2007Advances in Cardiovascular DiseasesRequires access

Advanced Research into Cardioprotective Mechanisms of Ischemic Postconditioning in Myocardial Ischemia-Reperfusion

Guoqin Feng

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Abstract

Postconditioning is defined as rapid intermittent periods of reperfusion and ischemia in the early phase of reperfusion after long ischemia. It has been found that ischemic postconditioning can reduce myocardial ischemia-reperfusion injury just as ischemic preconditioning. Mechanisms using postconditioning have been associated with a reduction in the generation of superoxide radicals and calcium overload, activation of protein kinases, preservation of endogenous autacoids (such as adenosine, opioids, and NO),opening of mitochondrial ATP-sensitive potassium channels and closing of mitochondrial transition permeability pore. This article summarizes the current information regarding the cardioprotection of postconditioning in ischemia-reperfusion and possible mechanisms involved.

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What this paper is about

Postconditioning is defined as rapid intermittent periods of reperfusion and ischemia in the early phase of reperfusion after long ischemia. It has been found that ischemic postconditioning can reduce myocardial ischemia-reperfusion injury just as ischemic preconditioning. Mechanisms using postconditioning have been associated with a reduction in the generation of superoxide radicals and calcium overload, activation of protein kinases, preservation of endogenous autacoids (such as adenosine, opioids, and NO),opening of mitochondrial ATP-sensitive potassium channels and closing of mitochondrial transition permeability pore. This article summarizes the current information regarding the cardioprotection of postconditioning in ischemia-reperfusion and possible mechanisms involved.

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Available abstract

Postconditioning is defined as rapid intermittent periods of reperfusion and ischemia in the early phase of reperfusion after long ischemia. It has been found that ischemic postconditioning can reduce myocardial ischemia-reperfusion injury just as ischemic preconditioning. Mechanisms using postconditioning have been associated with a reduction in the generation of superoxide radicals and calcium overload, activation of protein kinases, preservation of endogenous autacoids (such as adenosine, opioids, and NO),opening of mitochondrial ATP-sensitive potassium channels and closing of mitochondrial transition permeability pore. This article summarizes the current information regarding the cardioprotection of postconditioning in ischemia-reperfusion and possible mechanisms involved.

Key concepts: Cardioprotection, Medicine, Mitochondrial permeability transition pore, Ischemia, Reperfusion injury, Ischemic preconditioning, Cardiology, Pharmacology

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