Abstract: 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.