ABSTRACT
Acute haemorrhagic pancreatitis was induced in rats by injecting 5% sodium taurocholate into the common biliopancreatic duct. The condition was associated with an increase in the serum amylase levels as well as progressive pancreatic necrosis resulting in 100% mortality before 36 hours. This experimental model was documented by quantifying nine different parameters of pancreatic necrosis and giving more information about the induced lesion. The extent of pancreatic necrosis was evaluated at different intervals, 5.77% at 12 hours, 14.9% at 24 hours, and the rats died before 36 hours of pancreatitis induction with an average percentual necrosis of 29.9%. This model seems suitable for more pathogenic as well as therapeutic studies on acute pancreatitis in the rat.
Subject(s)
Disease Models, Animal , Pancreatitis/chemically induced , Taurocholic Acid/administration & dosage , Acute Disease , Animals , Injections/methods , Male , Necrosis , Pancreas/pathology , Pancreatic Ducts , Pancreatitis/pathology , Rats , Rats, Inbred Strains , Time FactorsABSTRACT
The effects of somatostatin (SS) on the treatment of acute pancreatitis were studied in rats. Acute pancreatitis was established by injecting 5% sodium taurocholate in the biliopancreatic duct. Previously, pancreatic necrosis was determined in this experimental model at several intervals without treatment. Treatment was started according different groups: at 12, 16 and 20 hours after induction of acute pancreatitis (IV bolus of 4 ug/kg body weight followed by a 24h continuous infusion of 4 ug/kg body wt/hour). When somatostatin was initiated at 12 or 16h a decrease in serum amylase and lactodehydrogenase was observed, as well as in pancreatic necrosis resulting in 0% mortality after 24h of treatment. When somatostatin was started at 20h there was no changes in the lethal outcome of the disease.
