蛛网膜下腔出血后基底动脉细胞间粘附分子-1的表达

目的：探讨蛛网膜下腔出血（SAH）后迟发性脑血管痉挛的病理过程中细胞间粘附分子－1（ICAM－1）与其发生时相间的关系。方法：采用49只雄性SD大鼠，随机分为实验组和对照组，实验组按存活时间分为6组，采用经额钻孔、注血的方法制作SAH动物模型。切取基底动脉，分别行HE染色和ICAM－1免疫组化染色，进行体视学图像分析。结果：病理切片经图像分析，在SAH后1h和48h管腔面积显缩小（P＜0．001），48h后基底动脉壁发生明显病理形态学变化。SAH后3h血管内皮细胞ICAM－1表达逐渐增强，48h后达到高峰。结论：SAH后可引发急性脑血管痉挛和迟发性脑血管痉挛。ICAM－1参与的炎症反应在SAH后迟发性脑血管痉挛的形成和发展过程中发挥关键性作用。

Expression of Intercellular Adhesion Molecule 1 ( ICAM - 1 ) Following Subarachnoid Hemorrhage in Basilar Artery of Rats

Objective:To study how the immune- inflammatory response is involved in the pathogenesis of cerebral vasospasm after subaraehnoid hemorrhage(SAH).Methods:We studied the intercellular adhesion molecules- 1 on the endothelial layer alter SAH in rats. SD rats(n = 49) were used in this study.The experimental SAH models of rats were completed by trans - cranal drilling a hole and injected oneself arterial blood.The animals were killed in sequential time points,from 1 hour to 3 days after SAH. The basilar artery was examined immunohistochemically and histologically for the presence of ICAM - 1 and the morphological lea-tures of vasospasm, respectively. Results: Morphometics analysis of the BA revealed twice significant narrowing of the lumen area 1 hour and 48 hours following the hemorrhage( P < 0.001). Endothelial cell ICAM - 1 immunoreactivity gradually increased 3 hours alter SAH and persisted for 48 hours.The peak morphological changes of chronic vasospasm correlated directly with the time of increased ICAM - 1 expression. Conclusion: ICAM - 1,as an early and specific signal of the immune - inflammatory response,plays an important role in the development of chronic vasospasm after SAH in rats.