摘要
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。
AIM: To explore the structural changes of brain microvasculature and mechanism in microvascular lesion after focal cerebral ischemia with reperfusion. METHODS: Using the techniques of immunohistochemical staining, in situ hybridization,optical microscopy and transmission electron microscopy, the expression of uPA, uPA mRNA, and changes in miocrovascular structure were examined in ischemic focus and perifocal areas after focal cerebral ischemia 2 hours with various time points of reperfusion in stroke-prone renovascular hypertensive rats (RHRSP). RESULTS: The brain edema and hemorrhage were severe 12 hours to 3 days after reperfusion. Ultrastructural change showed that the damage characterizations of the basement membrane were degradation, defection, and exfoliated of basement membrane, while uPA, which attack the basememt membrane around cerebral capillaries and extra-cellular matrix, and uPA mRNA expression increased significantly in ischemic and perifocal areas 12 hour to 3 day after reperfusion. CONCLUSION: The main pathologic mechanism of brain edema and hemorrhage after cerebral ischemia with reperfusion may result from the basement membrane lesion of brain microvasculature. The increase in the expression of uPA in reperfusion area may be the main cause of the basement membrane lesion .
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2000年第11期1189-1193,共5页
Chinese Journal of Pathophysiology
关键词
脑缺血
脑微血管
原位杂交
UPA
MRNA
Cerebral ischemia
Reperfusion
Brain microvasculature
Urokinase
In situ hybridization
