Metabolic and thermoregulatory responses to burn wound colonization.
This study was designed to determine whether there is a relationship between bacterial colonization of the burn wound and resting oxygen consumption (VO2) and colonic temperature (Tc) in burned rats. Resting VO2, Tc, and blood, spleen, and wound cultures were monitored for 2 weeks after 30% total body surface full-thickness burns. The wounds of 53 animals were seeded with 10(8) nonvirulent P. aeruginosa (NVP) at the time of injury, while the wounds of 33 rats were allowed to colonize spontaneously. The seeded wounds contained 10(6) colony forming units/gm (CFU/gm) by the fourth postburn day (PBD), while the unseeded wounds did not reach this level of colonization until after the first week postinjury. Wound seeding accelerated the metabolic and thermoregulatory responses to injury. Average VO2 and Tc of the seeded group were above the unseeded group on PBD's 3-4 and 7-8, but there were no significant differences between groups on PBD's 14-15. Although the unseeded animals were hypermetabolic during the first week, they remained afebrile. There was a significant correlation between wound bacterial counts and the increase in resting VO2 of 44 nonbacteremic animals, but variations in the data suggest that factors other than number of viable wound bacteria affect this relationship. Changes in Tc were unrelated to wound bacterial count but were correlated with changes in VO2. Taken together, the data suggest that bacteria in the burn wound contribute to the rise in energy expenditure following thermal injury.
Aulick
L H
LH
Department of Physiology, Marshall University School of Medicine, Huntington, WV 22704-2901.
Wroczyski
F A
FA
Coil
J A
JA
Mason
A D
AD
D000818:Animals; D001833:Body Temperature Regulation; D001835:Body Weight; D002056:Burns / Q000150:complications / Q000378:metabolism / Q000503:physiopathology*; D004734:Energy Metabolism; D008297:Male; D010101:Oxygen Consumption; D051381:Rats; D011919:Rats, Inbred Strains; D014946:Wound Infection / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*