The respiratory control ratio (RCR), the rate of O2 consumption in state 3 and the rate of ATP formation of liver mitochondria succinate respiratory chain were increased 30 min after Sprague-Dawley rats were injected with epinephnne or norepinephrine. The rate of O2 consumption in state 4 was increased or slightly increased. When rats were injected with adrenergic blocking agents, timolol and phenoxybenzamine, 1 h before burn, the activities of succinate respiratory chain were partly inhibited 30 min post-burn. All the results suggest that catecholamines play a main role in the increase of oxidative phosphorylation coupling in the early phase of burn injury.

The alterations in electron transport were studied in the myocardial mitochondria of rats with hemorrhagjc shock. Hemorrhagic shock model was induced by a modified Wigger procedure. Mitochondria were obtained by differential centrifugation. Succinate-, and NADH-respiratory chains were assayed by polarographically and spectrophotometrically in isolated myocardial mitochondria. The results showed that hemorrhagic shock led to progressive decrease in the enzymatic activities of two respiratory chains. The activities of Succinate-Co. Q reductase, Succinate-Cyt. C reductase, NADH-Co. Q reductase, NADH-Cty. C reductase and cytochrome oxidase were remarkably lower in shock 3 h group than those in the shamoperated. This implies that there is not only low-flow hypoxia, but inability to utilizer oxygen in the myocardial mitochondria

The effect of myocardium subjected to 60 min ischemia and 60 min reperfusion on the level of lipid peroxides (LPO) and function of myocardial mitochondria and activity of superoxide dismutase (SOD) was studied in cat cardiopulmonary bypass. Myocardial mitochondrial function was slightly depressed after 60 min ischemia but significantly depressed after 60 min reperfusion. Increased lipid peroxides content and decreased SOD activity were observed at 60 min ischemia. After reperfusion, the SOD activity continued decreasing, but LPO elevated apparently. These results support a hypothesis that the free radicals may contribute to the myocardial mitochondrial reperfusion injury.