Ghrelin abates bacterial translocation following burn injury by improving gastric emptying

AbstractBackgroundIn severe burns, increased intestinal permeability facilitates bacterial translocation, resulting in systemic endotoxemia and multi‐organ failure. We investigated the role of burn‐induced gastrointestinal dysmotility (BIGD) in promoting bacterial translocation following burn injury, and the protective effect of ghrelin in this process.MethodsWe assessed gastric emptying (GE%) and intestinal transit (IT by geometric center “GC”) in a 60% total body surface area scald burn rat model and measured bacterial counts in mesenteric lymph nodes (MLN) and distal small intestine by colony‐forming unit per gram of tissue (CFU/g). A group of animals was treated with ghrelin or saline after burn.Key ResultsScald burn was associated with a significant delay in GE (62% ± 4% vs 74% ± 4%; P = .02) and a trend of delay in intestinal transit (GC: 5.5 ± 0.1 vs 5.8 ± 0.2; P = .09). Concurrently, there was a marginal increase in small intestinal bacterial overgrowth (6 × 105 vs 2 × 105 CFU/g; P = .05) and significant translocation to MLN (2 × 102 vs 4 × 101; P = .03). We observed a negative correlation between GE and intestinal bacterial overgrowth (rs = −0.61; P = .002) and between IT and translocation (rs = −0.63; P = .004). Ghrelin administration significantly accelerated GE following burn injury (91% ± 3% vs 62% ± 4; P = .03), reduced small intestinal bacterial overgrowth, and completely inhibited translocation to MLN (0.0 vs 5 × 102; P = .01).Conclusions & InferencesBurn‐induced gastrointestinal dysmotility is correlated with the systemic translocation of gram‐negative gut bacteria that are implicated in multiple organ failure in burn patients. Therapeutic interventions to restore BIGD are warranted (Neurogastroenterol Motil, 2012, 24, 78).