Alterations of pancreatic acinar cells and biochemical changes in serum due to experimentally induced acute pancreatitis in dogs

Abstract

Experimentally induced acute pancreatitis was initiated in 16 male German shepherd dogs by application of sodium taurocholate into the pancreatic duct system. Potential effects of oxygen free radicals were evaluated by premedication with an antioxidant: superoxide dismutase (SOD). Therefore in 8 animals sodium taurocholate solution was applied simultaneously with intra-arterial inoculation of superoxide dismutase, while another 8 dogs were treated only with sodium taurocholate. The effects of sodium taurocholate solution and SOD were evaluated biochemically bi the amylase activity, the concentrations of ceruloplasmin (Cp) and PAGE (polyacrylamide gel electrophoresis) of serum proteins, together with the pathohistological observations. The results confirmed that bile salt injected into the pancreatic duct caused widespread progressive necrotic hemorrahagic lesions in the acinar, ductal and vascular cells. The biochemical injury response in all examined dogs was hyperamylasemia, increased amount of macroglobulin and decreased albumin and globulin fractions. There was a statistically significant increase in amylase activity and statistically significant differences in Cp concentrations between the examined groups. Pathohistological alterations were similar in both experimental groups, except in their rate, which was rather sluggish in the group treated with SOD. We therefore assumed that the oxygen free radicals as well as the detergent effect of the applied bile salt mediated the initial lesions in the induction of acute pancreatitis.