Wound endotoxin is not a principal mediator of postburn hypermetabolism in rats.

Localized bacterial colonization of a 30% total body surface burn (TBSB) wound raises the resting metabolic rate of rats. To determine whether endotoxin (LPS) released in the burn wound contributes to this response, the metabolic rates and colonic temperatures of male Sprague-Dawley rats were monitored before and for 1 week after thermal injury. Wounds were seeded with non-virulent P. aeruginosa (NVP), or S. epidermidis (SE) or were left unseeded at the time of injury. Non-bacteremic SE-seeded rats were as hypermetabolic as the NVP-seeded animals on postburn days (PBDs) 3-4 and 7-8, indicating that wound LPS is not an obligatory mediator of postburn hypermetabolism. Continuous subcutaneous infusion of NVPlps (2.6 and 12.6 micrograms/100 gm/hr) beneath unseeded burn wounds did not raise metabolic rates above those of burned, unseeded controls. Neither NVP seeding nor LPS infusion resulted in measurable endotoxemia on PBDs 7-8. These results indicate that the LPS released in the colonized burn wound does not serve as either a circulating mediator or the principal inducer of other mediators of postburn hypermetabolism in rats.