[Effect of nonachlazine on the energy provision for cardiac contractile activity in experimental myocardial infarct].
Experiments on 107 rabbits and 76 white rats with the use of electrophysiological, biochemical and electron microscopy research methods have shown that nonachlazine-induced improvement of heart contractility in microfocal myocardial infarction occurs as a result of the shortening of the systolic and lengthening of the diastolic phases of the heart cycle. Nonachlazine improves the processes of oxidative phosphorylation in heart mitochondria in myocardial infarction, which is accompanied by inhibition of the activity of succinate dehydrogenase and transition of oxidation from succinate to NAD-dependent substrates.
D000818:Animals; D004353:Drug Evaluation, Preclinical; D004734:Energy Metabolism / Q000187:drug effects*; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects*; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism; D009628:Nonachlazine / Q000627:therapeutic use*; D010085:Oxidative Phosphorylation / Q000187:drug effects; D010640:Phenothiazines / Q000627:therapeutic use*; D011817:Rabbits; D051381:Rats
D010640:Phenothiazines; D009628:Nonachlazine
Vliianie nonakhlazina na énergetichekoe obespechenie sokratitel'noĭ deiatel'nosti serdtsa pri éksperimental'nom infarkte miokarda.