Experimental acute necrotising pancreatitis: Evaluation and characterisation of a model of intraparenchymal injection of sodium taurocholate in rats

Objectives: To evaluate a simple model that produces progressive dose depen dent pancreatitis, by intraparenchymal injection of sodium taurocholate. Design: Open laboratory study. Setting: Teaching hospital, Israel. Materials: Forty eight Wistar rats. Interventions: 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, s aline was injected into the pancreas in similar fashion. Blood samples were withdrawn before, and 6, 24, 48, and 72 hours after induction of pancreati tis. Results: Six hours after taurocholate injection, there was a sharp increase in the plasma activities of amylase, lipase, and lactate dehydrogenase (LD H). After 24 hours plasma activities of amylase and Lipase decreased to nea r normal values while LDH remained slightly increased for 48 hours and decr eased only after 72 hours. At 6 hours after the injection, interleukin-6 (I L-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 va lues was significantly greater than in the 5% group (p = 0.04), and correla ted well with severity of pancreatitis as defined by histology (p = 0.01) a nd mortality (p = 0.037). Twenty four hours after injection of taurocholate , morphological changes comprising diffuse necrosis of the pancreas, fat ne crosis, 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 pa ncreas (sham control), and only mild rises of IL-6, lipase, amylase, and LD H 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 gro up, and 0 in the sham control group (p < 0.05). Conclusion: The intraparenchymal injection of taurocholate is easy to perfo rm 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.