大鼠急性局灶性脑缺血再灌注脑组织NO含量和NOS活性的变化  

The changes of NO content and NOS activity in cerebral tissue during acute focal cerebral ischemia and reperfusion in rats

作　　者：姜德华[1] 金男革[2] 玄汉石[3] 李在琉 

机构地区：[1]南京铁道医学院附属徐州医院神经外科,221009 [2]延边大学医学院生理学教研室 [3]延边大学医学院附属医院神经外科

出　　处：《临床神经病学杂志》2000年第4期201-203,共3页Journal of Clinical Neurology

摘　　要：目的　探讨一氧化氮 (NO)和神经元型 NO合酶 (n NOS)是否参与急性局灶性脑缺血再灌注的发病机理。方法　采用栓线法建立大鼠大脑中动脉阻塞 (MCAO)模型 ,观察脑组织 NO含量和一氧化氮合酶(NOS)活性的变化及 n NOS抑制剂 7-硝基吲唑 (7- NI)对再灌注期两者的影响。结果　缺血 30分钟 NO含量和 NOS活性显著升高 ,缺血 3小时两者下降 ;再灌注 30分钟 NO和 NOS再次升高 ,而再灌注 3小时两者又下降。 7- NI能显著降低再灌注期升高的 NO含量和 NOS活性。结论　 NO和 n NOS在急性局灶性脑缺血再灌注的病理过程中起重要作用。Objective To study whether nitric oxide (NO) and neuronal NO synthase (nNOS) were involved in the pathogenesis of acute focal cerebral ischemia and reperfusion.Methods Using rat model of a middle cerebral artery occlusion (MCAO) by suture mothod, NO content and NOS activity in brain during and after ischemia and the effect of nNOS inhibitor 7 nitroindazole(7 NI) on them were observed.Results NO content and NOS activity in cerebral tissue significantly increased after 30 min ischemia and then decreased after 3 h;NO content and NOS activity again increased in 30 min reperfusion, but in 3 h reperfusion they decreased. 7 NI could significantly inhibite NO content and NOS activity in 30 min reperfusion after 3 h MCAO.Conclusion NO and nNOS may play an importent role in acute focal cerebral ischemia and reperfusion during the pathologic process.

关 键 词：脑缺血再灌注 一氧化氮 一氧化氮合酶 7-NI 

分 类 号：R743[医药卫生—神经病学与精神病学]