Inflammatory/cardiovascular-metabolic responses in a rat model of burn injury with superimposed infection.

Infection remains the major cause of morbidity and mortality in burn patients. Furthermore, the use of antibiotics in such patients has led to the prevalence of antibiotic-resistant microbial infections; one such infection in intensive care unit turns out to be caused by the enterococcal organisms. Our laboratory studies have used a rat model of burn injury and Enterococcus faecalis infection. Sprague-Dawley male rats (similar to 250 g) were initially given an intragastric gavage of the antibiotic ciprofloxacin for 3 days. This procedure allowed for decontamination of intestine of gram-negative and some gram-positive organisms. The remainders of the gram-positive organisms were, to a large extent, Enterococci. After the decontamination procedure, rats were infra-abdominally inoculated with E. faecalis; inoculation involved preparation of sterilized rat fecal pellets impregnated with E. faecalis (10(4) colony-forming units) and their implants through a midline abdominal wall incision. Some of the rats that were implanted with the fecal pellets were subject to full-thickness skin burns (similar to 30% total body surface area; 95 degrees C water for 7 s). Sham abdominal infection rats received a sterile pellet only; sham burn procedure consisted of exposing the skin to room temperature water. All sham and burn and/or E. faecalis infection procedures were carried out on rats under pentobarbital anesthesia. Inflammation and innate host defense-related responses were assessed via measurements of neutrophil effector responses, i.e., oxygen anion free radical (O(2)(-))/elastase production, CD11b/CD18 expression, apoptosis, and tissue infiltration. Determining epithelial lactulose permeability, microvascular albumin leakage, and epithelial tight junction integrity assessed the status of intestinal function/structural derangements. The animals' metabolic and cardiovascular integrity was evaluated determining blood pH, pO(2), pCO(2), heart rate, respiratory rate, blood pressure, and cardiac output. Whereas the aforementioned measurements were carried out at 24 to 48 h postburn injury with and without the Enterococcal infection, animal mortality was determined for up to 5 days after the experimental injuries. The results of the studies indicated that whereas burn or E. faecalis infection alone did not produce significant mortality, the dual insult with burn and E. faecalis infection resulted in significant animal death accompanied by relatively more profound metabolic and cardiovascular derangements. Inappropriately heightened neutrophil effector responses were present with burn alone as well as with the dual burn and infection complications. These studies suggest that animal models of burn injury with Enterococcal infection complications simulate the adverse outcomes burn patients infected with Enterococcal organisms.