【摘要】 目的探讨蛛网膜下腔出血(SAH)后脑血管痉挛(CVS)的多因素影响机制。方法从SAH患者颈内静脉中抽取血样,检测血管内皮功能紊乱标志物、凝血因子、炎症介质及可溶性血管黏附分子浓度的变化。结果纤溶酶原激活物抑制剂-1(PAI-1)、凝血酶-抗凝血酶Ⅲ(TAT)、白介素-6(IL-6)及血小板活化因子(PAF)在SAH后3 d内浓度开始升高,并持续到第14天;细胞间黏附分子-1(ICAM-1)的浓度在SAH后9 d内明显升高;可溶性血栓调节素(sTM)浓度在SAH后4～9 d有短暂升高。在SAH后4～9 d时,有症状性CVS患者的PAI-1、sTM、TAT、IL-6、PAF和ICAM-1等物质的浓度明显高于无症状性CVS的患者,差异有统计学意义(P<0.05)。结论在SAH后CVS的发生和发展是受痉挛血管周围的血液刺激启动的,可能由包括血管内皮功能紊乱、炎症介质释放、血液的高凝状态及血管黏附分子的表达上调等众多因素参与和相互作用的结果,而血管壁的炎症反应则可能是其中不可避免的病理过程。更多还原

【Abstract】 Objective To explore the effects of varied factors in cerebral vasospasm (CVS) after subarachnoid hemorrhage (SAH).Methods The present study was undertaken to examine the changes of markers of endothelial dysfunction,coagulation factor,inflammatory mediators and vascular adhesion molecules in blood of the internal jugular vein in patients with SAH.Results Plasminogen activator inhibitor-1(PAI-1),interleukin-6(IL-6),thrombin-antithrombinⅢcomplex(TAT) and platelet activating factor(PAF) concentrations increased within first 3 days after SAH and remained elevated up to 14 days. intercellular adhesion molecule-1(ICAM-1) levels increased within 9 days after SAH.While it was showed a transient increase with soluble thrombomodullin(sTM) between the 4th day and 9th day.The patients with synptomatic vasospasm displayed the higher levels of PAI-1,sTM,TAT,IL-6,PAF and ICAM-1 than those without synptomatic vasospasm.Conclusion These results suggest that the CVS af- ter SAH is the pathophysiological consequence initiated by the blood surround spasmodic artery and may be developed by varied interactive factors,including vascular endothelial dysfunction,releasing of inflammatory mediators,blood hypercoagulant state and upregulated expression of vascular adhsion molecule,in which the inflammatory reaction in artery wall may be an inevitable pathological course.更多还原