间、意识清醒时间、DCVS的发生率等方面均少于脑脊液置换术组(p＜0.05)。
结论：1．腰池连续引流联合椎管注入尿激酶(uK)和地塞米松治疗蛛网膜下腔出血方法安全，临床综合效果优于常规脑脊液置换法，DCVS发生率低。2．脑脊液连续引流联合椎管内注入尿激酶和地塞米松治疗SAH的方法，简单易操作，治疗效果好，适合临床使用。
Obejective: subarachnoid hemorrhage (SAH) is one of the emergencies in neurology department, delayed cerebral vessels spasm (DCVS)is its common complication with high incidence rate about 30%-60%. DCVS is the most important death cause of SAIl patients. It is difficult to cure these patients with only medical treatment. Replacement of the cerebrospinal fluid by lumbar puncture can clean up haematocele in subarachnoid space quickly and decrease the incidence of mutilation and death and now it is widely used to treat SAH patients. But with this method the cerebrospinal fluid being drained is limited and patients are easy to be nervous. Persistent cerebrospinal fluid draining by putting a canal in lunar subarachnoid space, which abide by the physiological mechanisms of cerebrospinal fluid circulation and more cerebrospinal fluid could be replaced, more hematocele could be cleared. Combined treatment with Urokinase(UK) and dexamethasone can dissolve most of the hematocele, lower the intracranial pressure, palliate the blood irritation and decrease the incidence of cerebral vessel spasm. Some research have been done in overseas, we did not find any research about this field in china. In this research we investigate the curative effect of persistent cerebrospinal fluid draining by lumbosubarachnoid cannula combining with UK and dexamethasone intradural injection to SAH patients, compared with the common method of replacing the cerebrospinal fluid by lumbar puncture. We also investigate its preservation effect to DCVS diagnosed by TCD.
Method: Divide the SAH patients in our hospital from 2003.6 to 2006.6 into treatment group and control group. All these patients were diagnosed by the SAIl diagnostic criteria established by the chinese cerebrovascular disease metting 1996, and confirmed by computed tomography(CT). Hunt level were scored every patient.All of them were treated with dehydrater, haemostat, and calcium channel blocker. Patients in the control group received lumbar puncture and replacement of the cerebrospinal fluid,as 20ml cerebrospinal fluid was released and equal volume of normal saline was injected. In the first 4days once replacement every day, in the after days once every 2 or 3 days.Patients in the treatment group were dealt with persistent cerebrospinal fluid draining by lumbosubarachnoid cannula combining with Urokinase(UK) and dexamethasone intradural injection. Patients received normal lunar puncture. After measuring the intracranial pressure, a 16 code segmental eqidural catheter was put into the cephalad subarachnoid space. A tubing and an asepsis drainage pack were connected to the end of the catheter, controlling the drainage rate to 150～300ml/24h.In.the following 3 days, 20 thousand units UK was injected intradural and the catheter was clipped for 2h after 24h drainage. 12h after UK was injected, 10mg dexamethasone was injected intradural and the catheter was clipped for 2h again. In both group, when the routine and biochemistry examination of the cerebrospinal fluid was completely normal, the replacement or drainage ended. Record the time when the headache was relieved, the cerebrospinal fluid pressure was normal and the patients woke up,respectively. CT scans was done at 1, 2, 4, 7, 10 and 15 days after the drainage ended to record the time when the haematocele was cleared up. All these patients received TCD every day after the operation, to detect the blood flow rate of all intracranial vassels DCVS was diagnosed if the blood flow rate was beyond 140cm/s and identified by MRA. Compared the incidence of DCVS between these two groups.
Result: There were 39 patients in the treatment group and 35 patients in the control group. There were e in sex age and disease composition and the hunt level between these two groups,.There were significant differences in time of headache relief, haematocele disappearing, cerebrospinal fluid pressure becoming normal and patients waking up between these two groups. The incidence of DCVS was significant different between these two groups, too. Conclusion: Treating SAH patients with persistent cerebrospinal fluid draining by lumbosubarachnoid cannula combining with UK and dexamethasone intradural injection is safe and effective, which have a better curative effect and a lower incidence of DCVS.than the common method of replacing the cerebrospinal fluid by lumbar puncture
引文
[1] 陈国志，罗其中．蛛网膜下腔出血后CVS的研究进展[J]临床神经病学杂志，1999，12：126-127．
[2] 易利人．腰穿脑脊液置换治疗蛛网膜下腔出血36例[J]中国神经精神疾病杂志，1995，21：373
[3] 王维治．神经病学[M]人民卫生出版社(第4版)2002，15
[4] Li YH, Guo K, Zi XH, Song Z. Combining exchange of cerebrospinal fluid with small dose of urokinase injection for subarachnoid hemorrhage [J] . J Cent South Univ (Med Sci), 2005, 3:217—219.
[5] 王维治．神经病学[M]人民卫生出版社(第4版)2002，154
[6] Lysakowski C, Walder B, Costania MC, et al. Transcranial Doppler versus angiography in patients with vasospasm due to a ruptured cerebral aneurysm: a ystematic review[J]. Stroke, 2001, 32:2292-2298.
[7] 史玉泉．实用神经病学[M]上海科学技术出版社(第2版)，1994．，648-650
[8] Servadeif, Antongelliv, Giullantg, et al. Evolving lesions in tuanmatic subarachnoid hemorrhage: orospective study of 110 patients with emphasis on the role of ICP monitoring [J]. Acta Neurochirurgica—Supplement. 2002, 81:81-82.
[9] Kourtopoulosh, lindgrens, obergl. Ruptured intranranial aneuysms in infancy. Dianmostic difficulties and overall reflections associated with the surgical treatment and the treatment of vasospasm[J]. Acta Neurochir(wien). 2000, 142: 1425-1426
[10] Oyama K, Criddle L. Vasospasm after aneurysmal subarachnoid hemonftage[J] . Critical Care Nurse. 2004, 24: 58—67.
[11] Aiharay, JahromiBS, YassariR et al Molecular profile of vascularion channels after experimental subarachnoid hemorrhagee [J]. Cereb Blood Flow Metab, 2004, 24: 75-83
[12] Tran Dinh YR, Roche S, Debdi M, et al. Effects of oxyhemoglob in invitro in cerebral arteries from normal animals and animals subject to subarachnoid hemorrhage orindomethacin treatment [J]Brain Res, 1998, 790: 91-97.
[13] 冀勇，王中，周岱．动脉瘤性蛛网膜下腔出血病人血液NF-KB与sICAM-I，ET-1的动态变化[J]．中国急救医学．2005，25：17-19．
[14] 徐宗荣，贾志慧，朱慧云，等，脑脊液置换合用尼莫地平治疗蛛网膜下腔出血的疗效分析[J]．中风与神经疾病杂志．1998，15：307
[15] Lorenzi L, Kerr ME, Yonas H, et al. Influence of delaying treatment after symptoms develop from subarachnoid hemorrhage: a preliminary analysis. [J]. Neurosci Nuts, 2003, 35: 210-214.
[16] 黄清海，刘建民，许弈，等．腰椎穿刺蛛网膜下腔置管持续引流防治脑血管痉挛的初步观察．[J]．第二军医大学报，2001，22：784-786．
[17] Todo T, Udai M, Takakura K. Treatment of severe intraventricular hemorrhage by intraventricular infusion of urokinase[J]. Neurosury, 1991, 74-81.
[18] Lin Zh, Zhang Sl, Zwng Zb, et al. the clinicao study of ventuicular model hemorrhage treated by ventricular duainage combined with CSF replacement [J]. China Journal of moden Medicine, 2003, 13(2): 82-83. Chinese
[19] Wang XZ, Zhang ZT, Liu B. The treatment of venteicular model hemoohage by ventricular drainage irrigatin and CSF replacement[J]. Heillongjiang Medicine and Pharmacy, 2004, 27: 57. Chinese
[20] ZHANG TD, LI X. The clincal effects of 31 intraventricuar model hemorrhage patients treated by lateral ventricular duainage and terminal cistern CSF replacement [J]. China clinical neuroscience, 2004, 12: 421-422. Chinese
[21] Pang D, Sclabassi Rj, Horton Ja. Lysis of intraventricular blood clot with urokinase in a canine model: Part 1, part 2 [J]. Neurosurgery, 1986, 19:540-547.
[1] Suzuki N, Matsumoto H, Kitada C, et al. A sensitive sandwich enzyme immunoassay for human endothelin [J] immunol Methods, 989,118: 245—250 .
[2] Masaoka H, Suzuki R, Hirata Y, et al . Raised plasma endothelin in aneurismal subarachnoid haemorrhage [J] .Lancet, 1989, 11: 1402.
[3] Hacker G .The morphology of apoptosis[J].Cell Tiss Res, 2000, 301;5-17.
[4] Oginara K, Zubkov AY, B ernanke DH, et al. Oxyhemoglob ininduced a poptosis in cultured endothelial cells [J]. J Neurosurg, 1999, 91: 459-465.
[5] Yanagisawa M, Kurihara H, Kimura S, et al . A novel vasocontrictor peptide produced by vascular endothelin cells J. Nature, 1988, 322: 411—415.
[6]唐朝枢,谢选珠．内皮素(Edothelin)[J]．北京医科大学学报,1989,21： 163-164．
[7] Suauki R, Masaoka H, Hirata Y, et al. The role of endothelin-1 in the origin of cerebral vasospasm in patients with aneurismal subarachnoid haemorrhage [J] J Neurosurgery, 1992, 77:96-100.
[8] Mima T, Yanagisawa M, Shigeno T, et al. Endothelin acts in feline and canie cerebral arteries from the adventitial side. [J]. Stroke, 1989, 20:1553 .
[9] Ogihara K, Aoki K, Zubkov AY, et al. Oxyhemoglobin produces apoptosis and necrosis in cultured smooth muscle cells[J]. Brain Res, 2001, 889:89-97.
[10] Zubkov AY, tibbs RE, Clower B , et al.M orphological changes of cerebral arteries in a canine double hemorrhage model[J]. Neurosci Lett 2002, 326:137-141.
[11] Zhou C,Yamaguchi M, Kusaka G, et al.Caspase in hibitors preventen dothelial apoptosis and cerebral vasospasm in dog model of experimental subarachnoid hemorrhage [J]. J Cereb Blood Flow Metab, 2004, 24:419-431.
[12] Zhou C , Yamaguchi M , Colohan AR, et al.Role of p53 and apoptosis in cerebral vasospasm after experimental subarahnoid hemorrhage[J]. J Cereb Blood Flow Metab, 2005, 25: 572-582.
[13] Meguro T , Chen B, Lancon J, et al.Oxyhemoglobin induces caspase mediated cell death in cerebral endothelial cells [J]. Neurochem, 2001, 77.1128-1135.
[14] Meguro T, Chen, Parent AD, et al. Caspasin hibitors attenuate oxyhemoglobininduced apoptosis inendothelial cells [J] . Stroke, 2001, 32: 561-566.
[15] Sehnan WR. Vasospasm[J]. Neurosurgery, 2004, 100: 208-209.
[16] Dumont AS, Dumont RJ, Chow MM, et al. Cerebral vasospasm after subarachnoid hemorrhage: putative role of inflammation [J] Neurosurgery, 2003, 53:123-135.
[17] Biondi A, Ricciatdi GK, Puybasset L , et al. Intra arterial nimodipine for the treatment of symptomatic cerebral vasospasm after aneurysmal subarachnoid hemorrhage: preliminary results[J]. Neuroradiology, 2004, 25: 1067-1076.
[18] Bhardwaj A. SAH induced cerebral vasospasm: unravelin grnolecularmec hanisms of a complex disease[J]. Stroke, 2003, 134: 427-433.
[19] Hayashi T, Hasegawa K, Morimoto M, et al. Effect of antibodies to intercelular adhesion molecule (ICAM)-1 and lymphocyte function associated antigen(LFA)-1 on cytokine mRNA expression in reovirus type-2-triggered autoimmune insutitis in suckling DBA/1 mice[J] Comp Pathol, 2003, 128:283-288.
[20] Weil R, Israel AT-cell-receptor-and B-cell-receptor-mediated activation of NF-kappaB in lymphocytes [J] Curr Opin in Immunol, 2004, 16: 374-381.
[21] Mendel R, Carter LP. Evaluation and treatment of clinical J Neuro Shimoda M, following subaraclinoid aneurysms., 16: 6-12
[22] Tsugane R, et al. Intracranial complications of hypervolemic therapy inpatients with a delayed ischemic deficit atributed to vasospasm. J Neurosuryg, 1993, 78: 423-428
[23] Hirashima Y, Endo S, Otsuji T, KarasawaK, Nojima S, Takakua, Plateletactivating factor and cerebral vasospasm following subarachnoid hemorrhage. J Neurosurg 1998, 78: 592-599
[24] CammussiG, PiacribelloW, AglietaM, Codar, BussolinoF, TetaC, Release factor(PAF) and histamine Ⅱ. Of The platelet-activating cellularorigin of human PAF: monocytes, polymorphonuclear neutrophils and basophils. Immunology, 1998, 42: 191-197
[25] Freyssinet JM, WieselML, Gauchy J, Boneu B,CazenaveJ-P neutralizes the An IgM lupus anticoagulant thatenhancing efect of phospholipid on 39 purified endothelial thrombomodulin activity. A mechanism for thrombosis. Thromb Haemost 1996,53:309-315
[26] Harris EN, Gharvani AE, Hughes GRV, Anti-phospholipid antibodies. Clin Rheum Dis 1985,11:591-599
[27] Wachtfogel YT, Cadena RA, and Colman RW. Structural Biology ,cellular interactions and poathophysiology of the contact system. Thromb Res,1999, 72:1-9
[27] Mosesson MW The roles of fibrinogen and fibrin in hemostasis and thrombosis. 29:177-179 Semin Hematol, 1992,
[28] Colman RW, Hirsh J, Marder VJ, et al. Hemostasis and Thrombosis: Basic principles and clinical practice. 3'0 ed. Philadelphia: Lippincott Company, 1994,3-7
[29] Slack SM, Cui YW, and Turitto VT. The efect of flow on blood coagulation and thrombosis. Thromb Haemost, 1998, 70:129-136
[30] Hiroyuki Shibahashi Akira Yamaura, Coagulation-Fibrinolytic Abnormality and Symptomatic Vasospasm in the Acute Stage of Ruptured Cerebral Aneurysms. Neurol Med Chir(Tokyo)1991,43:239-246
[31] YHirashima, M.Kurimoto, E. Tsukamoto, S. Endo, Anti-Phospholipid Antibodies and cerebral vasospasm following subarachnoid haemorrhage. Actaneurochir (Wien) 1999,135:191—196
[32] Hidetoshi Kasuya,MDJakashi Shimizu, MD. Activated complement components C3a and C4a in cerebrospinal fluid and plasma following subarachnoid hemorrhage) Neurosurg 1999,71:741-749
[33] FeilJM, florWJ, CohanSL, ParkhurstJ, Sequential changes of vascular ultrastructure in experimental vasospasm. J Neurosurg 1994, 41:49-54
[34] Smith R R, Clower BP, Peeler DF,Yoshiokaj, The angiopathy of subarachnoid hemorrhage:angiographic and morphologic correlates. Stroke 1983,14:240-251
[35] Anderson GB, AshforthR, Steinke DE, et al. CT angiography for the detection of cerebral vasospasmin patients with acute subarachnoid hemorrhage [J].Am J Neuroradiolg 2000,21: 1011-1015.
[36]Lysakowski C,Walder B,Costania MC,et al.Transcranial Doppler versusangiography in patients with vasospasm due to a Ruptured cerebral aneurysml :a systematic reviewe[J].Stroke,2001.32,12292-2298.
[37]Harrigan MR,Magnano CR,Guterman LR,etal. Computed to mographic perfusion in the management of aneurismal subarachnoid hemorrhagel new application of an existent technique [J]Neurosurgeryg 2005,56: 304-317.
[38] GriffithsPD,Wilkinson ID,Mitchell P,etal.Multimodality MR imaging depiction of hemodynamic changes and cerebralischemia in subarachnoid hemorrhage[J].Am J Neuroradiolg 2001,22:1690-1697.
[39]Busch E, Beaulieu C, de Crespigny A, etal. Diffusion MR imaging during acute subarachnoid hemorrhage in rats[J].Strokeg 1998,29:12155-2161.
[40]Rowe J, Blamire AM, Domingo Z,etal.Discrepancies between Cerebral perfusion and metabolism after subarachnoid haemorrhagel a magnetic resonance approach[J].J NeurolNeurosurg Psychiatry,1998,64: 98-103.
[41]. Roski RA, Spetzler RF, Carotid ligation. In: Wilkins RH,Rengachary SS, eds. Neurosurgey, end ed, Vol II. New York: McGraw-HILL, 1996.2333-2340
[42] NishizawaY Doi M, Miura K, et al. Clinical andexperimental studies on the preventive efect of nicardipine for symptomatic vasospasm. 8' European Congress of Neurosurg. Barcelona, spain 1987, 279-283
[43] Fujita K, Yamashita H, Tamaki n, Matsumoto S. Et al.The efects of ticlopidine and nicardipine on the prevention of the symptomatic vasospasm after SAH. International Symosium on Surgery for Cerebral Stroke, Spain 1987,147-158
[44] Schneck SA, KrichefflI. Intracranial aneurysm rupture,vasospasm,and infarction. Arch Neurol, 1964,11:668-674
[45] Gruber A, Ungerbock K, Reinprecht A et al. Evaluation of cerebral vasospasm after early surgical and endovascular treatment of ruptured intracranial aneurysm. Neurosurgery 1998. 42:258-263
[46] Handa Y Weir BKA, Nosko M, et al. The efect of timing of clot removal on chronic vasospasm in a primate model, J Neurosurg, 1987, 67: 558-566
[47] Hijdra A, Van Gijn J, Nagelkerke NJ, et al. Prediction of delayed cerebral ischemia, rebleeding, and outcome after aneurysmal subarachnoid hemorrhage. Stroke, 1988, 1900: 1250-1256
[48] Hijdra A, Van Gijn J, S, et al. Delayed cerebral ischemia after aneurysm subrachnoid hemorrhage: clinicoanatomic correlations. Neurology, 1986, 36(3): 329-333.
[49] Weir B, Grace M, Hansen J, et al. Time course of vasospasm in man. J Neurosurg, 1978, 48(2): 173—178.
[50] Kassell NF, Peerless SJ, Durward QJ, er al. Treatment of ischmic deficits from vasospasm with intravascular volume expansion andf induced arterial hypertention. Neurosurgery, 1982, 11(3): 337-343.
[51] Hirashima Y, Endo S, Otsuji T, KarasawaK, Nojima S, Takakua, Platelet-activating factor and cerebral vasospasm following subarachnoid hemorrhage. J Neurosurg 1993, 78: 592-599
[52] CammussiG, AglietaM, Codar, BussolinoF, PiacribelloW, TettaC, Release of platelet-activating factor(PAF) and histamine Ⅱ. The cellular origin of human PAF: monocytes, polymorphonuclear neutrophils and basophils. Immunology, 1981, 42: 191—197
[53] Freyssinet JM, WieselML, Gauchy J, Boneu B, CazenaveJ-P An I9M lupus anticoagulant that neutralizes the enhancing efect of phospholipid on purified endothelial thrombomodulin active mechanism for thrombosis. Thromb Haemost 1986, 53: 309-315
[54] Harris EN, Gharvani AE, Hughes GRYAnti-phospholipid antibodies. Clin Rheum Dis 1985, 11: 591-599
[55] YHirashima, M. Kurimoto, E. Tsukamoto, S. Endo, Anti-Phospholipid Antibodies and cerebral vasospasm following subarachnoid haemorrhage. Acta neurochir (Wien) 1995, 135: 191—196
[56] Shinichi Tamatani, Osamu Sasaki. Detection of delayed cerebral vasospasm, after rupture of intracranial aneurysm, by magnetic resonance angiography. Neurosurgey 1997, 40: 748-753
[57] Keogh AJ, Vhora S. The usefulness of magnetic resonance angiography in surgery for intracranial aneurysm that have bled. Surg Neurol 1998 50: 122-127
[58] 魏东，万琪．核因子kappaB在脑缺血病理生理过程中的作用[J]．国外医学·脑血管疾病分册，2004，12：285-288．
[59] Wong CK, WK, Lam CW. Interleukin-3-5, and granulocyte macrophage colony-stimulating factor-induced adhesion molecule expression on eosinophils by p38 mitogen-activated protein kinase and nuclearfactor-[kappa]B [J] Am J of Respira Ceel & Mol Biol, 2003, 29(1): 133-147.
[60] Shumway SD, Berchtold CM, Gould MN, etal. Evidence for unique calmodulin-dependent nuclearfactor-KB regulation in WEHI-231B ceels [J] Mol Pharmacol, 2002, 61: 177-185.
[61] Li TL, Liu YJ. Diagnosis and treatment for subarachnoid hemorrhage patient [J]. Chinese Medical Journal, 2003; 83(1): 3-5.
[62] Ma L, Zhang HP, Zhang XM, Lu HB. Clinical observation of treating arachnoid hemorrhage by cerebrospinal fluid replacement[J]. Chinese Journal of the Practical Chinese with Modern Medicine, 2005; 18: 687-688.
[63] Zhang C. Emergency treatment of modern neurology [M]. Qingdao: Qingdao Publishing House; 1994. 145.
[64] Katoh H, Shima K, Shimizu A, et al. Clinical evaluation of the effect of percutaneous transluminal angioplasty and intra-arterial papaverine infusion forthe treatment of vasospasm following aneurysmal subarachnoid hemorrhage[J]. Neurol Res, 195-203.
[65] Zimmermann M, Seifert V. Endothelin thelin and subarachnoid hemorrhage an overview [J]. Neurosurgery, 1998, 43: 843-853.
[66] Kwan AL, Lin CL, Chang CZ, et al. Continuous intravenous infusion of CGS26303, an endothelin-converting enzyme inhibitor, prvene and reverses cerebral vasospasm after experimental subarachnoid hemorrhage[J]. Neurosurgery, 2001, 49: 422-427.
[67] Clatterbuck RE, Gailloud P, Ogata L, et al. Prevention of cerebral vasospasm by a humanized anti-CD11 / CD18 monoclonal antibody administered after experimental subarachnoid hemo- -rrhage in nonhuman primates [J].JNeurosurg, 2003, 99:376-382.
[68] Pradilla G, Wang PP, Legnani FG, et al, Prevention of vasospasm by anti-CD11 /CD18 monoclonal antibody therapy following subarachnoid hemorrhage in rabbits[J.J Neurosurg, 2004,101:88-92.
[69] Satoh M, Parent AD, Zhang J H.Inhibitory effect with antisense mitogen-activated protein kinase oligodeoxynucleotide against cerebral vasospasm in rats [ J] . Stroke, 2002, 33775-781.
[70] Kusaka G, Kimura H, Kusaka I, et al. Contribution of Srctyrosine kinase to cerebral vasospasm after subarachn oid hemorrhage [J] J Neurosurg, 2003, 99383-390.
[71] Treggiari MIU, Romand JA, Martin JB, et al. Cervical sympathetic block to reverse delayed ischemic neurological deficits after aneurysmal subarachnoid hemorrhage[J].Stroke, 2003, 34:961-967.
[72] Handa Y, Weir BK, Nosko M, et al. The effect of timing of clot removal onchronic vasopasm in a primate model [J].J Neurosurg, 1987, 67:558-564.
[73] Bejjani GK, Bank WO, Olan WJ, et al. The efficacy and safety of angioplasty for cerebral vasospasm after subarachnoid hemorrhage[J].Neurosurgery, 1998 , 42:979-986.
[74] Khurana VG, Smith LA, Bakert A, et al. Protective vasomotor effects of in vivo recombinant endothelial nitric oxide synthase gene expression in a canine model of cerebral vasospasm [ J] Stroke, 2002, 33 782 - 789.
[75] Petruk KC, Weir BK, Overton TR, Marriot, GraceMG, the efect of graded hypocapnia andhypercapnia on regional cerebral blood flow and cerebral vessel caliberhemodynamics in the rhesus monkey stuty of cerebral following subarachnoid hemorrahge and traumatic internal carotid spasm. Stroke 1973, 5:230-238
[76] Yamagata S, Kikuchi H, Ihara I ,Nagata 1, MorookaY,NaruoY, Koizumi T, Hashmoto K,Miyamoto S, Mitsuno K, MatsumotoMinamikawa J,M, Yamazoe N, Akiyama YCerebral blood flow as a prognostic indicationinsubarachnoid hemorrhage. Neurol Med Chir, 1988,28:333-338
[78] Lennihan L, Mayer SA, Fink ME, et al. Eefect of hypervolemic therapy on cerebral blood volume after subarachnoid hemorrhage: a randomized controlled trial.Stroke, 2000, 31(2):383-39125
[79] Juvela S. Aspirin and delayed cerebral ischemia after aneurismal subarachnoid hemorrhage. J Neurosurg,1995,82(6):945-952
[80] Hop JW Rinkel GJ, Algra, et al. Randomized pilot trial of postoperative aspirin in subarachnoid hemorrhage.Neurology, 2000, 54(4):872-878
[81] Shaw MD, Foy PM, Conway m, er al. Dipyridamole and postoperative ischemic deficits in aneurysmal subrachnoid hemorrhage. J Neurosurg,1985, 63(5):699-703
[82] Fuhrmeister U, Ruether P, Dommatsch D. Alterations of CSF hydrodynamics following meningitis and subarachnoid hemor-rhage, in Shulman K, Marmarou A, Miller JD (eds): Intracraniai Pressure IV. Berlin, Springer Verlag, 1980, pp 241— 244.
[83]Kosteljanetz M: CSF dynamics in patients with subarachnoid and/or intraventricular hemorrhage. J Neurosurg 60:940—946,1984.
[84] Sullivan MG, Sellar R, Statham PF, Whittle IR. Management of poor grade patients after subarachnoid haemorrhage: the importance of neuroradiological findings on clinical outcome. Br J Neurosurg 1996 Oct:10(5):445-5246
[85] Mase M, Yamada K, Banno T, Miyachi T, Ohara S, Matsumoto T. Quantitative analysis of CSF flow dynamicsusingMRI in normal pressure hydrocephalus. Acta Neurochir Suppl (Wien) 1998:71:350-3
[86] Marmarou A, Maset A, Ward JD, Choi S, Brooks D, Lutz HA, Moulton RJ, Muizelaar JP, DeSalles A, Young H. Contrihution of CSF and vascular factors to elevation of ICP in severely head-injured patients. J Neurosurg 66:883—890,1987.
[87] Mehta V, Holness R0, Connolly K, Walling S, Hall R. Acute hydrocephalus following aneurysmal subarachnoid hemorrhage. Can .1 Neurol Sci 1996Feb;23(1):40-5
[88] Gjerris F, Borgesen SE, Sorensen PS, Boesen F, Schmidt K, Harmsen A, Lester J. Resistance to cerebrospinal fluid outflow and intracranial pressure in patients with hydrocephalus after subarachnoid haemorrhage. Ac ta Neurochir (Wien) 1987:88(3-4):79-86
[89] Black PMcL. Hydrocephalus and vasospasm after subarachnoid hemorrhage from ruptured intracranial aneurysms. Neurosurgery 18:12—16,1986. 28:56—59,1991.
[90] Tomei G, Gaini SM, GiovaneJIi M, Rampini P, Granata G, Vi Ilani R. Intracranial pressure in subarachnoid hemorrhage. Preliminary report in 36 cases. J Neurosurg Sci 1981 Apr-,Jun;250 :57-66
[91]Andreas Gruber, M. D., Andrea Reinprecht, M. D., Gerhard Bavinzski, M. D., Thomas Czech, M. D. , Bernd Richling, M. D. Chronic Shunt-dependent Hydrocephalus after Early Surgical and Early Endovascular Treatment of Ruptured intracranial Aneurysms. Neurosurgery, March 1999;Vol. 44
[92] Galera RC, Greitz T. Hydrocephalus in the adult secondary to the rupture of intracranial arterial aneurysms. J Neurosurg 32:634—641,1970.
[93] Kol.luri VR, Sengupta RP. Symptomatic hydrocephalus following aneurysmal subarachnoid hemorrhage. Surg Neurol :402—404,1984.
[94] Suarez-Rivera O. Acute hydrocephalus after subarachnoid hemorrhage. Surg Neurol 1998 May;49(5):563-5
[2] 易利人．腰穿脑脊液置换治疗蛛网膜下腔出血36例[J]中国神经精神疾病杂志，1995，21：373
[3] 王维治．神经病学[M]人民卫生出版社(第4版)2002，15
[4] Li YH, Guo K, Zi XH, Song Z. Combining exchange of cerebrospinal fluid with small dose of urokinase injection for subarachnoid hemorrhage [J] . J Cent South Univ (Med Sci), 2005, 3:217—219.
[5] 王维治．神经病学[M]人民卫生出版社(第4版)2002，154
[6] Lysakowski C, Walder B, Costania MC, et al. Transcranial Doppler versus angiography in patients with vasospasm due to a ruptured cerebral aneurysm: a ystematic review[J]. Stroke, 2001, 32:2292-2298.
[7] 史玉泉．实用神经病学[M]上海科学技术出版社(第2版)，1994．，648-650
[8] Servadeif, Antongelliv, Giullantg, et al. Evolving lesions in tuanmatic subarachnoid hemorrhage: orospective study of 110 patients with emphasis on the role of ICP monitoring [J]. Acta Neurochirurgica—Supplement. 2002, 81:81-82.
[9] Kourtopoulosh, lindgrens, obergl. Ruptured intranranial aneuysms in infancy. Dianmostic difficulties and overall reflections associated with the surgical treatment and the treatment of vasospasm[J]. Acta Neurochir(wien). 2000, 142: 1425-1426
[10] Oyama K, Criddle L. Vasospasm after aneurysmal subarachnoid hemonftage[J] . Critical Care Nurse. 2004, 24: 58—67.
[11] Aiharay, JahromiBS, YassariR et al Molecular profile of vascularion channels after experimental subarachnoid hemorrhagee [J]. Cereb Blood Flow Metab, 2004, 24: 75-83
[12] Tran Dinh YR, Roche S, Debdi M, et al. Effects of oxyhemoglob in invitro in cerebral arteries from normal animals and animals subject to subarachnoid hemorrhage orindomethacin treatment [J]Brain Res, 1998, 790: 91-97.
[13] 冀勇，王中，周岱．动脉瘤性蛛网膜下腔出血病人血液NF-KB与sICAM-I，ET-1的动态变化[J]．中国急救医学．2005，25：17-19．
[14] 徐宗荣，贾志慧，朱慧云，等，脑脊液置换合用尼莫地平治疗蛛网膜下腔出血的疗效分析[J]．中风与神经疾病杂志．1998，15：307
[15] Lorenzi L, Kerr ME, Yonas H, et al. Influence of delaying treatment after symptoms develop from subarachnoid hemorrhage: a preliminary analysis. [J]. Neurosci Nuts, 2003, 35: 210-214.
[16] 黄清海，刘建民，许弈，等．腰椎穿刺蛛网膜下腔置管持续引流防治脑血管痉挛的初步观察．[J]．第二军医大学报，2001，22：784-786．
[17] Todo T, Udai M, Takakura K. Treatment of severe intraventricular hemorrhage by intraventricular infusion of urokinase[J]. Neurosury, 1991, 74-81.
[18] Lin Zh, Zhang Sl, Zwng Zb, et al. the clinicao study of ventuicular model hemorrhage treated by ventricular duainage combined with CSF replacement [J]. China Journal of moden Medicine, 2003, 13(2): 82-83. Chinese
[19] Wang XZ, Zhang ZT, Liu B. The treatment of venteicular model hemoohage by ventricular drainage irrigatin and CSF replacement[J]. Heillongjiang Medicine and Pharmacy, 2004, 27: 57. Chinese
[20] ZHANG TD, LI X. The clincal effects of 31 intraventricuar model hemorrhage patients treated by lateral ventricular duainage and terminal cistern CSF replacement [J]. China clinical neuroscience, 2004, 12: 421-422. Chinese
[21] Pang D, Sclabassi Rj, Horton Ja. Lysis of intraventricular blood clot with urokinase in a canine model: Part 1, part 2 [J]. Neurosurgery, 1986, 19:540-547.
[1] Suzuki N, Matsumoto H, Kitada C, et al. A sensitive sandwich enzyme immunoassay for human endothelin [J] immunol Methods, 989,118: 245—250 .
[2] Masaoka H, Suzuki R, Hirata Y, et al . Raised plasma endothelin in aneurismal subarachnoid haemorrhage [J] .Lancet, 1989, 11: 1402.
[3] Hacker G .The morphology of apoptosis[J].Cell Tiss Res, 2000, 301;5-17.
[4] Oginara K, Zubkov AY, B ernanke DH, et al. Oxyhemoglob ininduced a poptosis in cultured endothelial cells [J]. J Neurosurg, 1999, 91: 459-465.
[5] Yanagisawa M, Kurihara H, Kimura S, et al . A novel vasocontrictor peptide produced by vascular endothelin cells J. Nature, 1988, 322: 411—415.
[6]唐朝枢,谢选珠．内皮素(Edothelin)[J]．北京医科大学学报,1989,21： 163-164．
[7] Suauki R, Masaoka H, Hirata Y, et al. The role of endothelin-1 in the origin of cerebral vasospasm in patients with aneurismal subarachnoid haemorrhage [J] J Neurosurgery, 1992, 77:96-100.
[8] Mima T, Yanagisawa M, Shigeno T, et al. Endothelin acts in feline and canie cerebral arteries from the adventitial side. [J]. Stroke, 1989, 20:1553 .
[9] Ogihara K, Aoki K, Zubkov AY, et al. Oxyhemoglobin produces apoptosis and necrosis in cultured smooth muscle cells[J]. Brain Res, 2001, 889:89-97.
[10] Zubkov AY, tibbs RE, Clower B , et al.M orphological changes of cerebral arteries in a canine double hemorrhage model[J]. Neurosci Lett 2002, 326:137-141.
[11] Zhou C,Yamaguchi M, Kusaka G, et al.Caspase in hibitors preventen dothelial apoptosis and cerebral vasospasm in dog model of experimental subarachnoid hemorrhage [J]. J Cereb Blood Flow Metab, 2004, 24:419-431.
[12] Zhou C , Yamaguchi M , Colohan AR, et al.Role of p53 and apoptosis in cerebral vasospasm after experimental subarahnoid hemorrhage[J]. J Cereb Blood Flow Metab, 2005, 25: 572-582.
[13] Meguro T , Chen B, Lancon J, et al.Oxyhemoglobin induces caspase mediated cell death in cerebral endothelial cells [J]. Neurochem, 2001, 77.1128-1135.
[14] Meguro T, Chen, Parent AD, et al. Caspasin hibitors attenuate oxyhemoglobininduced apoptosis inendothelial cells [J] . Stroke, 2001, 32: 561-566.
[15] Sehnan WR. Vasospasm[J]. Neurosurgery, 2004, 100: 208-209.
[16] Dumont AS, Dumont RJ, Chow MM, et al. Cerebral vasospasm after subarachnoid hemorrhage: putative role of inflammation [J] Neurosurgery, 2003, 53:123-135.
[17] Biondi A, Ricciatdi GK, Puybasset L , et al. Intra arterial nimodipine for the treatment of symptomatic cerebral vasospasm after aneurysmal subarachnoid hemorrhage: preliminary results[J]. Neuroradiology, 2004, 25: 1067-1076.
[18] Bhardwaj A. SAH induced cerebral vasospasm: unravelin grnolecularmec hanisms of a complex disease[J]. Stroke, 2003, 134: 427-433.
[19] Hayashi T, Hasegawa K, Morimoto M, et al. Effect of antibodies to intercelular adhesion molecule (ICAM)-1 and lymphocyte function associated antigen(LFA)-1 on cytokine mRNA expression in reovirus type-2-triggered autoimmune insutitis in suckling DBA/1 mice[J] Comp Pathol, 2003, 128:283-288.
[20] Weil R, Israel AT-cell-receptor-and B-cell-receptor-mediated activation of NF-kappaB in lymphocytes [J] Curr Opin in Immunol, 2004, 16: 374-381.
[21] Mendel R, Carter LP. Evaluation and treatment of clinical J Neuro Shimoda M, following subaraclinoid aneurysms., 16: 6-12
[22] Tsugane R, et al. Intracranial complications of hypervolemic therapy inpatients with a delayed ischemic deficit atributed to vasospasm. J Neurosuryg, 1993, 78: 423-428
[23] Hirashima Y, Endo S, Otsuji T, KarasawaK, Nojima S, Takakua, Plateletactivating factor and cerebral vasospasm following subarachnoid hemorrhage. J Neurosurg 1998, 78: 592-599
[24] CammussiG, PiacribelloW, AglietaM, Codar, BussolinoF, TetaC, Release factor(PAF) and histamine Ⅱ. Of The platelet-activating cellularorigin of human PAF: monocytes, polymorphonuclear neutrophils and basophils. Immunology, 1998, 42: 191-197
[25] Freyssinet JM, WieselML, Gauchy J, Boneu B,CazenaveJ-P neutralizes the An IgM lupus anticoagulant thatenhancing efect of phospholipid on 39 purified endothelial thrombomodulin activity. A mechanism for thrombosis. Thromb Haemost 1996,53:309-315
[26] Harris EN, Gharvani AE, Hughes GRV, Anti-phospholipid antibodies. Clin Rheum Dis 1985,11:591-599
[27] Wachtfogel YT, Cadena RA, and Colman RW. Structural Biology ,cellular interactions and poathophysiology of the contact system. Thromb Res,1999, 72:1-9
[27] Mosesson MW The roles of fibrinogen and fibrin in hemostasis and thrombosis. 29:177-179 Semin Hematol, 1992,
[28] Colman RW, Hirsh J, Marder VJ, et al. Hemostasis and Thrombosis: Basic principles and clinical practice. 3'0 ed. Philadelphia: Lippincott Company, 1994,3-7
[29] Slack SM, Cui YW, and Turitto VT. The efect of flow on blood coagulation and thrombosis. Thromb Haemost, 1998, 70:129-136
[30] Hiroyuki Shibahashi Akira Yamaura, Coagulation-Fibrinolytic Abnormality and Symptomatic Vasospasm in the Acute Stage of Ruptured Cerebral Aneurysms. Neurol Med Chir(Tokyo)1991,43:239-246
[31] YHirashima, M.Kurimoto, E. Tsukamoto, S. Endo, Anti-Phospholipid Antibodies and cerebral vasospasm following subarachnoid haemorrhage. Actaneurochir (Wien) 1999,135:191—196
[32] Hidetoshi Kasuya,MDJakashi Shimizu, MD. Activated complement components C3a and C4a in cerebrospinal fluid and plasma following subarachnoid hemorrhage) Neurosurg 1999,71:741-749
[33] FeilJM, florWJ, CohanSL, ParkhurstJ, Sequential changes of vascular ultrastructure in experimental vasospasm. J Neurosurg 1994, 41:49-54
[34] Smith R R, Clower BP, Peeler DF,Yoshiokaj, The angiopathy of subarachnoid hemorrhage:angiographic and morphologic correlates. Stroke 1983,14:240-251
[35] Anderson GB, AshforthR, Steinke DE, et al. CT angiography for the detection of cerebral vasospasmin patients with acute subarachnoid hemorrhage [J].Am J Neuroradiolg 2000,21: 1011-1015.
[36]Lysakowski C,Walder B,Costania MC,et al.Transcranial Doppler versusangiography in patients with vasospasm due to a Ruptured cerebral aneurysml :a systematic reviewe[J].Stroke,2001.32,12292-2298.
[37]Harrigan MR,Magnano CR,Guterman LR,etal. Computed to mographic perfusion in the management of aneurismal subarachnoid hemorrhagel new application of an existent technique [J]Neurosurgeryg 2005,56: 304-317.
[38] GriffithsPD,Wilkinson ID,Mitchell P,etal.Multimodality MR imaging depiction of hemodynamic changes and cerebralischemia in subarachnoid hemorrhage[J].Am J Neuroradiolg 2001,22:1690-1697.
[39]Busch E, Beaulieu C, de Crespigny A, etal. Diffusion MR imaging during acute subarachnoid hemorrhage in rats[J].Strokeg 1998,29:12155-2161.
[40]Rowe J, Blamire AM, Domingo Z,etal.Discrepancies between Cerebral perfusion and metabolism after subarachnoid haemorrhagel a magnetic resonance approach[J].J NeurolNeurosurg Psychiatry,1998,64: 98-103.
[41]. Roski RA, Spetzler RF, Carotid ligation. In: Wilkins RH,Rengachary SS, eds. Neurosurgey, end ed, Vol II. New York: McGraw-HILL, 1996.2333-2340
[42] NishizawaY Doi M, Miura K, et al. Clinical andexperimental studies on the preventive efect of nicardipine for symptomatic vasospasm. 8' European Congress of Neurosurg. Barcelona, spain 1987, 279-283
[43] Fujita K, Yamashita H, Tamaki n, Matsumoto S. Et al.The efects of ticlopidine and nicardipine on the prevention of the symptomatic vasospasm after SAH. International Symosium on Surgery for Cerebral Stroke, Spain 1987,147-158
[44] Schneck SA, KrichefflI. Intracranial aneurysm rupture,vasospasm,and infarction. Arch Neurol, 1964,11:668-674
[45] Gruber A, Ungerbock K, Reinprecht A et al. Evaluation of cerebral vasospasm after early surgical and endovascular treatment of ruptured intracranial aneurysm. Neurosurgery 1998. 42:258-263
[46] Handa Y Weir BKA, Nosko M, et al. The efect of timing of clot removal on chronic vasospasm in a primate model, J Neurosurg, 1987, 67: 558-566
[47] Hijdra A, Van Gijn J, Nagelkerke NJ, et al. Prediction of delayed cerebral ischemia, rebleeding, and outcome after aneurysmal subarachnoid hemorrhage. Stroke, 1988, 1900: 1250-1256
[48] Hijdra A, Van Gijn J, S, et al. Delayed cerebral ischemia after aneurysm subrachnoid hemorrhage: clinicoanatomic correlations. Neurology, 1986, 36(3): 329-333.
[49] Weir B, Grace M, Hansen J, et al. Time course of vasospasm in man. J Neurosurg, 1978, 48(2): 173—178.
[50] Kassell NF, Peerless SJ, Durward QJ, er al. Treatment of ischmic deficits from vasospasm with intravascular volume expansion andf induced arterial hypertention. Neurosurgery, 1982, 11(3): 337-343.
[51] Hirashima Y, Endo S, Otsuji T, KarasawaK, Nojima S, Takakua, Platelet-activating factor and cerebral vasospasm following subarachnoid hemorrhage. J Neurosurg 1993, 78: 592-599
[52] CammussiG, AglietaM, Codar, BussolinoF, PiacribelloW, TettaC, Release of platelet-activating factor(PAF) and histamine Ⅱ. The cellular origin of human PAF: monocytes, polymorphonuclear neutrophils and basophils. Immunology, 1981, 42: 191—197
[53] Freyssinet JM, WieselML, Gauchy J, Boneu B, CazenaveJ-P An I9M lupus anticoagulant that neutralizes the enhancing efect of phospholipid on purified endothelial thrombomodulin active mechanism for thrombosis. Thromb Haemost 1986, 53: 309-315
[54] Harris EN, Gharvani AE, Hughes GRYAnti-phospholipid antibodies. Clin Rheum Dis 1985, 11: 591-599
[55] YHirashima, M. Kurimoto, E. Tsukamoto, S. Endo, Anti-Phospholipid Antibodies and cerebral vasospasm following subarachnoid haemorrhage. Acta neurochir (Wien) 1995, 135: 191—196
[56] Shinichi Tamatani, Osamu Sasaki. Detection of delayed cerebral vasospasm, after rupture of intracranial aneurysm, by magnetic resonance angiography. Neurosurgey 1997, 40: 748-753
[57] Keogh AJ, Vhora S. The usefulness of magnetic resonance angiography in surgery for intracranial aneurysm that have bled. Surg Neurol 1998 50: 122-127
[58] 魏东，万琪．核因子kappaB在脑缺血病理生理过程中的作用[J]．国外医学·脑血管疾病分册，2004，12：285-288．
[59] Wong CK, WK, Lam CW. Interleukin-3-5, and granulocyte macrophage colony-stimulating factor-induced adhesion molecule expression on eosinophils by p38 mitogen-activated protein kinase and nuclearfactor-[kappa]B [J] Am J of Respira Ceel & Mol Biol, 2003, 29(1): 133-147.
[60] Shumway SD, Berchtold CM, Gould MN, etal. Evidence for unique calmodulin-dependent nuclearfactor-KB regulation in WEHI-231B ceels [J] Mol Pharmacol, 2002, 61: 177-185.
[61] Li TL, Liu YJ. Diagnosis and treatment for subarachnoid hemorrhage patient [J]. Chinese Medical Journal, 2003; 83(1): 3-5.
[62] Ma L, Zhang HP, Zhang XM, Lu HB. Clinical observation of treating arachnoid hemorrhage by cerebrospinal fluid replacement[J]. Chinese Journal of the Practical Chinese with Modern Medicine, 2005; 18: 687-688.
[63] Zhang C. Emergency treatment of modern neurology [M]. Qingdao: Qingdao Publishing House; 1994. 145.
[64] Katoh H, Shima K, Shimizu A, et al. Clinical evaluation of the effect of percutaneous transluminal angioplasty and intra-arterial papaverine infusion forthe treatment of vasospasm following aneurysmal subarachnoid hemorrhage[J]. Neurol Res, 195-203.
[65] Zimmermann M, Seifert V. Endothelin thelin and subarachnoid hemorrhage an overview [J]. Neurosurgery, 1998, 43: 843-853.
[66] Kwan AL, Lin CL, Chang CZ, et al. Continuous intravenous infusion of CGS26303, an endothelin-converting enzyme inhibitor, prvene and reverses cerebral vasospasm after experimental subarachnoid hemorrhage[J]. Neurosurgery, 2001, 49: 422-427.
[67] Clatterbuck RE, Gailloud P, Ogata L, et al. Prevention of cerebral vasospasm by a humanized anti-CD11 / CD18 monoclonal antibody administered after experimental subarachnoid hemo- -rrhage in nonhuman primates [J].JNeurosurg, 2003, 99:376-382.
[68] Pradilla G, Wang PP, Legnani FG, et al, Prevention of vasospasm by anti-CD11 /CD18 monoclonal antibody therapy following subarachnoid hemorrhage in rabbits[J.J Neurosurg, 2004,101:88-92.
[69] Satoh M, Parent AD, Zhang J H.Inhibitory effect with antisense mitogen-activated protein kinase oligodeoxynucleotide against cerebral vasospasm in rats [ J] . Stroke, 2002, 33775-781.
[70] Kusaka G, Kimura H, Kusaka I, et al. Contribution of Srctyrosine kinase to cerebral vasospasm after subarachn oid hemorrhage [J] J Neurosurg, 2003, 99383-390.
[71] Treggiari MIU, Romand JA, Martin JB, et al. Cervical sympathetic block to reverse delayed ischemic neurological deficits after aneurysmal subarachnoid hemorrhage[J].Stroke, 2003, 34:961-967.
[72] Handa Y, Weir BK, Nosko M, et al. The effect of timing of clot removal onchronic vasopasm in a primate model [J].J Neurosurg, 1987, 67:558-564.
[73] Bejjani GK, Bank WO, Olan WJ, et al. The efficacy and safety of angioplasty for cerebral vasospasm after subarachnoid hemorrhage[J].Neurosurgery, 1998 , 42:979-986.
[74] Khurana VG, Smith LA, Bakert A, et al. Protective vasomotor effects of in vivo recombinant endothelial nitric oxide synthase gene expression in a canine model of cerebral vasospasm [ J] Stroke, 2002, 33 782 - 789.
[75] Petruk KC, Weir BK, Overton TR, Marriot, GraceMG, the efect of graded hypocapnia andhypercapnia on regional cerebral blood flow and cerebral vessel caliberhemodynamics in the rhesus monkey stuty of cerebral following subarachnoid hemorrahge and traumatic internal carotid spasm. Stroke 1973, 5:230-238
[76] Yamagata S, Kikuchi H, Ihara I ,Nagata 1, MorookaY,NaruoY, Koizumi T, Hashmoto K,Miyamoto S, Mitsuno K, MatsumotoMinamikawa J,M, Yamazoe N, Akiyama YCerebral blood flow as a prognostic indicationinsubarachnoid hemorrhage. Neurol Med Chir, 1988,28:333-338
[78] Lennihan L, Mayer SA, Fink ME, et al. Eefect of hypervolemic therapy on cerebral blood volume after subarachnoid hemorrhage: a randomized controlled trial.Stroke, 2000, 31(2):383-39125
[79] Juvela S. Aspirin and delayed cerebral ischemia after aneurismal subarachnoid hemorrhage. J Neurosurg,1995,82(6):945-952
[80] Hop JW Rinkel GJ, Algra, et al. Randomized pilot trial of postoperative aspirin in subarachnoid hemorrhage.Neurology, 2000, 54(4):872-878
[81] Shaw MD, Foy PM, Conway m, er al. Dipyridamole and postoperative ischemic deficits in aneurysmal subrachnoid hemorrhage. J Neurosurg,1985, 63(5):699-703
[82] Fuhrmeister U, Ruether P, Dommatsch D. Alterations of CSF hydrodynamics following meningitis and subarachnoid hemor-rhage, in Shulman K, Marmarou A, Miller JD (eds): Intracraniai Pressure IV. Berlin, Springer Verlag, 1980, pp 241— 244.
[83]Kosteljanetz M: CSF dynamics in patients with subarachnoid and/or intraventricular hemorrhage. J Neurosurg 60:940—946,1984.
[84] Sullivan MG, Sellar R, Statham PF, Whittle IR. Management of poor grade patients after subarachnoid haemorrhage: the importance of neuroradiological findings on clinical outcome. Br J Neurosurg 1996 Oct:10(5):445-5246
[85] Mase M, Yamada K, Banno T, Miyachi T, Ohara S, Matsumoto T. Quantitative analysis of CSF flow dynamicsusingMRI in normal pressure hydrocephalus. Acta Neurochir Suppl (Wien) 1998:71:350-3
[86] Marmarou A, Maset A, Ward JD, Choi S, Brooks D, Lutz HA, Moulton RJ, Muizelaar JP, DeSalles A, Young H. Contrihution of CSF and vascular factors to elevation of ICP in severely head-injured patients. J Neurosurg 66:883—890,1987.
[87] Mehta V, Holness R0, Connolly K, Walling S, Hall R. Acute hydrocephalus following aneurysmal subarachnoid hemorrhage. Can .1 Neurol Sci 1996Feb;23(1):40-5
[88] Gjerris F, Borgesen SE, Sorensen PS, Boesen F, Schmidt K, Harmsen A, Lester J. Resistance to cerebrospinal fluid outflow and intracranial pressure in patients with hydrocephalus after subarachnoid haemorrhage. Ac ta Neurochir (Wien) 1987:88(3-4):79-86
[89] Black PMcL. Hydrocephalus and vasospasm after subarachnoid hemorrhage from ruptured intracranial aneurysms. Neurosurgery 18:12—16,1986. 28:56—59,1991.
[90] Tomei G, Gaini SM, GiovaneJIi M, Rampini P, Granata G, Vi Ilani R. Intracranial pressure in subarachnoid hemorrhage. Preliminary report in 36 cases. J Neurosurg Sci 1981 Apr-,Jun;250 :57-66
[91]Andreas Gruber, M. D., Andrea Reinprecht, M. D., Gerhard Bavinzski, M. D., Thomas Czech, M. D. , Bernd Richling, M. D. Chronic Shunt-dependent Hydrocephalus after Early Surgical and Early Endovascular Treatment of Ruptured intracranial Aneurysms. Neurosurgery, March 1999;Vol. 44
[92] Galera RC, Greitz T. Hydrocephalus in the adult secondary to the rupture of intracranial arterial aneurysms. J Neurosurg 32:634—641,1970.
[93] Kol.luri VR, Sengupta RP. Symptomatic hydrocephalus following aneurysmal subarachnoid hemorrhage. Surg Neurol :402—404,1984.
[94] Suarez-Rivera O. Acute hydrocephalus after subarachnoid hemorrhage. Surg Neurol 1998 May;49(5):563-5