[Mitochondrial oxidation in the liver during visceral-ischemic shock].

Distinct decrease in respiratory and phosphorylating functions of liver mitochondria was found under conditions of visceral-ischemic shock induced in rabbits after 2 hrs occlusion of superior mesenteric artery and the subsequent step-by-step revascularization. Endogenous intoxication was mainly responsible for inhibition of electron transport through respiratory chain. Impairment of mitochondrial oxidation is one of important factors related to development of the shock "irreversible" phase.

[The mechanism of action of a synthetic derivative of 1,4-naphthoquinone on the respiratory chain of liver and heart mitochondria].

It was found that the 1.4-naphthoquinone derivative AK-135 (2-methyl-3-piperidine-methyl-1.4-naphthoquinone hydrochloride) possesses a marked acceptor capacity during succinate and glutamate oxidation by rat liver and rabbit heart mitochondria.

[Characteristics of biochemical processes of the liver in rats with various types of open-field behavior].

Respiration and phosphorylation of liver mitochondria, lipid spectrum of the blood serum activity of hepatocytes main microsomal enzymes were studied in outbred rats with various emotionality. It was found that in low-emotional rats, the intensity of phosphorylation processes in liver mitochondria and enzymes activity of hematocytes microsomal oxidative system responsible for detoxication processes,-- was significantly higher than in low-emotional animals. Analogous differences were found in the lipid blood spectrum and in liver mitochondria antioxidant activity of animals with different emotionality.

[Mitochondrial oxidation in the rat liver during acute blood loss].

Acute hemorrhage was accompanied by impairments in electron transport and energy functions of rabbit liver mitochondria as well as by a decrease in activity of multienzyme systems responsible for electron transfer via redox chain. The impairments observed correlated distinctly with the rate of hypoxia and of metabolic acidosis. In the hemorrhage NADH oxidation occurred mainly via rotenon-insensitive NADH oxidase while the cytochrome oxidase activity was maintained at a relatively high level.