一氧化氮和内皮素在蛛网膜下腔出血后脑血管痉挛发生机制中的作用  

Effect of Nitric Oxide and Endothelin on Cerebral Vasospasm after Subarachnoid Hemorrhage in Rats

作　　者：戴小牛[1] 夏作理[2] 陈连璧[3] 

机构地区：[1]南京铁道医学院生理教研室,邮政编码南京210009 [2]泰山医学院微循环研究所 [3]山东医科大学生理教研室

出　　处：《微循环学杂志》1998年第4期11-13,共3页Chinese Journal of Microcirculation

摘　　要：采用不开颅法造成实验性大鼠蛛网膜下腔出血（SAH）模型，检测脑血流中一氧化氮（NO）和内皮素（ET－1）含量。结果发现，SAH后1h脑血流ET－1浓度升高（P＜0．001），NO浓度降低。并且在SAH后即刻开始，脑血流NO／ET－1比值下降（P＜0．001）L-精氨酸可增加脑血流NO含量，减少ET－1含量，使NO／ET－1比值降低幅度减小。结果表明，脑血流内皮舒张因子和内皮收缩因子之间的平衡紊乱是SAH后脑血管痉挛发生的机制之一。Subarachnoid hemorrhage(SAH) in rats was induced by advancing an intraluminal suture through the internal carotid artery to pierce a hole in the circle of Willis. The levels of ET-1 (endothelin-1 ) and NO(nitric oxide) in cerebral plasma were determined. Results showed that the levels of ET-1 in cerebral plasma increased significantly(PM＜0. 001 ), the levels of NO decreased after SAH.Administration of L-arginine inhibited the elevation of plasma ET-1 and the decline of plasma NO. It indicated that the imbalance of endothelium derived relaxing factor(NO) and the endothelium derived constricting factor(ET) was a major cause of vasospasm after SAH.

关 键 词：蛛网膜下腔出血 内皮素 一氧化氮 脑血管痉挛 

分 类 号：R743.350.2[医药卫生—神经病学与精神病学]