| Reperfusion after cerebral ischemia can induce more serious damage than of cerebral ischemia itself. An pathologic phenomenon occurring after the reestablishment of circulation has causative role in this reperfusion, included microvascular endothelial cell swelling necrosis and dysfunction of synthesizing cytokines by microvascular endothelium. Then the function and integrity of the microvessels are damaged and the normal cerebral blood is not supplied properly, and the normal cerebral function is damaged too . So it is very important to investigate the microvascular lesions after cerebral ischemia-reperfusion(I-R) and mechanism of microvascular ultrastructural characteristics and expression of cytokines hi endothelial cell. The animals were subjected to reperfusion following 30min of global ischemia induced by 3-vessel occlusion. The experimental studies investigate not only the change of microvascular intergrity and cytokines synthesized by microvascular endothelium but also the microvascular structure perfused by performed polymer of polyresin after global cerebral ischemia-reperfusion in rats. In this way we want to interpret the change of microvascular ultrastructure and endothelium after cerebral ischemia-reperfusion.In this study, the healthy male Sprague-Dawley (SD) rats were divided into two groups randomly, one was cerebral ischemia-reperfusion group and another was sham operated control ischemia-reperfasion group. The global cerebral ischemia-reperfusion model was formed by 3-vessel occlusion (30min) and reperfuse in rats (lh,3h,6h,12h,24h,48h,72h), VII factor related antigen (von willebrand7Factor, vWF) was detected by immunohistochemical SABC staining method in order to mark the change of microvascular damage after cerebral ischemia-reperfusion, and we detected the expression of PAI-lmRNA in situ hybridization and observed its alteration, and we investigate the mivrovascular casts by scanning electron microscope to study the ultrastructural characteristics of cortical microvasculature. The findings of experiments are lined in the following.1. The experiment of vascular endothelial cell (VEC)injury: Positive immunoreactivity of vWF was on microvascularendothelial cells surface. At Ih after cerebral I-R, the expression of vWF in microvascular endothelial cells began to decrease (P<0.05), then slightly decreased at 3h and the lowest at 24~48h after reperfusion(P< 0.01). The expression of vWF increased at 72h after reperfusion but still lower than control level. There was statistical significance among strong positive in every sham operated central group, and there was no statistical significance among the defferent groups(P>0.05).2. The expression of PAI-lmRNA in situ hybridization: PAI-lmRNA was detected in sham operated control group andincreased at Ih after cerebral ischemia-reperfusion(P < 0.05), The expression were the highest at 12~24h after reperfusion(P<0.01), The expression was higher than that of control at 72h (P<0.05) . The defference of each group has statistical significance(P<0.01).3. The change of cortical microvascular ultrastructural characteristics:It was found, under scanning electron microscope, that the microvascular casts from cortex showed evidence such as capillary spasm and narrowing, the ratio of inmer diameter of capillariesdecreased significantly, at Ih after cerebral ischemia-reperfusion, then partial or total disconnection of microvessels and presence of microvessels, and presence of vessel-disappeared areas at 3~48h after ischemia-reperfusion.In summary. This finding suggest the following that: (1)The endothelial cells injury was occurred and BBB was damaged when global cerebral ischemia-reperfusion, then cerebral function was damaged but part of that could be reversed in beginning period of ischemia-reperfusion. (2) The global cerebral ischemia-reperfusion is capable of leading to the damage of cerebral microvasculature in ultrastructure. The abnormality of cerebral microcirculation is...
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