title: Beneficial effects of growth hormone on bacterial translocation during the course of acute necrotizing pancreatitis in rats.
abstract: 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 the intestinal epithelial proliferation, we investigated the effects of GH on bacterial translocation in a rat 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 standard techniques. Intestinal mucosal permeability was assessed by measuring the movement of 125I-labeled albumin from blood to intestinal lumen. Insulin-like growth factor-1 (IGF-1) mRNA was detected in the liver and ileum by reverse transcriptase-polymerase chain reaction (RT-PCR). Morphologic changes of pancreas and ileum were also analyzed. Administration of GH significantly 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 was alleviated by GH treatment. Ileal mucosal thickness, villus height, and crypt depth in GH treatment rats were obviously increased compared with those 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-1 mRNA expression in ileum, but not in liver. These results suggested that exogenous GH had beneficial effects in maintaining the integrity of intestinal mucosal barrier and reducing the incidence of bacterial translocation in rats with ANP. One of the mechanisms might be the up-regulation of IGF-1 mRNA in intestine by GH treatment.
authors.affiliation: Department of Gastroenterology, Shanghai First People's Hospital, People's Republic of China. xpwcn@public7.Sta.Net.Cn
authors.forename: X
authors.initials: X
authors.lastname: Wang
authors.forename: B
authors.initials: B
authors.lastname: Wang
authors.forename: J
authors.initials: J
authors.lastname: Wu
authors.forename: G
authors.initials: G
authors.lastname: Wang
mesh_terms: D000681:Amylases / Q000097:blood; D000818:Animals; D001424:Bacterial Infections / Q000188:drug therapy* / Q000382:microbiology; D004195:Disease Models, Animal; D004731:Endotoxins / Q000097:blood; D019382:Human Growth Hormone / Q000627:therapeutic use*; D006801:Humans; D007334:Insulin-Like Growth Factor I / Q000235:genetics; D007413:Intestinal Mucosa / Q000187:drug effects / Q000382:microbiology; D008049:Lipase / Q000097:blood; D008297:Male; D008854:Microscopy, Electron; D019283:Pancreatitis, Acute Necrotizing / Q000188:drug therapy* / Q000382:microbiology* / Q000473:pathology; D010539:Permeability / Q000187:drug effects; D012333:RNA, Messenger / Q000235:genetics; D051381:Rats; D017207:Rats, Sprague-Dawley; D013656:Taurocholic Acid / Q000633:toxicity
chemical_list: D004731:Endotoxins; D012333:RNA, Messenger; D019382:Human Growth Hormone; D013656:Taurocholic Acid; D007334:Insulin-Like Growth Factor I; D008049:Lipase; D000681:Amylases