Impaired intracellular signal transduction via cyclic AMP contributes to cerebral vasospasm in rats with subarachnoid hemorrhage

No drug can completely prevent vasospasm after subarachnoid hemorrhage. Impaired intracellular signal transduction by cyclic nucleotides might be involved. We investigated effects of intravenous isoproterenol and NKH477 on cerebral blood flow in rats with or without intracisternal injection of autologous blood one week previously. In controls without hemorrhage, isoproterenol at 0.01, 0.1, 1, and 10 mg kg(-1) min(-1) increased cerebral blood flow by 1.2%+/-9.5%, 19.7%+/-12.8%, 46.8%+/-23.5%, and 63.8%+/-32.9% respectively; 10mg kg(-1) min(-1) of isoproterenol increased systemic blood pressure by 66.6%+/-58.1%, while other doses decreased blood pressure. In the subarachnoid hemorrhage group, isoproterenol increased cerebral blood flow by -20.0%+/-6.5%, -7.6%+/-8.7%, 8.2%+/-8.8%, and 35.9%+/-83.1% respectively; 10 mg kg(-1) min(-1) of isoproterenol increased systemic blood pressure by 68.8%+/-79.5%, while other doses decreased blood pressure. In controls, NKH477 at 3, 10, and 30 mg kg(-1) increased cerebral blood flow by 2.3%+/-3.6%, 14.4%+/-7.0%, and 50.7%+/-14.6%, respectively; in the subarachnoid hemorrhage group, NKH477 changed cerebral blood flow by -1.3%+/-2.4%, 4.6%+/-2.8%, and -12.6%+/-10.8% (not significant difference from controls). NKH477 at 30 mg kg(-1) min(-1) decreased systemic blood pressure in both groups, but the effect in the hemorrhage group was greater. Either isoproterenol or NKH477 at appropriate doses can increase cerebral blood flow in vasospasm following subarachnoid hemorrhage without decreasing blood pressure.     

Cerebral vasospasm after subarachnoid hemorrhage: An update

Symptomatic vasospasm, or delayed cerebral ischemia associated with arteriographic evidence of arterial constriction, is currently the most important cause of morbidity after acute subarachnoid hemorrhage. The development of vasospasm is directly correlated with the presence of thick blood clots in the basal subarachnoid cisterns, which can be detected by an early computed tomographic scan. Symptomatic vasospasm usually develops between 4 and 12 days after subarachnoid hemorrhage. The onset is gradual, occurring over hours or days. There is typically a gradual deterioration of the level of consciousness, accompanied by focal neurological deficits that are determined by the arterial territories involved. Hyponatremia frequently occurs and may exacerbate the symptoms. The patients are usually volume depleted, and therefore many authorities now treat them with replenishment and expansion of their intravascular volume with colloid and blood. Volume expansion, together with elevation of the systemic blood pressure and reduction of the intracranial pressure when elevated, constitute the only currently available effective therapy for symptomatic vasospasm. The cause of vasospasm remains obscure. Mechanisms of smooth muscle cell contraction and relaxation and experimental efforts to elucidate the nature of vasospasm are reviewed.     

Correlations between cerebral arterial velocities, blood flow, and delayed ischemia after subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: Elevated middle cerebral erythrocyte velocities and tissue hypoperfusion have been correlated with delayed ischemia after subarachnoid hemorrhage, but few studies have compared serial arterial velocities with cerebral blood flow and neurological deficits. METHODS: Serial measurements of middle cerebral velocities, using transcranial Doppler ultrasonography, were performed in 34 patients after subarachnoid hemorrhage and correlated with cerebral blood flow, measured in 20 of the 34 using single-photon emission computed tomography with technetium-99m hexamethylpropylene amine oxime and neurological evidence of delayed ischemia. RESULTS: In 16 patients without delayed ischemia, eight had evidence of vasospasm (greater than 120 cm/sec), but only one of seven had hypoperfusion, suggesting that vasospasm might be more common than hypoperfusion in this group (p = 0.1). In 10 patients with delayed ischemia and a lateralizing deficit, both asymmetrical middle cerebral vasospasm (eight of nine with vasospasm) and hypoperfusion (six of six studied) were concordant with the clinically ischemic hemisphere (p less than 0.05). Vasospasm occurred with nonlateralized delayed ischemia in seven of eight patients and with hypoperfusion in five of six, affecting the anterior cerebral territory in three. CONCLUSIONS: Concordant vasospasm and hypoperfusion were most often present in patients with delayed ischemia and lateralizing neurological deficits. Discordant results reflect inherent limitations and the different levels of the circulation monitored by the two techniques.     

动脉瘤性蛛网膜下腔出血后脑血管痉挛和脑低灌注的相关性分析

目的分析动脉瘤性蛛网膜下腔出血(aSAH)后脑血管痉挛及脑灌注异常的相关性。方法回顾性分析52例aSAH病人的临床资料。在出血后3～15d内均接受CT血管造影(CTA)和CT灌注成像(CTP)检查,了解大脑前动脉(ACA)和大脑中动脉(MCA)血管痉挛的严重程度,以及相关供血区域的脑灌注情况,对获取的参数进行统计学分析和比较。结果无脑血管痉挛23例,其中发生脑低灌注5例(21%)(位于脑分水岭区4例,在脑沟积血附近1例)。轻中度脑血管痉挛18例,其中存在相关供血区域脑低灌注7例(38%)。重度脑血管痉挛11例,其中发生相关供血区域脑低灌注9例(81%)。比较无脑血管痉挛与重度脑血管痉挛血管节段的血流灌注区域,在局部脑血流量(rCBF)和平均通过时间(MTT)两方面,差异均存在统计学意义(P0.05)。结论重度脑血管痉挛是相关供血区域发生脑低灌注的高危因素。无明显脑血管痉挛的病人,在脑分水岭区和脑沟积血附近也可发生脑低灌注,可能与脑微血管痉挛有关。     

Cerebrovascular CO2 reactivity during delayed vasospasm in a canine model of subarachnoid hemorrhage

While the in vitro reactivity of cerebral conducting vessels following subarachnoid hemorrhage has been extensively studied, in vivo cerebrovascular CO2 reactivity has not been systematically investigated. We tested the hypothesis that, in the canine model of subarachnoid hemorrhage, the rise in cerebral blood flow normally seen with hypercapnia is blunted during delayed vasospasm. Four groups of animals were studied: one received two 4-ml subarachnoid injections of nonheparinized arterial blood into the cisterna magna (n = 8), one received three subarachnoid injections of 5 ml blood (n = 5), one received two subarachnoid injections of 4 ml saline (n = 5), and a control group (n = 5) had no subarachnoid injections or angiography. Basilar artery diameter was measured from baseline and follow-up angiography. We determined CO2 reactivity by randomly varying the concentration of inspired CO2 and measuring regional cerebral blood flow with radiolabeled microspheres. Basilar artery diameter was not affected by saline injection and was reduced by 26 +/- 2.9% in the two-hemorrhage group and 55 +/- 1.9% in the three-hemorrhage group. Baseline cerebral blood flow and CO2 reactivity were similar in all four groups. We conclude that, in this model of delayed vasospasm, regional cerebral vascular CO2 reactivity is intact and extrapolation of in vitro data regarding basilar artery diameter and reactivity to cerebral blood flow must be done cautiously.     

Cyclosporine A reduces cerebral vasospasm after subarachnoid hemorrhage in dogs

The double subarachnoid hemorrhage canine model was used to test the prophylactic value of immunosuppression in the prevention of cerebral vasospasm after subarachnoid hemorrhage. Dogs treated with cyclosporine A following the regimen prescribed for organ transplant procedures in patients showed a significant reduction in the severity of angiographic constriction of cerebral arteries. While basilar artery diameter after double experimental subarachnoid hemorrhage in a series of untreated dogs (n = 34) averaged 65% of baseline diameter, arterial diameter in dogs treated prophylactically (n = 18) with 6 mg/kg/day cyclosporine A and adjunct low-dose steroid averaged 80% of baseline diameter, for a mean reduction in the severity of chronic arterial constriction of 42%. More important than the average effect, however, is the statistical observation that this mean improvement was obtained primarily by a dramatic reduction in the incidence of severe cerebral vasospasm, the situation most likely to account for morbidity and mortality after aneurysmal rupture.     

The Effectiveness of Lumbar Cerebrospinal Fluid Drainage to Reduce the Cerebral Vasospasm after Surgical Clipping for Aneurysmal Subarachnoid Hemorrhage

ObjectiveRemoval of blood from subarachnoid space with a lumbar drainage (LD) may decrease development of cerebral vasospasm. We evaluated the effectiveness of a LD for a clinical vasospasm and outcomes after clipping of aneurysmal subarachnoid hemorrhage (SAH).MethodsBetween July 2008 and July 2013, 234 patients were included in this study. The LD group consisted of 126 patients, 108 patients in the non LD group. We investigated outcomes as follow : 1) clinical vasospasm, 2) angioplasty, 3) cerebral infarction, 4) Glasgow outcome scale (GOS) score at discharge, 5) GOS score at 6-month follow-up, and 6) mortality.ResultsClinical vasospasm occurred in 19% of the LD group and 42% of the non LD group (p<0.001). Angioplasty was performed in 17% of the LD group and 38% of the non LD group (p=0.001). Cerebral infarctions were detected in 29% and 54% of each group respectively (p<0.001). The proportion of GOS score 5 at 6 month follow-up in the LD group was 69%, and it was 58% in the non LD group (p=0.001). Mortality rate showed 5% and 10% in each group respectively. But, there was no difference in shunt between the two groups.ConclusionLD after aneurysmal SAH shows marked reduction of clinical vasospasm and need for angioplasty. With this technique we have shown favorable GOS score at 6 month follow-up.     

Delayed Cerebral Ischemia in Patients with Aneurysmal Subarachnoid Hemorrhage – Serum D-dimer and C-reactive Protein as Early Markers

BackgroundIdentifying patients at risk for delayed cerebral ischemia after an aneurysmal subarachnoid hemorrhage remains challenging and both delayed treatment and over-treatment are reasonable concerns.ObjectiveTo evaluate the role of the serum markers C-reactive protein, white blood count, and d-dimer as prognostic factors for the occurrence of delayed cerebral ischemia.MethodsAll patients admitted within 24 hours after an aneurysmal subarachnoid hemorrhage were included over a 6-year period. The World Federation of Neurosurgery and Fisher grading scales as well as the extended Glasgow Outcome Scale were documented at discharge and after a 3-to-6-month follow-up period. C-reactive protein, d-dimer, white blood count, and procalcitonin were assessed on admission, day 1, day 4, day 9, day 14, and at discharge. Radiologically confirmed delayed cerebral ischemia before discharge was the primary endpoint. Severe angiographic vasospasm and outcome were used as secondary endpoints.ResultsDelayed cerebral ischemia occurred in 19.6% of the 138 patients included. Delayed cerebral ischemia correlated with severe vasospasm and with a worse outcome. Serum C-reactive protein levels were higher in patients with severe vasospasm during the period of vasospasm. D-dimer levels on admission correlated with Fisher grades. Delayed cerebral ischemia occurred more frequently in patients with Fisher grade IV hemorrhage, if d-dimer levels were higher on admission. The cut-off was .445 µg/ml.ConclusionOur observations support a multifactorial genesis for delayed cerebral ischemia, including vasospasm and microthrombotic and inflammatory processes. Serum d-dimer levels greater than .445 µg/ml might be a predictor for the occurrence of delayed cerebral ischemia in patients with a Fisher grade IV aneurysmal subarachnoid hemorrhage.     

Clentiazem protects against chronic cerebral vasospasm in rabbit basilar artery.

BACKGROUND AND PURPOSE: Experiments were carried out in rabbits to determine whether clentiazem (8-chlorodiltiazem), a cerebrovascular-selective calcium channel blocker, administered 24 hours before subarachnoid hemorrhage influenced the subsequent cerebral vasospasm. METHODS: Subarachnoid hemorrhage was induced by multiple injections of blood into the prepontine cisterns of 35 male New Zealand White rabbits, and clentiazem (5 mg/kg) was administered 4 times daily until sacrifice. Cerebral artery diameter was assessed in vivo by angiography. Functional features of basilar arteries were measured using conventional in vitro methodology. RESULTS: Clentiazem reduced the angiographic narrowing seen on days 2 and 5 from 35% and 34%, respectively (sham control, 1.42 +/- 0.31 mm [n = 22]), to 8% and 11%, respectively, and prevented the narrowing (32%) that occurred on day 9. Narrowing in the untreated rabbits was only partly reversed by papaverine; all narrowing in clentiazem-treated animals was papaverine sensitive. Clentiazem prevented or reduced many of the changes in the basilar artery caused by the subarachnoid hemorrhage. Of particular relevance to arterial narrowing were the increased wall stiffness, the transient spontaneous changes in wall force, and the reduction in relaxation to acetylcholine. Reduction of the changes in wall force induced by agonists and by stimulation of intramural sympathetic nerves was observed. CONCLUSIONS: The vascular damage associated with chronic cerebral vasospasm is related to calcium entry into the smooth muscle and endothelial cells, and possibly sympathetic nerve terminals, through calcium channels sensitive to clentiazem, which suggests that clentiazem may be of value in the management of chronic cerebral vasospasm.     

血浆PTX3对动脉瘤性蛛网膜下腔出血后脑血管痉挛的预测价值

目的 分析血浆正五聚蛋白3(Pentraxin 3,PTX3)对动脉瘤性蛛网膜下腔出血后脑血管痉挛的预测价值。方法 收集本院2016年2月-2019年2月186例动脉瘤性蛛网膜下腔出血患者作为研究对象,经颅多普勒检测仪检测大脑中动脉(Middle cerebral artery,MCA)流速,MCA平均流速(Mean velocity of MCA,MCA Vm)>120 cm/s,且同侧Lindegaard≥3为血管痉挛组(92例),其余为无血管痉挛组(94例); 收集2组一般资料; 酶联免疫吸附(Enzyme linked immunosorbent assay,ELISA)法检测血浆中PTX3水平; 绘制受试者工作特性曲线(Receiver operator characteristic curve,ROC)分析血浆中PTX3对动脉瘤性蛛网膜者发生脑血管痉挛的诊断价值; 以血浆PTX3水平<4.73 ng/mL和≥4.73 ng/mL分为PTX3低表达组和PTX3高表达组,分析血浆PTX3水平与一般资料的关系; Logistic分析影响动脉瘤性蛛网膜下腔出血患者发生脑血管痉挛的因素。结果 无血管痉挛组与血管痉挛组年龄、治疗方法、高血压病史、Fisher分级、Hunt-Hess分级存在明显差异(P<0.05); 与无血管痉挛组比较,血管痉挛组血浆PTX3水平升高(P<0.05); ROC曲线显示,血浆PTX3水平预测动脉瘤性蛛网膜下腔出血患者发生脑血管痉挛的ROC曲线下面积为0.777,截断值为4.73 ng/mL,其敏感性为68.50%、特异性为74.50%; 血浆PTX3水平与年龄、治疗方法、Fisher分级、Hunt-Hess分级关系密切(P<0.05); Logistic分析显示,PTX3、年龄、Fisher分级、Hunt-Hess分级是影响动脉瘤性蛛网膜下腔出血患者发生脑血管痉挛的独立危险因素。结论 动脉瘤性蛛网膜下腔出血脑血管痉挛患者血浆PTX3水平升高,PTX3对动脉瘤性蛛网膜下腔出血患者发生脑血管痉挛具有一定诊断价值。     

动脉瘤性蛛网膜下腔出血并发脑血管痉挛患者血清血管内皮生长因子表达的变化

目的:探讨动脉瘤性蛛网膜下腔出血(SAH)并发脑血管痉挛(CVS)与血清血管内皮生长因子(VEGF)表达的关系.方法:27例动脉瘤性SAH患者为试验组(SAH组),再依据是否并发不同程度CVS分为:无CVS亚组(11例),轻度CVS亚组(9例)、中度CVS亚组(4例)和重度CVS亚组(3例);另设10名健康体检者为对照组.采用ELISA法检测血清VEGF水平.结果:SAH各时间点各组血清VEGF水平为①SAH组发病第1天起即明显高于对照组;②无CVS组不增高.SAH后第1、3、5、7天时血清VEGF水平为①轻度CVS组与中度CVS组相同时间点比较,差异无统计学意义;②重度CVS组明显高于轻度和中度CVS组.SAH后出现脑梗死患者血清VEGF水平明显高于未出现脑梗死患者.结论:SAH后出现CVS患者和出现脑梗死的患者血清VEGF水平明显增高,血清VEGF水平能反映脑血管痉挛的程度.     

Intracranial aneurysms and subarachnoid hemorrhage. A cooperative study. Antifibrinolytic therapy in recent onset subarachnoid hemorrhage.

In this cooperative study among 13 institutions, 502 patients were treated with antifibrinolytic medication (epsilon-aminocaproic acid or tranexamic acid) within a 14-day period following rupture of an intracranial aneurysm. Mortality at the end of 14 days was 11.6%; proved rebleed rate was 12.7%. Patients with an internal carotid or anterior cerebral aneurysm had the highest mortality and rebleed rate. Most rebleeds occurred between the sixth and eleventh days following the initial bleed. Significantly higher mortality was reported among patients with cerebral vasospasm, yet rebleed rate was no different among those patients with or without vasospasm. The same pattern was observed among patients with a mean blood pressure value above and below 110 mm Hg. We conclude that antifibrinolytic therapy provides beneficial treatment to patients with recent onset subarachnoid hemorrhage (SAH) following rupture of an intracranial aneurysm.     

An overview of new pharmacological treatments for cerebrovascular dysfunction after experimental subarachnoid hemorrhage

Cerebral vasospasm and the resulting cerebral ischemia occurring after subarachnoid hemorrhage (SAH) are still responsible for the considerable morbidity and mortality in patients affected by cerebral aneurysms. Mechanisms contributing to the development of vasospasm, abnormal reactivity of cerebral arteries and cerebral ischemia after SAH have been intensively investigated in recent years. It has been suggested that the pathogenesis of vasospasm is related to a number of pathological processes, including endothelial damage, smooth muscle cell contraction resulting from spasmogenic substances generated during lyses of subarachnoid blood clots, changes in vascular responsiveness and inflammatory or immunological reactions of the vascular wall.A great deal of experimental and clinical research has been conducted in an effort to find ways to prevent these complications. However, to date, the main therapeutic interventions remain elusive and are limited to the manipulation of systemic blood pressure, alteration of blood volume or viscosity, and control of arterial dioxide tension.Even though no single pharmacological agent or treatment protocol has been identified which could prevent or reverse these deadly complications, a number of promising drugs have been investigated. Among these is the hormone erythropoietin (EPO), the main regulator of erythropoiesis. It has recently been found that EPO produces a neuroprotective action during experimental SAH when its recombinant form (rHuEPO) is systemically administered.This topic review collects the relevant literature on the main investigative therapies for cerebrovascular dysfunction after aneurysmal SAH. In addition, it points out rHuEPO, which may hold promise in future clinical trials to prevent the occurrence of vasospasm and cerebral ischemia after SAH.     

腰穿枕大池置管2次注血的迟发性脑血管痉挛动物模型

目的 :制作一种操作简便、重复性好的蛛网膜下腔出血 (SAH)脑血管痉挛 (CV)动物模型。方法 :选取家猪 12头 ,随机分成SAH组和生理盐水对照组 ;SAH组经腰穿枕大池置管 2次注血 ,制成SAH模型 ,对照组注入生理盐水 ;以脑血管造影和基底动脉组织学改变判定脑血管痉挛。结果 :SAH组双侧颈内动脉和基底动脉明显痉挛 (P <0 0 1) ,基底动脉有典型病理改变 ,对照组未见异常。结论 :腰穿枕大池置管 2次注血法 ,是一种简便、可靠的SAH诱发CV动物模型制作方法。     

Hyponatremia and cerebral vasospasm in patients with aneurysmal subarachnoid hemorrhage]

We studied retrospectively the relationship between hyponatremia and cerebral vasospasm in 121 consecutive patients with aneurysmal subarachnoid hemorrhage. In 19 patients sodium levels fell below 130 mEq/l on at least two consecutive days. Hyponatremia developed at average 8.9 hospital day and lasted for 4.4 days. It was mild (126 to 130 mEq/l) in 15 patients, moderate (121 to 125 mEq/l) in 3 patients, and severe (116 to 120 mEq/l) in 1 patient. Cerebral vasospasm was evaluated by angiography, symptoms and CT finding. Angiographical vasospasm was found in 57 patients, symptomatic vasospasm in 38 patients and low density area on CT in 20 patients. Angiographical vasospasm developed in 15 of the 19 patients (78.9%) with hyponatremia, symptomatic vasospasm in 16 patients (84.2%), low density area on CT in 8 patients (42.1%), the difference being significantly high. (respectively, p < 0.01, p < 0.001 and p < 0.01 by chi-square test) Polyuria of 2500 ml or more immediately before the onset of hyponatremia developed in 14 patients (87.5%). When symptomatic vasospasm and hyponatremia coincided, there were only 4 patients in which symptomatic vasospasm was preceded by hyponatremia. So, it is difficult to predict the development of vasospasm from that of hyponatremia. This study found incidence of cerebral vasospasm after aneurysmal subarachnoid hemorrhage to be significantly higher in patients who developed hyponatremia, which raised suspicion about the presence of dehydration. Hyponatremia with central origin generally remains asymptomatic, but it is important to treat positively when the pathology of cerebral vasospasm is taken into consideration.     

甲基强的松龙对兔实验性脑血管痉挛的作用

目的探讨大剂量甲基强的松龙对蛛网膜下腔出血(SAH)后脑血管痉挛(CVS)的作用。方法将24只雄性新西兰白兔随机分成2组:SAH对照组和SAH 大剂量甲基强的松龙(MP,18mg/kg)治疗组。通过枕大池二次注血法构建SAH模型,观察MP对脑基底动脉的影响。应用酶联免疫生化技术检测各组兔基底动脉血管平滑肌细胞膜蛋白激酶C(PKC)活性。结果经脑血管造影证实该剂量甲基强的松龙明显减轻实验性脑血管痉挛的严重程度,与对照组相比,PKC活性在大剂量甲基强的松龙治疗组没有明显提高。结论大剂量甲基强的松龙能够明显减轻脑血管痉挛程度,通过抑制血管平滑肌细胞来防治脑血管痉挛的发生发展。     

Postoperative hemodynamic and metabolic changes in patients with subarachnoid hemorrhage

Positron emission tomography was performed using an oxygen-15 gas inhalation technique to measure regional cerebral blood flow, metabolic rate for oxygen, oxygen extraction fraction, and cerebral blood volume in 13 patients with subarachnoid hemorrhage during the period of delayed vasospasm after surgery as well as in 10 volunteers as controls. Compared with the controls, the patients showed decreased hemoglobin concentration and decreased total arterial oxygen content due to postoperative hemodilution. Global reductions in the metabolic rate for oxygen and in the tissue oxygen supply were noted even in the apparently normal cortex of the patients in spite of adequate blood flow and adequate oxygen extraction fraction. In addition, regional reductions in blood flow and in perfusion reserve were seen in the cortical territory corresponding to cerebral vasospasm. Our results indicate that two processes are involved in the pathophysiology of cerebral vasospasm: 1) generalized impairment of oxygen metabolism with a reduced tissue oxygen supply, even in the apparently normal cortex, and 2) additional impairment of regional perfusion in the territory of vasospasm.     

Single-Photon Emission Computed Tomography,Transcranial Doppler Ultrasound,and Cerebral Angioplasty for Posttraumatic Vasospasm

Intracranial arterial vasospasm is an important consequence of subarachnoid hemorrhage. In posttraumatic patients, this phenomenon is becoming increasingly recognized with noninvasive techniques that evaluate (1) vascular stenosis, such as transcranial Doppler (TCD) ultrasound, and (2) regional cerebral blood flow, such as single-photon emission computed tomography (SPECT). A posttraumatic patient developed symptomatic vasospasm that was detected by TCD and SPECT and then treated with percutaneous transluminal balloon cerebral angioplasty, which improved the symptoms. The anatomical and functional results of angioplasty were evaluated also by TCD and SPECT, which showed a reduction in the severity of stenosis and improved blood flow, respectively.     

Effect of tissue plasminogen activator on intimal platelet accumulation in cerebral arteries after subarachnoid hemorrhage in cats

Recombinant tissue plasminogen activator may be effective in preventing cerebral vasospasm after subarachnoid hemorrhage by resolving subarachnoid clots. We previously demonstrated that blood placed on the adventitial surface of cerebral arteries enhances intimal platelet accumulation, positively correlating with endothelial damage and other pathologic changes in vessel walls. In this study, we investigated the ability of a single bolus injection of tissue plasminogen activator to prevent platelet accumulation in cerebral vessels after subarachnoid hemorrhage. Subarachnoid hemorrhage was produced in cats by the transorbital intracisternal injection of 2.5 ml autologous arterial blood around the proximal part of the right middle cerebral artery. In 10 animals, 25 micrograms tissue plasminogen activator was injected at intervals of 10 (five cats) and 60 minutes (five cats) after subarachnoid hemorrhage. Intracisternal physiological saline (0.5 ml) was injected in six cats 10 minutes after subarachnoid hemorrhage. Platelets labeled with indium-111 were injected intravenously just before subarachnoid hemorrhage, and their radioactivity was measured in cerebral arteries at death. The results indicated that, after subarachnoid hemorrhage, early injection of tissue plasminogen activator inhibited intimal platelet accumulation, but later injection did not, although the extent of subarachnoid clot was reduced at both plasminogen injection times.     

颅内动脉瘤性蛛网膜下腔出血血管痉挛治疗的临床探讨

目的探讨颅内动脉瘤性蛛网膜下腔出血脑血管痉挛的治疗方法。方法回顾性分析颅内动脉瘤性蛛网膜下腔出血合并脑血管痉挛患者临床资料67例。结果 23例并发脑血管痉挛,6例发生一侧肢体功能障碍,3例发生脑血栓形成。经治疗后61例C-反应蛋白恢复正常,6例明显下降,4例肢体功能恢复正常,1例恢复到4级,1例死亡。结论炎症因子在脑血管痉挛中明显升高;钙离子拮抗剂尼莫地平加抗氧化剂依达拉奉中药川芎嗪联合治疗动脉瘤性蛛网膜下腔出血所致的脑血管痉挛有较好疗效。