脑缺血—再灌注损伤细胞间粘附分子—1的表达

本文用暂时性脑缺血的大鼠模型，对细胞间粘分子－１（ＩＣＡＭ－１）的表达进行了研究。免疫组化结果显示ＩＣＡＭ－１在正常大鼠脑血内皮有向量表达，经缺血１ｈ，再灌３ｈ、６ｈ、９ｈ、１２ｈ后其表达量呈时间领事性增加，于再灌６ｈ后达到高峰，病理切片再灌９ｈ后缺血区白细胞渗出明显并见局灶变性坏死的神经细胞。结果说明ＩＣＡＭ－１表达量的增加与脑血－再灌注损伤的病理过程密切相关。

Intercellular adhesion molecule 1 expression after cerebral ischemia reperfusion injury

Activated neutrophils contribute to tissue injury after organic ischemia and reperfusion. Increased expression of cellular adhesion molecules are prerequiste for leukocytes adhesion to vascular endothelial cells and migration into surrounding tissues. We therefore used rat transient cerebral ischemic model to investigate the expression of intercellular adhesion molecule 1 (ICAM 1) and found that the up regulation of ICAM 1 on cerebral microvessels was time depedent and markedly increased after 1 h ischemia following 6h reperfusion. While leukocytes highly adhered to vessel walls and infiltrated into injury tissue after 9 h reperfusion. Our data indicate that ICAM 1 may mediate the pathologic process of ischemia reperfusion injury.