iNOS抑制剂对海马缺血/再灌注损伤保护作用研究

目的：进一步证实诱导型一氧化氮合酶（ｉＮＯＳ）催化所形成的一氧化氮（ＮＯ）在脑缺血／再灌注损伤中具有毒性作用。方法：将Ｓ－Ｄ大鼠双侧颈总动脉短暂夹闭３分钟，然后分成应用药物组－氨基胍（ＡＧ）和非药物组．４８小时后取海马脑片，观察顺向群峰电位（ｏＰＳ）以及组织学改变。结果；给药组大部分可见ｏＰＳ发放．而对照组只见有突触前排放（ｐｖ）无ｏＰＳ（Ｐ＜０．０５），两组超微结构也有明显差异。结论：本实验证明大鼠海马短暂缺血／再灌注后ｉＮＯＳ抑制剂可减轻神经元损害，即可抑制血由ｉＮＯＳ诱生表达所形成的ＮＯ在脑缺血／再灌注损伤中的毒性作用。

Research on protective role of iNOS Inhibitor In hippocampus of the rats exposed to transient forebrain ischemia and reperfusion Injury

Objective: To confirm a neurotoxic action for NO generated by immunologic nitric oxide synthase (iNOS) in the rats exposed to transient foredrain ischemia/reperfusion injury. Methods: The transient forebrain ischemia/reperfusion was induced by transient clipping double side common carotid arteries for 3 mins in rats, then they were divided into non-medicine treatment group and medicine treatment group (Aminoguandine,AG). The hippocampal slices had been made in 48h after the transient forebrain ischemia/reperfusion in rats, the orthodromic population spike (oPS) in hippocampal slices and changes of histology in hippocampus of the rats between two groups were compared. Results: The occurrence rate of oPS obtained in the rats treated with AG after transient forebrain ischemia/reperfusion was higher than that of the control (P<0. 05) and there were marked differences between two groups in histologic ultrastructure. Condusion: NO generated by iNOS in the rats exposed to transient forebrain ischemia/rperfusion had neurotoxic action and iNOS inhibitor-AG could be resistant to NO neurotoxicity.