[Myocardium mitochondria functional state during adaptation to intermittent hypoxia and treatment with L-arginine].
Processes of respiration and oxidative phosphorylation in myocardium mitochondria after 14 days of intermittent hypoxia training method (IHT) and IHT with L-arginine (600 mg/kg) as a precursor of nitric oxide have been investigated. ADP-stimulated respiration (under 0.35 mM succinate, 1 mM alpha-ketoglutarate, inhibitor of succinate dehydrohenase--2 mM malonate and inhibitor MFC I 10 microM rothenone) have been studied. The intensivity of lipid peroxidation processes was studied under the increase of 2-thiobarbituric acid products in blood and myocardium. Our investigations deal with the valuation of dynamic support of myocardium mitochondria functional parameters (respiration control by Chance, respiration rate, efficiency of phosphorylation) on 1, 30, 60 and 180th days after the last adaptation terms. It has been shown that the preservation of the main NAD-dependent substrates of mitochondria respiratory chain oxidation is the basis for increasing functional efficiency in myocardium mitochondria after the adaptation. The changes were accompanied by the decrease of lipid peroxidation processes. These effects were intensified under L-arginine treatment during IHT.
Kurhaliuk
N M
NM
Tkachenko
H M
HM
D000222:Adaptation, Physiological / Q000187:drug effects / Q000502:physiology*; D000818:Animals; D001120:Arginine / Q000494:pharmacology*; D000860:Hypoxia / Q000378:metabolism / Q000503:physiopathology*; D015227:Lipid Peroxidation / Q000187:drug effects; D008054:Lipid Peroxides / Q000378:metabolism; D008297:Male; D008929:Mitochondria, Heart / Q000187:drug effects* / Q000378:metabolism; D009569:Nitric Oxide / Q000096:biosynthesis*; D010101:Oxygen Consumption / Q000187:drug effects; D010766:Phosphorylation; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors
D008054:Lipid Peroxides; D009569:Nitric Oxide; D001120:Arginine