Actions of glucocorticosteroids on ischemic-reperfused muscle and cutaneous tissue

Abstract

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.

Mechanisms of the anti‐inflammatory effects of the natural secosteroids physalins in a model of intestinal ischaemia and reperfusion injury

“…By activating these GRs, glucocorticoids may affect reperfusion injury in a multitude of ways, including inhibition of leucocyte recruitment ( Perretti & Flower, 1993 ; Pitzalis et al ., 1997 ), reduction of vascular permeability ( Evans & Whittle, 2003 ; Romero et al ., 2003 ; Su et al ., 2004 ), inhibition of formation of cytokines or other mediators ( Almawi et al ., 1998 ; Turesin et al ., 2003 ) and modulation of enzyme systems involved in inflammation ( Koehler et al ., 1990 ; Kleinert et al ., 1996 ; Wallerath et al ., 2004 ). Potential mechanisms may involve modulation of neutrophil and endothelial function ( Korompilias et al ., 1996 ; Tjandra et al ., 1996 ; Takahira et al ., 2001 ), inhibition of formation of arachidonic acid products ( Turesin et al ., 2003 ) and attenuation of lipid peroxidation of biological membranes through membrane stabilization and scavenging of toxic‐free radicals ( Korompilias et al ., 1996 ; Marumo et al ., 1998 ). Here, treatment with dexamethasone totally suppressed the increase in vascular permeability, neutrophil influx and haemorrhage induced by reperfusion of the ischaemic SMA.…”

Activation of HSF and selective increase in heat-shock proteins by acute dexamethasone treatment

“…Glucocorticoids have a plethora of effects, including inhibition of lipid peroxidation, inhibition of formation of arachidonic acid products and modulation of neutrophil and endothelial function (19). Chronic glucocorticoid administration is known to alter protein metabolism (7,8).…”

Extracorporeal Shock Wave Therapy (ESWT) Minimizes Ischemic Tissue Necrosis Irrespective of Application Time and Promotes Tissue Revascularization by Stimulating Angiogenesis

“…These include the postoperative administration of topical agents such as fibrin, soluble mediators and growth factors (eg, recombinant human vascular endothelial growth factor), 1,2 and antiischemic pharmacotherapeutics (nitroglycerine, trolamine salicylate, and nifedipine). 3 Systemically administered agents with some protective effect in ischemic tissue have been tested to include hyperbaric oxygen, 4 corticosteroids, 5 thrombolytics, 6 free radical scavengers, 7 and vasoactive agents (potassium channel agonists like nicorandil, prostacyclin, and other prostanoid modifiers). 8,9 However, no single pharmacological intervention has proven consistently effective.…”