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

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OBJECTIVE: Because bacterial translocation from the gut is one of the important sources of bacterial infection in acute necrotizing pancreatitis (ANP), and growth hormone (GH) has the ability to promote intestinal epithelial proliferation, we investigated the effects of GH on bacterial translocation in a rat ANP model. METHODS: Acute necrotizing pancreatitis was induced in rats via injection of 5% sodium taurocholate into the biliopancreatic duct. The rats with ANP were treated with either human recombinant GH or a placebo. Laparotomized animals without ANP induction (sham operation) served as controls. Twenty‐four hours after the operation, blood was drawn for bacterial culture and determinations of amylase, lipase and endotoxin. Peritoneal fluid and specimens of mesenteric lymph nodes (MLN), liver, pancreas and spleen were taken for bacterial culture by standard techniques. Intestinal mucosal permeability was assessed by measuring the movement of [125I]‐labeled albumin from blood to the intestinal lumen. Insulin‐like growth factor‐1 (IGF‐1) mRNA was detected in the liver and ileum by reverse transcription–polymerase chain reaction (RT‐PCR). Morphological changes in the pancreas and ileum were also analyzed. RESULTS: Administration of GH significantly decreased the activity of serum amylase and lipase, decreased the plasma endotoxin level and reduced the incidence of bacterial translocation. Moreover, the survival rate of ANP rats was improved. The severity of inflammation in the pancreas and ileum was reduced by GH treatment. Ileal mucosal thickness, villus height and crypt depth in GH‐treated rats were obviously increased as compared with those of ANP rats. The intestinal permeability was markedly decreased in the GH group as compared with the ANP group. GH treatment resulted in upregulation of IGF‐1 mRNA expression in ileum, but not in liver. CONCLUSIONS: These results suggest that exogenous GH has beneficial effects in maintaining the integrity of the intestinal mucosal barrier and reducing the incidence of bacterial translocation in rats with ANP. One of the mechanisms might be the upregulation of IGF‐1 mRNA in the intestine by GH.
Title: Beneficial effects of growth hormone on bacterial translocation during the course of acute necrotizing pancreatitis in rats
Description:
OBJECTIVE: Because bacterial translocation from the gut is one of the important sources of bacterial infection in acute necrotizing pancreatitis (ANP), and growth hormone (GH) has the ability to promote intestinal epithelial proliferation, we investigated the effects of GH on bacterial translocation in a rat ANP model.
METHODS: Acute necrotizing pancreatitis was induced in rats via injection of 5% sodium taurocholate into the biliopancreatic duct.
The rats with ANP were treated with either human recombinant GH or a placebo.
Laparotomized animals without ANP induction (sham operation) served as controls.
Twenty‐four hours after the operation, blood was drawn for bacterial culture and determinations of amylase, lipase and endotoxin.
Peritoneal fluid and specimens of mesenteric lymph nodes (MLN), liver, pancreas and spleen were taken for bacterial culture by standard techniques.
Intestinal mucosal permeability was assessed by measuring the movement of [125I]‐labeled albumin from blood to the intestinal lumen.
Insulin‐like growth factor‐1 (IGF‐1) mRNA was detected in the liver and ileum by reverse transcription–polymerase chain reaction (RT‐PCR).
Morphological changes in the pancreas and ileum were also analyzed.
RESULTS: Administration of GH significantly decreased the activity of serum amylase and lipase, decreased the plasma endotoxin level and reduced the incidence of bacterial translocation.
Moreover, the survival rate of ANP rats was improved.
The severity of inflammation in the pancreas and ileum was reduced by GH treatment.
Ileal mucosal thickness, villus height and crypt depth in GH‐treated rats were obviously increased as compared with those of ANP rats.
The intestinal permeability was markedly decreased in the GH group as compared with the ANP group.
GH treatment resulted in upregulation of IGF‐1 mRNA expression in ileum, but not in liver.
CONCLUSIONS: These results suggest that exogenous GH has beneficial effects in maintaining the integrity of the intestinal mucosal barrier and reducing the incidence of bacterial translocation in rats with ANP.
One of the mechanisms might be the upregulation of IGF‐1 mRNA in the intestine by GH.

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