title: [Effect of energostim on myocardial damage during coronary artery occlusion].
abstract: In contrast to traditional therapy (beta-adrenoblocker and nitrates), energostim improves the systolic and diastolic functions of myocardium during 120-min occlusion of the left descending coronary artery. The energostim-induced improvement in the central hemodynamics is correlated with an adaptive increase in activity of the antioxidant system enzymes in response to the ischemic production of reactive oxygen species, which is evidence of the mobilization of reserves of the enzymatic link in the antioxidant defense system of cardiomyocytes. Analogous pattern is observed in the blood. In the control group of traditional therapy, a decrease in the superoxide dismutase (SOD) activity and the redox potential (NAD/NADH) in myocardium are correlated with a decrease in the maximum rate of pressure increase in the left ventricle (R 6.4, p < 0.01) observed 2 h after the coronary occlusion. In the energostim treated group, there is a correlation between the SOD activity and the content of cytochrome C in mitochondria (R 6.1, p < 0.01): a change in the level of cytochrome C during 2-h acute ischemia is correlated with the decrease in redox potential (NAD/NADH) and in the ratio of glutathione peroxidase to Mn-dependent SOD (r 0.64, p < 0.01). Thus, disturbances in the antioxidant defense system of both myocardium and blood plasma of the patients with acute myocardium infarction are correlated with inability of the energy supply system to utilize oxygen in the process of glycolysis and oxidative phosphorylation in mitochondria. Stable adaptive increase in activity of the antioxidant defense system enzymes and a decrease in the content of cytochrome C in the blood plasma are probably the independent indications of beneficial prognosis and high efficacy of the proposed treatment of the ischemic damage of myocardium.
authors.affiliation: Republic Research Center for Medical Biophysics and Novel Biomedical Technologies, Ministry of Public Health of the Republic of Georgia, Gudamakarskii per. 2, Tbilisi, Georgia.
authors.forename: N V
authors.initials: NV
authors.lastname: Karsanov
authors.forename: G V
authors.initials: GV
authors.lastname: Sukoian
authors.forename: A V
authors.initials: AV
authors.lastname: Antelava
authors.forename: N A
authors.initials: NA
authors.lastname: Varazanashvili
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage / Q000494:pharmacology*; D003327:Coronary Disease / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D003331:Coronary Vessels / Q000187:drug effects / Q000473:pathology*; D045304:Cytochromes c / Q000008:administration & dosage / Q000494:pharmacology; D004195:Disease Models, Animal; D004285:Dogs; D004338:Drug Combinations; D005260:Female; D007288:Inosine / Q000008:administration & dosage / Q000494:pharmacology; D008297:Male; D009206:Myocardium / Q000201:enzymology / Q000378:metabolism / Q000473:pathology*; D009243:NAD / Q000008:administration & dosage / Q000494:pharmacology; D018384:Oxidative Stress / Q000187:drug effects; D016277:Ventricular Function, Left / Q000187:drug effects
chemical_list: D000975:Antioxidants; D004338:Drug Combinations; D009243:NAD; D007288:Inosine; D045304:Cytochromes c