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目的 :探讨脑缺血再灌注区脑微血管结构损害特征及发生机制。方法 :应用光镜、透射电镜、免疫组织化学、原位分子杂交等技术 ,观察易卒中型肾血管型高血压大鼠局灶脑缺血 2h再灌注 6h至 7d ,再灌注区脑微血管结构改变、尿激酶型纤溶酶原激活物 (uPA)表达。结果 :局灶脑缺血再灌注区的脑水肿加重及并发出血以再灌注 12h至 3d最为严重 ,脑微血管基底膜溶解、缺损。同时使基底膜及细胞外间质降解的主要酶类uPA及uPAmRNA表达增加 ,以再灌注 12h至 3d达高峰。结论 :脑缺血再灌注区脑微血管基底膜破坏是导致再灌注后脑水肿、出血的主要病理基础 ,内皮细胞、胶质细胞uPA表达的增加可能是引起微血管基底膜及细胞外间质损害的主要机制之一。
Objective: To investigate the characteristics and mechanism of cerebral microvascular structure damage in cerebral ischemia-reperfusion area. Methods: The morphological changes of cerebral microvessels in reperfusion area were observed by light microscopy, transmission electron microscopy, immunohistochemistry and in situ hybridization. The changes of cerebral microvessels in reperfusion area were observed after focal cerebral ischemia 2h and reperfusion 6h to 7d in stroke prone renovascular hypertensive rats , Urokinase-type plasminogen activator (uPA) expression. Results: Cerebral edema in focal cerebral ischemia-reperfusion area was aggravated and concurrent hemorrhage occurred at 12h to 3d after reperfusion. The basement membrane of cerebral microvascular was dissolved and damaged. At the same time, the expression of uPA and uPA mRNA, the major enzymes responsible for the degradation of the basement membrane and extracellular matrix, was increased to the peak of reperfusion 12h to 3d. CONCLUSION: The destruction of cerebral microvascular basement membrane in cerebral ischemia-reperfusion area is the main pathological basis of cerebral edema and hemorrhage after reperfusion. The increase of uPA expression in endothelial cells and glial cells may be the main cause of microvascular basement membrane and extracellular matrix damage One of the mechanisms.