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Anastasios V. Korompilias; Long-En Chen; Anthony V. Seaber; James R. Urbaniak (Profiled Author: James Randolph Urbaniak)
Ischemia-reperfusion injury represents a complex series of vascular and cellular events that resembles an acute inflammatory reaction within the reperfused tissue. This article provides an overview of glucocorticosteroid effects on cells and tissues involved in inflammatory reaction following ischemia-reperfusion of muscle and cutaneous tissue. Glucocorticosteroids exert a variety of effects that influence the microcirculation. These effects include leukocyte recruitment, reduction of vascular permeability, inhibition of formation of cytokines or other mediators, and modulation of enzyme systems involved in inflammation. The current view is that glucocorticosteroids act through cytoplasmic receptors by controlling the transcription of certain genes encoding regulatory proteins, but the exact mechanisms of glucocorticoid action on ischemia-reperfusion are not completely understood. Potential mechanisms may involve modulation of neutrophil and endothelial function, inhibition of formation of arachidonic acid products, and attenuation of lipid peroxidation of biological membranes through membrane stabilization and scavenging of toxic free radicals.
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