After long-term adaptation to intermittent hypoxia, rats with an initially low resistance to acute oxygen deficiency were 2 to 4 times more resistant to it, while highly resistant rats did not show a significant change in resistance. The adaptation was accompanied by weakening of the electron-transporting function of the respiratory chain and increasing efficiency of oxidative phosphorylation in the brain mitochondria oxidizing NAD-dependent substrates, indicating that energy was produced in a more economical way. The succinate oxidase pathway of oxidation was found to be utilized to only a limited extent as a compensatory mechanism in animals exposed to intermittent hypoxia over a prolonged period. The effects of adaptation were more marked in the brain mitochondria of rats initially highly sensitive to oxygen deficiency.
It is demonstrated that energostim, an aqueous mixture of NAD § cytochrome c, and inosine possesses pronounced antihypoxic activity. Energostim increases by 26-fold the survival rate of rats with low resistance to hypoxia under conditions of hypobaric hypoxia. Administration of energostim before the "rise" in a pressure chamber prevents a decrease in the brain content of ATP in rats with high resistance to hypoxia under the conditions of maximum hypoxia and increases it in rats with low resistance to hypoxia. Energostim has no effect on the survival rate of high-resistant rats in acute hypobaric hypoxia and on the brain content of macroergic substances in low-and high-resistant rats when agony is not developed on "the critical height" and there is no deficiency of macroergic substances.
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