title: Inhibition of inducible nitric oxide synthase reduces bacterial translocation in a rat model of acute pancreatitis.
abstract: BACKGROUND
  Translocation of bacteria from the gut into pancreatic necrosis is an important factor in the development of septic complications and mortality in acute pancreatitis. S-methylisothiourea (SMT) is an inducible nitric oxide synthase inhibitor that has been shown to decrease bacteria] translocation in sepsis and thermal injury.
  
  
  OBJECTIVE
  To investigate whether SMT could affect bacterial translocation in acute necrotizing pancreatitis.
  
  
  METHODS
  Forty-five Sprague-Dawley rats were studied. Acute pancreatitis was induced in Group I and Group II by injection of taurocholate and trypsin into the common biliopancreatic duct. Group III underwent laparotomy with the manipulation (but not cannulation) of the pancreas and received saline injection. Group I rats received normal saline as a placebo, and Group II rats received SMT after surgery for 2 days. At 48 hours, blood was drawn for serum amylase determinations. Bacterial translocation to mesenteric lymph nodes and distant sites (pancreas, liver, and peritoneum) were examined. A point scoring system of histologic features was used to evaluate the severity of pancreatitis.
  
  
  RESULTS
  Plasma amylase levels and pancreatic histologic score were significantly reduced in Group II rats given SMT compared with those in Group I rats given saline (p < 0.01, p < 0.05, respectively). All Group I rats had bacterial translocation to mesenteric lymph nodes compared with 7 of 12 rats in Group II (p < 0.05). There was no difference in bacterial translocation to distant organs between the two groups, although rates tended to be lower in Group II compared with Group I (p > 0.05). Bacterial counts in the pancreas were significantly reduced in Group II rats compared with those in Group I rats (p < 0.05).
  
  
  CONCLUSIONS
  Treatment with SMT appears to have ameliorated the course of acute pancreatitis; however, mortality was not affected.
authors.affiliation: Department of Internal Medicine, Gulhane School of Medicine, Ankara, Turkey. isimsek1@yahoo.com
authors.forename: I
authors.initials: I
authors.lastname: Simsek
authors.forename: M R
authors.initials: MR
authors.lastname: Mas
authors.forename: M
authors.initials: M
authors.lastname: Yasar
authors.forename: M
authors.initials: M
authors.lastname: Ozyurt
authors.forename: U
authors.initials: U
authors.lastname: Saglamkaya
authors.forename: S
authors.initials: S
authors.lastname: Deveci
authors.forename: B
authors.initials: B
authors.lastname: Comert
authors.forename: A
authors.initials: A
authors.lastname: Basustaoglu
authors.forename: F
authors.initials: F
authors.lastname: Kocabalkan
authors.forename: M
authors.initials: M
authors.lastname: Refik
mesh_terms: D000208:Acute Disease; D000681:Amylases / Q000097:blood; D000818:Animals; D018988:Bacterial Translocation / Q000187:drug effects*; D002432:Cecum / Q000382:microbiology; D004195:Disease Models, Animal; D016983:Enterococcus / Q000502:physiology; D004791:Enzyme Inhibitors / Q000494:pharmacology*; D004926:Escherichia coli / Q000502:physiology; D007550:Isothiuronium / Q000031:analogs & derivatives* / Q000494:pharmacology; D008099:Liver / Q000382:microbiology; D008198:Lymph Nodes / Q000382:microbiology; D008297:Male; D008643:Mesentery; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors*; D052247:Nitric Oxide Synthase Type II; D009924:Organ Culture Techniques; D010179:Pancreas / Q000382:microbiology; D010195:Pancreatitis / Q000382:microbiology* / Q000473:pathology; D010537:Peritoneum / Q000382:microbiology; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D004791:Enzyme Inhibitors; D007550:Isothiuronium; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; C496318:Nos2 protein, rat; D000681:Amylases; C027744:S-methylisothiopseudouronium