Myocardial ischemia-reperfusion injury: Possible role of melatonin

Our knowledge and understanding of the pathophysiology of coronary atherosclerosis has increased enormously over the last 20 years. Reperfusion through thrombolysis or percutaneous coronary angioplasty is the standard treatment for preventing acute myocardial infarction. Early reperfusion is an absolute prerequisite for survival of the ischemic myocardium, but reperfusion itself may lead to accelerated and additional myocardial injury beyond that generated by ischemia alone. These outcomes, in a range of reperfusion-associated pathologies, are collectively termed "reperfusion injuries". Reactive oxygen species are known to be produced in large quantities in the first few minutes of the post-ischemia reperfusion process. Similarly, scientific evidence from the last 15 years has suggested that melatonin has beneficial effects on the cardiovascular system. The presence of vascular melatoninergic receptor binding sites has been demonstrated; these receptors are functionally linked to vasoconstrictor or vasodilatory effects of melatonin. It has been shown that patients with coronary heart disease have a low melatonin production rate, especially those with higher risk of cardiac infarction and/or sudden death. Melatonin attenuates molecular and cellular damage resulting from cardiac ischemia-reperfusion in which destructive free radicals are involved.