title: Beneficial effect of octreotide treatment in acute pancreatitis in rats.
abstract: CONCLUSIONS
  Octreotide treatment contributes to the regulation of tumor necrosis factor (TNF) production in sodium taurocholate-induced acute necrotizing pancreatitis in rats. Owing to its complex effect, octreotide can partially ameliorate the deleterious consequences of acute necrotizing pancreatitis. Elevated TNF and interleukin-6 (IL-6) levels in the peritoneal fluid may be considered a consequence of the activation of peritoneal macrophages.
  
  
  BACKGROUND
  The effects of octreotide on exocrine pancreatic function have been investigated in numerous studies, but little attention has been paid to its influence on cytokine production in acute pancreatitis.
  
  
  METHODS
  Acute pancreatitis was induced by the retrograde injection of taurocholic acid into the pancreatic duct in male Wistar rats. Serum amylase activity, wet pancreatic weight/body weight (pw/bw) ratio, and TNF and IL-6 levels were measured. Four micrograms/kg of octreotide was administered subcutaneously at the time of induction of pancreatitis and 24 or 48 h later. Rats were sacrificed 6, 24, 48, or 72 h after the operation.
  
  
  RESULTS
  The serum amylase level and pancreatic weight to body weight ratio were decreased significantly in the octreotide-treated group. The serum TNF level was decreased significantly in the octreotide-treated group as compared with the control group at 6, 24, and 48 h (0.6 +/- 1.5, 2.0 +/- 3.3, and 0 vs 50 +/- 15.5, 37.5 +/- 18.4, and 13.1 +/- 12.5 U/mL, respectively). The ascites TNF level was decreased to 0 in the octreotide-treated group and was elevated in the control group at 72 h (28.0 +/- 49.0 U/mL). IL-6 production in ascites was extremely high in both groups at 6 h (80,000 +/- 43,817 pg/mL and 58,500 +/- 33,335 pg/mL), but the difference was not significant.
authors.affiliation: Department of Surgery, Albert Szent-Gyorgyi Medical University, Szeged, Hungary.
authors.forename: J
authors.initials: J
authors.lastname: Marton
authors.forename: Z
authors.initials: Z
authors.lastname: Szasz
authors.forename: Z
authors.initials: Z
authors.lastname: Nagy
authors.forename: K
authors.initials: K
authors.lastname: Jarmay
authors.forename: T
authors.initials: T
authors.lastname: Takacs
authors.forename: J
authors.initials: J
authors.lastname: Lonovics
authors.forename: A
authors.initials: A
authors.lastname: Balogh
authors.forename: G
authors.initials: G
authors.lastname: Farkas
mesh_terms: D000681:Amylases / Q000097:blood; D000818:Animals; D001202:Ascitic Fluid / Q000378:metabolism; D004195:Disease Models, Animal; D005765:Gastrointestinal Agents / Q000627:therapeutic use*; D015850:Interleukin-6 / Q000097:blood / Q000378:metabolism; D008262:Macrophage Activation; D008297:Male; D015282:Octreotide / Q000627:therapeutic use*; D019283:Pancreatitis, Acute Necrotizing / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology; D051381:Rats; D017208:Rats, Wistar; D013656:Taurocholic Acid / Q000008:administration & dosage / Q000633:toxicity; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D005765:Gastrointestinal Agents; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D013656:Taurocholic Acid; D000681:Amylases; D015282:Octreotide