To review the mechanisms responsible for bacterial translocation after thermal injury. Areas investigated were the rate of bacterial translocation, blood flow to the gastrointestinal tract, potential of reversibility of mesenteric vasoconstriction, specific vasomediators responsible for postburn mesenteric vasoconstriction, potential reversal of gut mucosal atrophy with decreased translocation, and evidence of gut mucosal damage after thermal injury.
Using three different animal models consisting of rats, sheep, and minipigs, the objectives were defined. Using the sheep model, the relationship of decreased mesenteric blood flow after thermalinjury was defined along with rates of translocation, and the potential reversibility of the postburn mesenteric vasoconstriction and its effect on translocation. The effect of smoke inhalation and the combination of thermal injury and inhalation injury on rates of translocation are explained. Using minipigs, the role that thromboxane A2 plays on the postburn mesenteric vasoconstriction was defined by blocking thromboxane A2 synthesis with OKY046, a specific thromboxane synthetase inhibitor. Evidence of gut mucosal injury was determined using ornithine decarboxylase as an indicator of gut mucosal damage and subsequent repair in the minipig model. The rat model was used to demonstrate gut mucosal atrophy after thermal injury and the potential for reversal of atrophy with the use of bombesin, a specific gut mucosal growth stimulator.
After thermal injury, there were significant decreases in mesenteric blood flow. There was also an increase in bacterial translocation. Selective infusion of nitroprusside into the cephalic mesenteric artery prevented the postburn mesenteric vasoconstriction and attenuated bacterial translocation. Smoke inhalation and smoke inhalation with thermal injury resulted in mesenteric vasoconstriction and increased rates of bacterial translocation. OKY046 infusion prevented the postburn increase in mesenteric vascular resistance. There were increased concentrations of ornithine decarboxylase within the colonic mucosa, indicating a previous injury and the presence of ongoing repair. Likewise, there was gut mucosal atrophy after thermal injury with bacterial translocation. Treating with bombesin attenuates the postburn mucosal atrophy and prevents bacterial translocation.
Thermal injury is associated with mesenteric vasoconstriction. This postburn mesenteric vasoconstriction results in damage to gut mucosa and allows for increases in bacterial translocation. The postburn mesenteric ischemia can be ameliorated with nitroprusside infusion, thus preventing translocation. Thromboxane A2 appears to be a major mediator of the postburn decrease in mesenteric blood flow. Likewise, prevention of postburn gut mucosal atrophy with bombesin attenuates bacterial translocation. (Crit Care Med 1993; 21:S50-S54)