Myocardial Ischemia Reperfusion Injury

Abstract

Myocardial ischemia reperfusion injury contributes to adverse cardiovascular outcomes after myocardial ischemia, cardiac surgery or circulatory arrest. Primarily, no blood flow to the heart causes an imbalance between oxygen demand and supply, named ischemia (from the greek isch-, restriction and -haema, blood), resulting in damage or dysfunction of the cardiac tissue. Instinctively, early and fast restoration of blood flow has been established to be the treatment of choice to prevent further tissue injury. Indeed, the use of thrombolytic therapy or primary percutaneous coronary intervention is the most effective strategy for reducing the size of a myocardial infarct and improving the clinical outcome. Unfortunately, restoring blood flow to the ischemic myocardium, named reperfusion, can also induce injury. This phenomenon was therefore termed myocardial ischemia reperfusion injury. Subsequent studies in animal models of acute myocardial infarction suggest that myocardial ischemia reperfusion injury accounts for up to 50% of the final size of a myocardial infarct. Consequently many researchers aim to understand the underlying molecular mechanism of myocardial ischemia reperfusion injury to find therapeutic strategies ultimately reducing the final infarct size. Despite of the identification of numerous therapeutic strategies at the bench, many of them are just in the process of being translated to bedside. In the current review, we will discuss the most striking basic science findings made during the last decades that are currently under clinical evaluation, with the ultimate goal to treat patients who are suffering from myocardial ischemia and reperfusion associated tissue injury.

Cardioprotective effect of preconditioning is more efficient than postconditioning in rats submitted to cardiac ischemia and reperfusion

“…The coronary reperfusion therapy constitutes the major therapeutic strategy to salvage the myocardium from tissue injury following prolonged ischemia in acute myocardial infarction (AMI) patients [1][2][3] . However, the beneficial effect of this therapy is compromise by myocardial injuries caused during coronary reperfusion that subsequently lead to cardiac dysfunctions, including arrhythmias, caused by bioenergetic and electrochemical misbalance caused mainly by reduction of ATP production by mitochondria and cytosolic Ca 2+ overload in cardiomyocytes 4,5 .…”

Embelin as a Potential Drug Molecule: A Review

“…Siddharthan Surveswaran et al [68] illusteated crude E. ribes displaying free radical scavenging activities when tested using DiPhenyl-2-picryl Hydrazyl (DPPH). Uma et al [69] described antioxidant activity against streptozotocin induced diabetic rats using aqueous extract of E. ribes administered orally (100 and 200 mg/kg body weight) and whereas Venkateshwar rao et al [70][71][72][73][74][75][76][77][78][79] substantiates the antioxidant activity of embelin. Dharmendra Singh et al reported antioxidant activity of embelin against hepatotoxicity induced rats (at concentration of 25 mg/kg body weight).…”

Real-Time Monitoring of Nitric Oxide Dynamics in the Myocardium: Biomedical Application of Nitric Oxide Sensor

“…In particular, remote ischemic preconditioning (RIPC) is a novel method where ischemia followed by reperfusion of one organ is believed to protect remote organs either by the release of biochemical messengers into circulation or by the activation of nerve pathways, resulting in the release of messengers that have a protective effect [60][61][62]. This preserves the target tissue without trauma to major vessels or direct stress to the target organ [63].…”