Ischemic preconditioning: Interruption of various disorders

Abstract

Ischemic heart diseases are the leading cause of morbidity and mortality worldwide. Reperfusion of an ischemic heart is necessary to regain the normal functioning of the heart. However, abrupt reperfusion of an ischemic heart elicits a cascade of adverse events that leads to injury of the myocardium, i.e., ischemia-reperfusion injury. An endogenous powerful strategy to protect the ischemic heart is ischemic preconditioning, in which the myocardium is subjected to short periods of sublethal ischemia and reperfusion before the prolonged ischemic insult. However, it should be noted that the cardioprotective effect of preconditioning is attenuated in some pathological conditions. The aim of this article is to review present knowledge on how menopause and some metabolic disorders such as diabetes and hyperlipidemia affect myocardial ischemic preconditioning and the mechanisms involved.

Keywords: Diabetes; Hyperlipidemia; Ischemic preconditioning; Menopause.

Fig. 1

Mechanisms involved in hyperglycemia induced attenuation of cardioprotective effect of preconditioning. eNOS = endothelial nitric oxide synthase; GSK3β = glycogen synthase kinase-3β; K_ATP = adenosine triphosphate-sensitive potassium channels; NO = nitric oxide.

Fig. 2

Mechanisms involved in hyperlipidemia induced attenuation of cardioprotective effect of preconditioning. mitoK_ATP = mitochondrial adenosine triphosphate-sensitive potassium channels; MMP = matrix metalloproteinases; NO = nitric oxide.

Fig. 3

Mechanisms involved in menopause-induced attenuation of cardioprotective effect of preconditioning. eNOS = endothelial nitric oxide synthase; mitoK_ATP = mitochondrial adenosine triphosphate-sensitive potassium channels; mPTP = mitochondrial permeability transition pore; PKC = protein kinase C; TNF = tumor necrosis factor.