Although initially controversial, reperfusion injury is now recognized as a distinct entity. This refers to the sudden and brisk reperfusion of ischemic myocardium that may induce injury that was not originally present-paradoxically exaggerating the end result of an ischemic event. Reperfusion injury may increase infarct size, decrease myocardial contractile function and induce or exaggerate vascular endothelial dysfunction. The pathophysiology is not well understood, but some of the effects of reperfusion injury have been attributed to the generation of free oxygen radical and increased oxidative stress possibly related to the abnormalities of the nitric oxide synthase (NOS) enzyme and its byproducts. These cellular events lead to the endothelial dysfunction, a pivotal event in the development of reperfusion injury.