Remote postconditioning of myocardium: mechanisms, efficacy in metabolic syndrome in experimental and clinical studies (review)

Abstract

Remote postconditioning of the heart (RPost) – performed several periods of short-term ischemia-reperfusion of an remote organ after a long period of ischemia immediately before the resumption or in the early reperfusion, which leads to a reduction in the size at the subsequently formed infarction – represents a great therapeutic potential for clinical practice. The mechanism of remote postconditioning includes a trigger that can be played by adenosine, opioids, cannabinoids, bradykinin, CGRP, and substance P. Protein kinase C, PI3 kinase, Akt kinase, and JAK play an important role in the signaling mechanism of remote postconditioning. Experimental studies found that genetically determined or diet-induced metabolic changes reduce the effectiveness of cardioprotection in RPost. As possible mechanisms of cardioprotection inefficiency, we can suggest a decrease in the release of humoral factors, dysfunction of the receptor and signaling link of RPost, the effect of metabolic disorders on the functioning of KATP channel, mPTP, and on the state of mitochondrial respiration. However, these assumptions need experimental substantiation. The results of clinical studies show both the antinecrotizing and infarct-limiting effect of RPost in AMI and cardiac surgery, and the lack of its effectiveness. The role of metabolic disorders in the absence of the effectiveness of RPost in patients requires substantiation.