老龄大鼠脑缺血再灌注海马神经元iNOS的表达及超微结构改变

目的：观察老年大鼠脑缺血再灌注后海马神经元诱导型一氧化氮合酶（induced nitric oxide synthase iNOS）的表达及超微结构变化。方法：建立老年大鼠不完全性全脑缺血动物模型，应用免疫组织化学染色和透射电镜，观察海马神经元iNOS的表达及超微结构变化。结果：缺血30min后再灌注24h组海马神经元iNOS活性显著升高；缺血30min再灌注21h和48h组中量表达；假手术组、缺血30min即刻取材、再灌注1h、6h、96h组iNOS几乎无表达；再灌注超过48h组海马神经元损伤较重。结论：NO是脑缺血后神经元迟发性死亡的重要因素之一。

iNOS expression and ultrastructural changes in hippocampal neurons of the aged rats with cerebral ischemia and reperfusion

Objective:To observe expression of induced nitric oxide synthase(iNOS) and ultrastructural changes in hippocampal neurons of the aged rats with incomplete brain ischemia and reperfusion. Methods:The aged SD rats were made as models for incomplete brain ischemia. The expression of iNOS was examined by immunohistochemistry and neuronal ultrastructural changes were observed by the transmission electron microscopy (TEM) at different time after reperfusion. Results:Rats subjected to incomplete brain ischemia of 30min and reperfusion 24h showed high expression of iNOS in the neurons hippocampus. When the duration of reperfusion was changed to be 12h or 48h, the expression of iNOS became moderate. It was nearly no expression of iNOS in the neurons of hippocampus in the aged rats treated with reperfusion of 0 min, 1h, 6h, 96h respectively, and the sham operation and control group as well. Ultrastructure of neurons in hippocampus of rats which reperfusion over 48h was damaged more severely. Conclusion: NO may be one of the important factors inducing delayed neuronal death after ischemia / reperfusion.