The results of pharmacological correction of experimental mitochondrial dysfunction in brain stem neurons after single injection of specific respiratory complex I inhibitor rotenone by complex agents mildronate and rhytmocor have been presented. It was shown that 14-days rhytmocor injection promoted the rise of mitochondrial reserve capacity under glutamate and malate oxidation as well as under succinate oxidation. The mildronate injection was accompanied by enhancement of the velocity of phosphorilated mitochondrial respiration in the presence and absence of ADP when both substrates of oxidation were used. Under the brain stem experimental mitochondrial dysfunction, mildronate improved a decreased velocity of phosphorilated mitochondrial respiration and the respiratory control in a more significant degree under glutamate malate as the substrates of oxidation. Simultaneous increase in the respiratory control and in the coefficient of efficacy ofphosphorilation during the correction of experimental mitochondrial dysfunction by rhytmocor could suggest about essential economization of processes in mitochondrial respiratory chain. It was concluded that the main mechanisms of influence on mitochondrial disturbances of both agents were connected to the powerful rise of NAD-related oxidation which allowed to enhance a resistance of mitochondrial respiratory chain and to optimize the mitochondrial function.
