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Updated: Aug 3, 2026

Sodium Taurocholate Induced Severe Acute Pancreatitis in C57BL/6 Mice
Published on: June 28, 2021
Splanchnic and pancreatic tissue perfusion in experimental acute pancreatitis
P J Kinnala1, K T Kuttila, J M Grönroos
1Dept of Surgery, University of Turku, Finland.
Background:
Gut hypoperfusion has a major role in the pathogenesis of multiple organ failure, which is the main cause of death in severe acute pancreatitis. The effects of experimental acute pancreatitis on splanchnic and pancreatic perfusion and oxygenation were studied to find out whether gut hypoperfusion occurs already at the same time as changes in pancreatic perfusion.
Methods:
Twenty-four domestic pigs weighing 21-27 kg were randomized to severe or mild acute pancreatitis or control groups. Eight anaesthetized and mechanically ventilated pigs were intraductally infused with taurocholic acid to induce severe acute pancreatitis and eight received intraductal saline to induce mild acute pancreatitis. Eight pigs served as controls.
Results:
Intraductally infused taurocholic acid rapidly induced severe necrotizing acute pancreatitis as assessed macroscopically and histologically. Histological changes of mild acute pancreatitis were seen in animals after intraductal saline infusion. After the induction, pancreatic tissue oxygen tension decreased promptly in severe acute pancreatitis and increased in mild acute pancreatitis. Laser-Doppler red cell flux decreased in severe acute pancreatitis. Gut pH gap and pCO2 gap decreased in 2 h after the induction of severe acute pancreatitis. Central haemodynamics were fairly stable throughout the study period in all groups.
Conclusion:
In experimental severe acute pancreatitis, splanchnic malperfusion seems to begin with pancreatic hypoperfusion before disturbances in gut microcirculation.
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