Abstract
Ischemia and reperfusion (IR) injury causes a variety of changes in tissue homeostasis that lead to necrosis and/or programmed cell death. Due to its strategic location at the luminal surface of vessels, the vascular endothelium is particularly sensitive to IR. In particular, endothelial biosynthetic activities (and their protective effects) appear to be impaired by the oxidative burst induced by a sudden increase in oxygen free radical species upon reperfusion. Importantly, this endothelial damage can be easily assessed in vivo in humans by measuring endothelium-dependent vasorelaxation. Paradoxically, recent studies have emphasized the central role of free radicals (including oxygen free radicals and nitric oxide) also in a protective process, denominated ischemic preconditioning, i.e. a condition whereby a given stimulus can increase the tolerance of a tissue to IR damage. We discuss the role of the endothelium in determining the mechanism of IR injury, and on the other side, the effect of IR injury on endothelial function. In particular, we focus on the role of reactive free radicals in endothelial IR injury and in the development of ischemic preconditioning.
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