Reperfusion of ischemic tissues is associated with a sequence of events that closely resembles an acute inflammatory response. The increased leukocyte rolling, adherence and emigration in postcapillary venules elicited by ischemia/reperfusion appear to result from an accumulation of mediators such as platelet activating factor and leukotriene B4. These adhesive interactions between circulating leukocytes and venular endothelium are modulated by adhesion glycoproteins expressed on the surface of activated neutrophils and endothelial cells, reactive oxygen metabolites and granule-associated proteins produced by neutrophils, and by hydrodynamic forces generated within the microcirculation. Therapeutic interventions directed against either of these factors may prove to be effective in reducing ischemia/reperfusion injury.