Experimental pancreatitis in the rat. Development of pancreatic necrosis, ischemia and edema after intraductal sodium taurocholate injection.
Acute hemorrhagic pancreatitis was induced in rats by injecting sodium taurocholate into the common biliopancreatic duct. The extent of pancreatic necrosis was quantified in histological sections during the course of the disease. The proportion of necrotic acini was low, although the amount of necrosis increased from 3.3% of pancreatic parenchyma at 15 min to 10.5% at 12 h. The degree of ischemia in the inflamed pancreas was estimated by extracting intravenously injected toluidine blue from the gland. The amount of the dye in the gland decreased progressively during 12 h to 58.8% of the amount in normal pancreas. The development of pancreatic edema was studied by recording the water content of the gland. The edema was maximal at 3 h and resolved partly in 12 h after the induction of the disease. Necrosis and ischemia become progressively more pronounced in the edematous pancreas during sodium taurocholate-induced acute hemorrhagic pancreatitis. This kind of pathophysiologic course is also thought to characterize human pancreatitis. The present simple model of acute hemorrhagic pancreatitis in the rat is suitable for quantitative observations on the development of pancreatic damage under various experimental conditions.
D000818:Animals; D004487:Edema / Q000473:pathology*; D005260:Female; D007263:Infusions, Parenteral; D007511:Ischemia / Q000473:pathology*; D009336:Necrosis; D009929:Organ Size; D010179:Pancreas / Q000098:blood supply* / Q000473:pathology; D010195:Pancreatitis / Q000139:chemically induced / Q000473:pathology*; D051381:Rats; D011919:Rats, Inbred Strains; D013656:Taurocholic Acid / Q000008:administration & dosage; D013997:Time Factors
D013656:Taurocholic Acid