Abstract

Cardiovascular diseases are the main cause of death and disability in the economically developed countries of the world. Taking into account the high medical, social, and economic importance of the problem of treating patients with coronary heart disease and acute myocardial infarction, the search for new effective methods how to prevent or weaken the unfavorable effects of ischemic and reperfusion myocardial injury and to find out the mechanisms of their implementation is an urgent task of modern experimental and clinical medicine. The aim of the study was to elucidate the participation of nitric oxide (NO) in the mechanisms of realization of the infarct-limiting effect of post-conditioning (PostC) with lactate during myocardial ischemia-reperfusion in young and old rats. According to the study results, it was found that PostC with lactate (10 mg/kg), carried out at the 25th minute of myocardial reperfusion after 30-minute acute coronary occlusion, has an infarction-limiting effect in both young and old rats. However, in the animals under the conditions of systemic action of an inhibitor of NO-synthase of NG-nitro-L-arginine methyl ester at a dose of 25 mg/kg (intravenous administration 5 minutes before the start of reperfusion and 30 minutes before PostC), the cardioprotective effect of PostC with lactate was preserved only partially in young rats. The infarction-limiting effect of PostC with lactate was fully preserved in old rats. The data obtained suggest that the activity of NO-synthase and the NO level in the blood are significant in the mechanisms of implementation of the infarct-limiting effect of PostC with lactate in young, but not in old rats.

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