Neutrophil and endothelial changes in reperfusion injury.

Reperfusion of the ischemic myocardium alleviates the hypoxic insult, but promotes the influx of neutrophils. The rapidity and site-specificity of neutrophil accumulation, initially noted as adhesion to the vascular endothelium, implies functional alterations in the endothelium, which subserve neutrophil sequestration and reperfusion injury. Elucidation of the underlying mechanisms that predispose one to endothelial dysfunction, leukocyte sequestration, and neutrophil-mediated exacerbation of myocardial injury may provide a basis for the development of adjunctive pharmacologic therapies to enhance the benefits of restoring blood flow to the ischemic heart.