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脑血管痉挛大鼠血和脑组织ET 1、NO含量动态变化的研究
作者:戴小牛1 王翠芬1 孙保亮2 夏作理2 杨明峰2 邱平明2 
单位:1.东南大学医学院,生理学教研室,; 2.泰山医学院附属医院,微循环研究所,
关键词:蛛网膜下腔出血 脑血管痉挛 一氧化氮 内皮素 1 脑微区血流 大鼠 
分类号:R743.35, R332
出版年·卷·期(页码):2001·20·第四期(222-224)
摘要:

目的:探讨内皮素(ET) 1和一氧化氮(NO)在蛛网膜下腔出血(SAH)后脑血管痉挛(CVS )及脑缺血性损害中的作用.方法:采用非开颅法大鼠SAH模型,检测24 h内血及脑组织中NO和ET 1含量,并测定脑微区血流(rCBF)和基底动脉管径. 结果:大鼠SAH后30 min基底动脉管径缩小,rCBF持续下降;血NO减少,ET 1增多;脑组织NO和ET 1均增加.结论:血NO减少,ET增多系SAH后CVS发生的原因之一;脑组织NO和ET增多则加重脑损伤.

Objective  To investigate the possible roles of endothelin?1 (ET?1)and nitric oxide (NO) in the development of cerebral vasospasm(CVS) and related brain ischemic damage following subarachnoid hemorrhage (SAH).Methods  90 Wistar rats were divided into SAH group and sham  operated group. Regional cerebral blood flow (rCBF),NO and ET?1 in both blood and brain tissue within 24?h after operation were detected.Diameter of basilar artery(BA) was measured.Results  rCBF decreased rapidly and persistently within 24?h after induction of SAH. Spasm of BA occurred 30?min after SAH.NO in blood was decreased while that in brain tissue increased. Both blood and brain tissue ET?1 levels were increased.Conclusion  Decrease of NO and increase of ET?1 in blood are involved in the development of CVS following SAH while increase of NO and ET?1 in brain tissue contributes to brain damage due to ischemia.

参考文献:

[1] Bederson J B, GERMANO M, GUARINO L. Cortical blood flow an d cerebral perfusi on pressure in a new noncraniotomy model of subarachnoid hemorrhage in rats, 1995
[2] 王成彬, 沈文梅, 田亚平. 铜离子活化镉还原法测定血清中硝酸盐浓度, 1996
[3] 高树生, 徐有奇. 正常妊娠中内皮素的测定, 1993
[4] ZELLERS T M, MCCOMICK J, WU Y Q. Interaction among ET 1 endothelium derive d nitric oxide and prostacyclin in pulmonary arteries and veins, 1994
[5] HARBERCHT B G, STADLER J, DEMETRICS A J. Nitric oxide and prost aglandi ns interact to prevent hepatic damage during murine endotoxemia, 1994
[6] Nishikawa T. Effect of nitric oxide synthase inhibition on cerebral blood flow and injury volume during focal ischemia in cats, 1993
[7] Ziv I, FLEMINGER G, DYALDETTI R. Increased plasma endothelin 1 in acute ischemic stroke, 1992 

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