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目的 探讨脑缺血再灌注后脑微血管结构损害的特征及发生机制。 方法 应用光镜、透射电镜、免疫组织化学等技术 ,观察易卒中型肾血管性高血压大鼠局部脑缺血 2h再灌注 6h至7d时脑微血管结构、基底膜Ⅳ型胶原抗原和层连蛋白抗原变化。 结果 局部脑缺血再灌注病灶区脑水肿及并发出血以再灌注 12h至 3d最为严重 ,脑微血管基底膜大片溶解、缺损。再灌注 12h后脑微血管基底膜主要成分Ⅳ型胶原抗原、层连蛋白抗原减少 ,其阳性单位 (PU值 )分别为 2 0 17± 2 91和15 96± 4 81,与对照组比较差异有显著性 (均为P <0 0 5 ) ;再灌注 7d分别为 5 12± 2 70和 5 2 6±2 17,与对照组比较差异有极显著性 (均为P <0 0 1)。 结论 脑缺血再灌注后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 ,脑微血管基底膜成分的减少是基底膜破坏的根本原因。
Objective To investigate the characteristics of cerebral microvascular structure damage after cerebral ischemia and reperfusion and its mechanism. Methods Using light microscopy, transmission electron microscopy and immunohistochemical techniques, we observed the changes of cerebral microvascular structure, type IV collagen antigen and laminin in rat with stroke-induced renovascular hypertension at 6 hours and 6th to 7th days after focal cerebral ischemia. Antigen changes. Results Cerebral edema in focal cerebral ischemia-reperfusion area and concurrent hemorrhage were most severe in 12h to 3d after reperfusion, and the large area of cerebral microvascular basement membrane was dissolved and impaired. After 12h of reperfusion, the main component of cerebral microvascular basement membrane type Ⅳ collagen antigen, laminin antigen decreased, the positive units (PU) were 2017 ± 2191 and 15 96 ± 4 81, compared with the control group, the difference was significant (All P <0 05). At 7 days after reperfusion, they were 5 12 ± 2 70 and 52 6 ± 2 17, respectively, which were significantly different from those of the control group (P <0.01). Conclusions The destruction of cerebral microvascular basement membrane after cerebral ischemia-reperfusion is the main pathological basis of cerebral edema and hemorrhage after reperfusion. The decrease of basement membrane components of cerebral microvascular is the underlying cause of basement membrane destruction.