| BACKGROUND & AIMWhen acute myocardial infarction occurs, revascularization therapy should be performed as soon as possible to minimize the myocardial damage. However, reoxygenation of ischemic heart induces ischemia-reperfusion injury. Oxidative stress seems to play important roles in ischemia-reperfusion injury.Carbon monoxide(CO) is usually regarded as a toxic species that disrupts cellular respiration. However, recently, CO has been shown to be an important signaling molecule and protects tissues against injuries induced by several types of stress. CO is now regarded as a versatile signaling molecule having essential regulatory roles in a variety of physiological and pathophysiological processes that take place within the cardiovascular, nervous, and immune systems.CO, a gaseous second messenger, arises in biological systems during the oxidative catabolism of heme by the heme oxygenase (HO) enzymes. Endogenous CO appears to control the proliferation of vascular smooth muscle cells 12 and suppress the rejection of transplanted hearts. The biological action of heme oxygenase- derived CO is substantiated by the pharmacological effects observed when this gas is applied exogenously to in vitro and in vivo systems. Recently study reported that certain transition metal carbonyls possess the ability to liberate CO under appropriate conditions...
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