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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 explore the mechanism of cerebral edema and hemorrhage secondary to cerebral ischemia and reperfusion. Methods The effects of light microscope, transmission electron microscopy, immunohistochemistry and microscope - computerized image analysis were used to observe the changes of cerebral microvascular structure, type Ⅳ collagen antigen and urokinase - type plasminogen after reperfusion for 2 hours after focal cerebral ischemia in rats Activator (u-PA) expression. Results 24 hours after focal cerebral ischemia and reperfusion, MCA in ischemic MCA had the most severe interstitial edema in the MCA. The basement membrane was dissolved and damaged in a segmental manner with leakage of erythrocytes, and a large amount of microvascular wall and extracellular matrix interstitial u-PA The expression peaked at the same time as the type Ⅳ collagen antigen in the capillary basement membrane decreased. With the prolonged reperfusion time, the damage of capillary basement membrane was aggravated, the type Ⅳ collagen antigen gradually disappeared and the expression of u-PA decreased. Conclusions Cerebral microvascular damage after cerebral ischemic reperfusion is the main pathological basis leading to cerebral edema and hemorrhage. The expression of u-PA on the cerebral microvascular wall and extracellular matrix may be one of the main mechanisms of microvascular damage.