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

目的探讨一氧化氮（ＮＯ）和神经元型ＮＯ合酶（ｎＮＯＳ）是否参与急性局灶性脑缺血再灌注的发病机理。方法采用栓红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ｎＮＯＳ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分种ＮＯ含量和ＮＯＳ活性显著升高，缺血３小进两者下降；再灌注３０分种ＮＯＴ和ＮＯＳ再次升高，而再灌注３小时两者又下降。７－Ｎ

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

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.