脑缺血再灌流脑微血管损害及u-PA表达的实验研究

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。

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

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.