Increased Mitochondrial Oxygen Consumption in the Hypermetabolic Injured Rat

THE RISE IN total body oxygen consumption after severe thermal injury r-04 is accompanied by an increase in visceral oxygen utilization and substrate turnover, in part to meet the metabolic demands of the wound (1). The 4 increased heat production after injury is the consequence not of altered thermoregulatory drives, but of an elevated metabolic state (2). The extent of this increased heat production suggests that accelerated intracellular oxidative processes may be primarily functioning to produce heat rather than energy to be used for synthetic and transport reactions. To assess the cellular basis for this increased oxygen utilization, we examined the function of mitochondria isolated from the liver, the metabolically most active organ.