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.
出处
《临床神经病学杂志》
CAS
2000年第4期201-203,共3页
Journal of Clinical Neurology
关键词
脑缺血再灌注
一氧化氮
一氧化氮合酶
7-NI
Cerebral ischemia and reperfusion Nitric oxide Nitric oxide synthase 7 nitroindazole
