title: Experimental acute necrotising pancreatitis: evaluation and characterisation of a model of intraparenchymal injection of sodium taurocholate in rats.
abstract: OBJECTIVE
  To evaluate a simple model that produces progressive dose dependent pancreatitis, by intraparenchymal injection of sodium taurocholate.
  
  
  METHODS
  Open laboratory study.
  
  
  METHODS
  Teaching hospital, Israel.
  
  
  METHODS
  Forty eight Wistar rats.
  
  
  METHODS
  Sodium taurocholate was injected, 0.3 ml/100 g body weight, in concentrations of 5% and 10% into the pancreatic parenchyma of 32 Wistar rats, resulting in two distinct groups of severity. In 16 sham controls, saline was injected into the pancreas in similar fashion. Blood samples were withdrawn before, and 6, 24, 48, and 72 hours after induction of pancreatitis.
  
  
  RESULTS
  Six hours after taurocholate injection, there was a sharp increase in the plasma activities of amylase, lipase, and lactate dehydrogenase (LDH). After 24 hours plasma activities of amylase and lipase decreased to near normal values while LDH remained slightly increased for 48 hours and decreased only after 72 hours. At 6 hours after the injection, interleukin-6 (IL-6) concentrations had increased slightly in the 5% group and decreased to the baseline values at 24 hours. In the 10% group, the increase in IL-6 values was significantly greater than in the 5% group (p = 0.04), and correlated well with severity of pancreatitis as defined by histology (p = 0.01) and mortality (p = 0.037). Twenty four hours after injection of taurocholate, morphological changes comprising diffuse necrosis of the pancreas, fat necrosis, and intestinal dilatation secondary to paralytic ileus were severe. Histopathological examination of the pancreas showed good correlation with the clinical findings and with mortality. No morphological changes were detected when saline was injected into the pancreas (sham control), and only mild rises of IL-6, lipase, amylase, and LDH activities were seen at 6 hours after injection. The mortality, after 10 days, was 80% in the 10% taurocholate group, 30% in the 5% taurocholate group, and 0 in the sham control group (p < 0.05).
  
  
  CONCLUSIONS
  The intraparenchymal injection of taurocholate is easy to perform and highly reproducible. The histopathological injury is dose-dependent, as is the mortality. We conclude that this model is valuable for the study of new treatments for pancreatitis.
authors.affiliation: Department of Surgery A, Meir Hospital, affiliated with the Sackler School of Medicine, Tel-Aviv University, Kfar-Sava, Israel.
authors.forename: H
authors.initials: H
authors.lastname: Paran
authors.forename: A
authors.initials: A
authors.lastname: Mayo
authors.forename: D
authors.initials: D
authors.lastname: Kidron
authors.forename: G
authors.initials: G
authors.lastname: Sivak
authors.forename: T
authors.initials: T
authors.lastname: Reshef
authors.forename: T
authors.initials: T
authors.lastname: Vider
authors.forename: O
authors.initials: O
authors.lastname: Ziv
authors.forename: U
authors.initials: U
authors.lastname: Freund
mesh_terms: D000818:Animals; D002756:Cholagogues and Choleretics / Q000008:administration & dosage*; D004796:Clinical Enzyme Tests; D004195:Disease Models, Animal; D007267:Injections; D015850:Interleukin-6 / Q000097:blood; D010179:Pancreas / Q000473:pathology; D019283:Pancreatitis, Acute Necrotizing / Q000097:blood / Q000175:diagnosis / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D013656:Taurocholic Acid / Q000008:administration & dosage*; D013997:Time Factors
chemical_list: D002756:Cholagogues and Choleretics; D015850:Interleukin-6; D013656:Taurocholic Acid