Journal of the Pancreas Open Access

  • ISSN: 1590-8577
  • Journal h-index: 82
  • Journal CiteScore: 35.06
  • Journal Impact Factor: 24.75
  • Average acceptance to publication time (5-7 days)
  • Average article processing time (30-45 days) Less than 5 volumes 30 days
    8 - 9 volumes 40 days
    10 and more volumes 45 days

Abstract

Histopathological Sequential Changes in Sodium Taurocholate-Induced Acute Pancreatitis

Rajesh Gupta, Kim Vaiphei, Rakesh Kochhar, Jai Dev Wig, Thakur Deen Yadav, Ashwinikumar Kudari, Rudra Prasad Doley, Siddarth Majumdar

Context Experimental models of acute pancreatitis have been developed in order to understand its pathophysiology and extrapancreatic manifestations. Objective The objective of our study was to study sequential changes in the pancreas and distant organs in sodium taurocholate-induced acute pancreatitis in a rat model. Animals Sixteen male Wistar rats weighing 250-300 g. Design The rats were distributed into two groups: induced acute pancreatitis (study group: 8 rats) and a control group (8 rats). Within each group, the animals were divided into subgroups: those who were sacrificed early (24 h and 72 h; two each) and those who were sacrificed late (120 h and 240 h; two each). Intervention Acute pancreatitis was induced in the rats by multiple intraparenchymal injections of 10% sodium taurocholate solution. In the controls, the same amount of normal saline was injected into the pancreatic parenchyma. Main outcome measures Pathological examination of the pancreas, lungs, kidneys, intestine and liver was done. Results In this model of taurocholate-induced acute pancreatitis, the early changes observed in the pancreas were focal hemorrhages, parenchymal necrosis and neutrophil infiltration. At 72 hours, the changes observed were acinar necrosis, edema, fibrin deposition and inflammatory cell infiltration. Late changes were fibrinoid necrosis and fibroblast proliferation. In the acute phase, the histological changes in the lungs were congestion, focal pulmonary edema and intraalveolar hemorrhages while, in the late stage, there was persistence of vascular congestion. The changes observed in the kidneys were vacuolization of tubular epithelium in the subcapsular region and areas of hemorrhage in the interstitium. Intestinal changes included degenerative changes in the villous epithelium in the acute phase with normalization of the histology in the late phase. Conclusion Our findings correlate with the clinical observation of multisystem organ failure in acute pancreatitis. Early changes in these organs suggest that careful observation is mandatory in patients with acute pancreatitis in order to institute supportive treatment.