Metabolic cardioprotection: new concepts in implementation of cardioprotective effects of meldonium

Abstract

Recent studies confirm the need to find means to correct ischemic / reperfusion injury due to the hemodynamic medicine, which are already known do not have the proper cardioprotective effects. Key issue is the possibility of drug effects on the mitochondria of cardiomyocytes that controls the aerobic metabolism and maintenance of ATP admission into cardiomyocytes. Moreover mitochondria are the target of ischemia / reperfusion injury and involved in the cardioprotective mechanism ischemia and pharmacologic pre- and postconditioning. Effect of nitric oxide during ischemic reperfusion directed to mitochondria, is considered as the ultimate goal of cardioprotection. Preconditioning effects is begun from sarcolemmal membrane and then is directed to the cytoplasm through a plurality of stages of enzymes, including nitric oxide synthase (NOS), soluble guanylatecyclase (sGC) and protein kinase G (PKG). Thus, the signal is transmitted to the mitochondria, where it occurs cardioprotection. It is proved that the mitochondria provides protection of the heart against ischemia-reperfusion injury by opening the mitochondrial ATP-sensitive K + channels and by converting the capacity of mitochondria. Metabolic modulation concept can be used in the development of strategies cardioprotection for treatment in ischemic / reperfusion myocardial injury.