Beneficial effects of growth hormone on bacterial translocation during thecourse of acute necrotizing pancreatitis in rats

Because bacterial translocation from the gut is one of the important source s of bacterial infection in acute necrotizing pancreatitis (ANP) and growth hormone (GH) has the ability to promote the intestinal epithelial prolifer ation, we investigated the effects of GH on bacterial translocation in a ra t ANP model. ANP was induced in rats by injection of 5% sodium taurocholate into the biliopancreatic duct. The rats with ANP were treated with either human recombinant GH or placebo. Laparotomized animals without induction of ANP (sham operation [SO]) served as controls. At 24 hours after operation, blood was drawn for bacterial culture and determination of amylase, lipase , and endotoxin. Peritoneal fluid and specimens of mesenteric lymph nodes ( MLN), liver, pancreas, and spleen were taken for bacterial culture by stand ard techniques. Intestinal mucosal permeability was assessed by measuring t he movement of I-125-labeled albumin from blood to intestinal lumen, insuli n-like growth factor-1 (IGF-1) mRNA was detected in the liver and ileum by reverse transcriptase-polymerase chain reaction IRT-PCR). Morphologic chang es of pancreas and ileum were also analyzed. Administration of CH significa ntly decreased the serum amylase, lipase activities, plasma endotoxin level , and incidence of bacterial translocation. Moreover, the survival rate of ANP rats was improved. The severity of inflammation in pancreas and ileum w as alleviated by GH treatment. Ileal mucosal thickness, villus height, and crypt depth in GH treatment rats were obviously increased compared with tho se of ANP rats. The intestinal permeability was markedly improved in the GH group versus the ANP group. GH treatment resulted in up-regulation of IGF- I mRNA expression in ileum, but not in liver. These results suggested that exogenous GH had beneficial effects in maintaining the integrity of intesti nal mucosal barrier and reducing the incidence of bacterial translocation i n rats with ANP. One of the mechanisms might be the up-regulation of IGF-I mRNA in intestine by GH treatment.