Ischemia and reperfusion result in leukocyte activation, adhesion and infiltration, which can extend tissue injury in experimental stroke and myocardial infarction. Activated neutrophils are considered the primary mediators of tissue destruction following ischemia and reperfusion. This involves adhesion to the endothelial surface and tissue infiltration, followed by eventual release of toxic reactive oxygen metabolites and proteases by neutrophils. The activation of neutrophils and monocytes is accompanied by an increase in cell-surface density of the adhesion molecules CD1 lb and CD 18, which play an important role in leukocyte adhesion and infiltration. The critical role of these adhesion molecules is clearly demonstrated by the observations that inhibition of leukocyte adhesion with antibodies directed against CD 18 or the CD18/CD11 dimers can reduce the extent of injury.