Injury associated with ischemia and reperfusion is a significant factor in a number of clinical diseases. Reactive oxygen species generated during the reperfusion of ischemic tissues is known to directly cause injury (Serrano et al., 1996). Reperfusion of ischemic tissue is also associated with an acute inflammatory response that may exacerbate vascular and tissue damage further. Compelling evidence from a variety of animal models indicates that neutrophils are the principal effector cells of reperfusion injury and that the blockade of neutrophil adhesion to endothelium attenuates ischemia-reperfusion injury (Thiagarajan et al., 1997). Monoclonal antibodies directed to CD 18, P-selectin, and L-selectin have been shown to be effective in reducing ischemia-reperfusion injury to the rabbit ear and in reducing injury following hemorrhagic shock in both rabbits and nonhuman primates (Winn et al., 1997,1998). Antioxidants have been shown to suppress leukocyte adhesion and CD 18 expression following ischemia-reperfusion, resulting in a marked suppression of leukocyte-mediated injury in the postischemic heart (Serrano et al., 1996).
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