大鼠急性局灶性脑缺血再灌注NO含量和NOS活性的变化及7-NI对其影响的实验研究

目的探讨一氧化氮和神经元型一氧化氮合酶是否参与了急性脑缺血再灌注的发病机制.方法采用栓线法复制大鼠大脑中动脉阻塞模型,观察血清和脑组织NO含量和NOS活性的变化及神经元型一氧化氮合酶抑制剂7-硝基吲唑对再灌注期间两者的影响.结果脑缺血45 min再灌注2 h后血清及脑组织中NOS活性及NO含量增加,再灌注8 h达高峰.7-NI能显著抑制再灌注期间血清及脑组织中NOS的活性及NO的含量.结论 NO和nNOS在急性局灶性脑缺血再灌注的过程中起着重要的作用.

The Changes of NO Content and NOS Activity During Acute Focal Cerebral Ischemia Reperfusion and the Effect of 7-nitroindazole

ObjectiveTo study whether nitric oxide and neuronal NO synthase(nNOS) were involved in the pathogenesis of acute focal cerebral ischemia reperfusion.MethodsUsing rat model of a middle cerebral artery occlusion by suture, NO content and NOS activity in brain and serum during reperfusion were detected and the effect of nNOS activity inhibitor(7-nitroindazole) on them was observed.ResultsThe NO content and NOS activity in brain tissue and serum increased at 2h of reperfusion after 45min of ischemia. They reached peak at 8h of reperfusion. 7-NI could inhibit NO content and NOS activity obviously during reperfusion.ConclusionNO and nNOS may play an important role in acute focal cerebral ischemia reperfusion.