Роль натрийуретических пептидов и эритропоэтина в регуляции толерантности сердца к действию ишемии и реперфузии. Анализ экспериментальных и клинических данных

Abstract

Experimental studies show that natriuretic peptides have an infarct-limiting effect both in vitro and in vivo. In studies performed on animals, it was shown that erythropoietin is able to prevent ischemic and reperfusion damage of the heart both in vitro and in vivo by activating a number of kinases and by inactivating GSK-3β kinase. These data suggest that the cardioprotective effect of erythropoietin and natriuretic peptides appears to be associated with the activation of cardiac receptors. Erythropoietin had an anti-apoptotic effect both in vitro and in vivo. In the infarct-limiting effect of the atrial natriuretic peptide, NO synthase, protein kinase C, and the mitoKATP channel are involved. It was found that the in vivo infarct-reducing effect of erythropoietin is associated with the activation of PI3 kinase and ERK1/2 kinase. Brain natriuretic peptide prevents post-infarction cardiac remodeling and increases the survival rate of rats with experimental myocardial infarction. Erythropoietin inhibits post-infarction cardiac remodeling and enhances the process of myocardial neovascularization in rats and dogs. Natriuretic peptides have an infarct-reducing effect in patients with acute myocardial infarction (AMI). Atrial natriuretic peptide prevents post-infarction cardiac remodeling in patients with AMI. Erythropoietin does not affect infarct size in patients with AMI. A single injection of erythropoietin does not affect the post-infarction remodeling of the heart.