title: [THE ENERGY FUNCTION OF RAT CARDIAC MITOCHONDRIA UNDER ARTIFICIAL HYPOBIOSIS].
abstract: We investigated the energy activity of mitochondria from rat cardiomyocytes under the artificial carbon dioxide hypobiosis, which led to physiological changes in the organism (the decrease of body temperature, the reduction of heart rate, etc.). The respiratory and phosphorylation activities in mitochondria of cardiomyocytes is reduced when using two oxidation substrates (succinate and malate), which characterize the rate of the oxygen consumption by the mitochondria. The partial uncoupling of the oxidation and phosphorylation processes when using the malate unlike succinate was established. The activity of NADH-KoQ-oxidoreductase (complex I of the respiratory chain) is inhibited, but the activities of succinate dehydrogenase and cytochrome oxidase don't change. Probably, the priority of the succinate use under the artificial hypobiosis provides the support of the mitochondria functional activity on a sufficient energy level. It is evidenced by the ATP-synthetase activity. The modifications of the structural and functional state of the inner mitochondria membrane of the cardiomyocytes are directed to the adaptation under the artificial carbon dioxide hypobiosis.
authors.forename: S D
authors.initials: SD
authors.lastname: Melnytchuk
authors.forename: S V
authors.initials: SV
authors.lastname: Khyzhnyak
authors.forename: V S
authors.initials: VS
authors.lastname: Morozova
authors.forename: L I
authors.initials: LI
authors.lastname: Stepanova
authors.forename: A A
authors.initials: AA
authors.lastname: Umanskaya
authors.forename: V M
authors.initials: VM
authors.lastname: Voitsitsky
mesh_terms: D000818:Animals; D021461:Animals, Outbred Strains; D001831:Body Temperature / Q000187:drug effects; D002245:Carbon Dioxide / Q000494:pharmacology*; D002458:Cell Fractionation; D004579:Electron Transport / Q000187:drug effects / Q000502:physiology; D042967:Electron Transport Complex I / Q000378:metabolism; D003576:Electron Transport Complex IV / Q000378:metabolism; D006339:Heart Rate / Q000187:drug effects; D007035:Hypothermia / Q000378:metabolism / Q000503:physiopathology; D000860:Hypoxia / Q000378:metabolism / Q000503:physiopathology; D008293:Malates / Q000378:metabolism; D008297:Male; D008929:Mitochondria, Heart / Q000187:drug effects* / Q000378:metabolism; D051336:Mitochondrial Membranes / Q000187:drug effects* / Q000378:metabolism; D025261:Mitochondrial Proton-Translocating ATPases / Q000378:metabolism; D032383:Myocytes, Cardiac / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D010085:Oxidative Phosphorylation / Q000187:drug effects*; D010100:Oxygen / Q000494:pharmacology*; D010101:Oxygen Consumption / Q000187:drug effects*; D051381:Rats; D013385:Succinate Dehydrogenase / Q000378:metabolism; D019802:Succinic Acid / Q000378:metabolism
chemical_list: D008293:Malates; D002245:Carbon Dioxide; C030298:malic acid; D019802:Succinic Acid; D013385:Succinate Dehydrogenase; D003576:Electron Transport Complex IV; D025261:Mitochondrial Proton-Translocating ATPases; D042967:Electron Transport Complex I; D010100:Oxygen