[Oxidative metabolism and myocardial function in rats with different sensitivities to oxygen deficiency in hypoxia]

In exposure to mild hypoxia, the electron-transport function of the myocardial respiratory chain in the NAD-cytochrome b area is limited in a different manner in animals highly resistant (HR) and those poorly resistant (PR) to hypoxia. In PR animals this process develops very rapidly, leads to diminution of the oxidative capacity of the respiratory chain and of ATP production, and, as a consequence, to suppression of the energy-dependent contractile function of the myocardium. In HR animals this process is less manifest and develops very slowly, which confirms the lesser role of NAD-dependent oxidation of substrates in the metabolism of the myocardium of these animals. The ability of the HR animals to maintain in mild hypoxia a higher ATP level than that in PR animals suggests that ATP synthesis in them occurs through oxidation of endogenous substrates which enter the respiratory chain by bypassing the NAD-dependent area. Compounds of the group of quinones, which facilitate removal of the block of the electron-transport function of the respiratory chain on the level of the first enzyme complex, normalize processes of ATP production and myocardial contractility and may be used as antihypoxic agents.