脑缺血再灌流脑微血管损害及u-PA表达的实验研究

The experimental study on cerebral microvascular and u-PA after local cerebral ischemia with reperfusion.

目的探讨脑缺血再灌流后继发的脑水肿、出血的发生机制。方法应用光镜、透射电镜、免疫组织化学、显微镜－计算机图像分析等技术，观察大鼠局部脑缺血２小时再灌流不同时间，脑微血管结构、Ⅳ型胶原抗原及尿激酶型纤溶酶原激活物（ｕ－ＰＡ）表达。结果局部脑缺血再灌流２４小时，缺血侧ＭＣＡ区脑微血管外细胞间质水肿最严重，基底膜节段性溶解、缺损，有红细胞漏出，微血管壁及管外细胞间质ｕ－ＰＡ大量表达达高峰，同时微血管基底膜Ⅳ型胶原抗原减少。随再灌流时间延长，微血管基底膜损害加重，Ⅳ型胶原抗原逐渐消失，ｕ－ＰＡ表达减少。结论脑缺血再灌流后脑微血管结构损害是导致脑水肿、出血的主要病理基础，而脑微血管壁和管外细胞间质ｕ－ＰＡ表达可能是引起微血管损害的主要机制之一。

Objective To investigate the mechanism of brain edema and hemorrhage after focal cerebral ischemia with reperfusion. Methods The cerebral microvascular ultrastructure and the product of u-PA in microvascular and intercellular substance after focal cerebral ischemia with reperfusion were observed by transmission electron microscope, immunohistochemical method and morphological analysis. Results The results showed that u-PA on cerebral ischemic area was significantly increased after focal cerebral ischemia with reperfusion 6 hours. By 12-hour reperfusion, cerebral microvascular structure was damaged and type IV collagen of microvascular reduced at the ischemic area. Conclusions These results suggest that u-PA might play an important role in microvascular lesion after reperfusion following cerebral ischemia.