Correction of mitochondrial dysfunction of rabbit cardiomyocytes using substrate antihypoxants

Abstract

Features of energy metabolism in children with cardiovascular diseases are of great practical importance. It is prognostically important to determine the status of the energy of cardiomyocytes to normalize bioenergetic deficit cardiomyocytes in rheumatoid arthritis, myocarditis, congenital heart diseases to decrease reduction in myocardial contractility and reduce precondition for the progression of heart failure. The experimental and clinical studies of the pathogenesis of idiopathic cardiomyopathy in children in recent years indicate directly the damage of oxidative phosphorylation in myocardial tissue due to decreased activity of the mitochondrial electron transport system. Numerous congenital diseases like syndrome Ivemark, Holt-Oram, Ellis-Van Creveld, Ivemark, Noonan, Greeg, Kugel-Stoloff, Werner, West, Adams-Stokes, MERRF include cardiomyopathy in their symptoms. Vibration-type model of hypoxic cell metabolism was suggested to estimate antihypoxant succinic acid as cardioprotective substance in in drug “Amber-antitoks” on rabbit cardiomyocytes. The experiment of bioenergy dependent reaction of native heart mitochondria was studied by polarographic method performed using a closed membrane Clarke’ electrode. Pharmacological drug “Amber-antitoks” in dose as 8.4 mg/kg prevents the formation of bioenergy dependent hypoxia of cardiomyocytes and restore the activity of NAD-dependent, and suppress hyperactivity suktsinat-degidrogenaze enzyme-substrate complex of the respiratory chain. It causes reduction of the severity of mitochondrial dysfunction and the degree of morphological myocardial tissue damage. The protective properties of drug “Amber-antitoks” allow to recommend it for using in the treatment in combination with other drugs of cardiovascular disease in children.