缺血再灌脑血管内皮损伤及GPⅢ_a表达的研究

Studies of Endothelial Injury and GPⅢ_a Expression at Ischemia_reperfusion Gerbil Brain

研究沙土鼠缺血再灌注后微血管内皮损伤和GPⅢa的表达。方法用夹闭沙土鼠双侧颈总动脉、30min再通造成灌注模型 ,由颈动脉注入FITC标记血小板。荧光显微镜下观察活体软脑膜微血管中血小板对内皮细胞的粘附 ,用CD61抗体经免疫组化方法观察缺血再灌注沙土鼠脑组织血管内血小板和内皮细胞上GPⅢa糖蛋白的表达。结果再灌注后即刻 ,软脑膜细静脉内有白细胞和血小板粘附 ,呈星点状分布 ;再灌注(30～60)min ,可观察到小动脉和细动脉内皮形成的空泡和血栓形成。免疫组化显示缺血再灌注(1～6)h血小板和内皮细胞膜上GPⅢa表达增强。

Objective To study endothelial injury and GPⅢa expression of microvessels at ischemia_reperfusion in gerbil brain. Methods Ischemia_reperfusion model was established by occlusion of common jugular artery and reperfusion in gerbil. The platelets were labeled by FITC injected by jugular artery. Adherence of platelets to endothelial cells in pial vessel was observed by fluorescent microscope. The expression of GPⅢa protein was identified by CD61 histochemistry. Results After onset of reperfusion, the adhesion of platelet to endothelia was observed at veins of pial vessel. they distributed as tiny spots, 30～60 minutes after reperfusion, we observed the vacuole formation in endothelial cells of artery and thrombosis could be seen at the injurious area. Immunohistochemistry examination shows the increased expression of GPⅢa at EC and platelet. Conclusions Ischemia_reperfusion can induce the increased expression of platelets and endothelial GPⅢa and cause the endothelial injury of cerebral microvessel.