【摘要】 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。更多还原

【Abstract】 Objective To approach the structural changes of brain microvasculature and the possible mechanism of microvascular lesion after focal cerebral ischemia and reperfusion. Methods Reperfusion in renovascular hypertensive stroke prone rats (RHRSP) model were performed. Using immunohistochemical staining, optical microscopy and transmission electron microscopy, changes of type Ⅳ collagen and laminin antigens, the main components of the microvascular basement membrane, and the changes of miocrovascular structure were observed in ischemic focus and perifocal areas 2 hours after focal cerebral ischemia at various time points. Results The brain edema and hemorrhage were most severe between 12 hours and 3 days after reperfusion. Ultrastructural changes showed that the basement membrane damages included degradation, defection and exfoliation. Twelve hours after reperfusion, the main components of the basement membrane such as type Ⅳ collagen and laminin being 20 17±2 91 positive unit and 15 96±4 81 positive unit respectively, significantly decreased compared with that of the control group (P<0 05). Seven days after reperfusion the positive unit of type Ⅳ collagen and laminin were 5 12±2 70 and 5 26±2 17, respectively (P<0 01 ). Conclusions The mechanism of main pathologic changes such as brain edema and hemorrhage after cerebral ischemia with reperfusion were resulted from the basement membrane damages of brain microvasculature, and the decreases in the components of basement membrane contributed to the basement membrane lesion and the loss of microvascular integrity.更多还原