The effects of thermal injury on mitochondrial oxygen consumption and the glycerol phosphate shuttle

Since many of the physiologic adaptations to postburn hypermetabolism must be related to alterations in mitochondrial function, the effects of thermal injury on rat liver mitochondrial oxygen consumption were studied. A 60% full-thickness thermal injury was found to cause a significant increase in mitochondrial oxygen consumption, peaking at postburn day 12, without the loss of respiratory control. The same thermal injury was also found to cause a significant increase in glycerol-3-phosphate dehydrogenase (GPD) activity, which also peaks at postburn day 12. The increase in GPD activity and the resultant increase in the flow through the glycerol phosphate shuttle might be related to the increase of postburn mitochondrial oxygen consumption. It is also shown that although the loss of respiratory control could also be a contributing factor to postburn hypermetabolism at postburn days 15 and 18, this was not observed during the early days after thermal injury.