大鼠脑缺血再灌注后微血管通透性变化

目的 :了解大鼠脑缺血再灌注后微血管通透性的变化。方法 :用暂时性脑缺血的大鼠模型 ,以右旋糖酐分子为示踪剂对缺血再灌注后微血管通透性的变化进行观察。结果 :电镜下见缺血 1h和再灌注后 1、2、3、4、6、9、12h各时点均可见右旋糖酐颗粒穿出血管外 ,微血管通透性增高有二个高峰 ,一是单纯缺血 1h ,另一是再灌注 6h以后。胞浆内出现的大量吞饮小泡 ,细胞间连接的增宽和开放 ,内皮细胞胞膜表面的凹陷及多量微绒毛的出现是微血管通透性增高的结构基础。结论 :单纯缺血和再灌注损伤都可引起微血管通透性的改变 ,但超微结构的变化提示有不同的机制参与通透性变化的调节。

Changes of Rat Brain Microvascular Permeability after Cerebral Ischemia-Reperfusion Injury

Objective: Microvascular permeability to high molecular weight Dextran was examined in the rat transient cerebral ischemic-reperfusion model.Method: The rat brain ischemia-reperfusion injury was induced using the method of Bannister and the microvessel permeability was determined by Dextran which was injected intravenously.Results: The increased permeability presented a biphasic nature,the first peak appeared immediately after ischemia,and the second peak at 6 hours after reperfusion.Intermittent enlargement of intercellular junctions,and numerous microvesicles,perivascular edema,deep invagination of the endothelial surface,were the most impressive characteristics which contribute to the breakdown of blood brain barrier.Conclusion: Both ischemia and reperfusion injury cause increase of endothelial permeability.The difference in ultrastructural change indicates that there are different machanismes in the regulation of permeability.