Alterations in intestinal function in acute pancreatitis in an experimental model
Version of Record online: 8 DEC 2005
Copyright © 1996 British Journal of Surgery Society Ltd.
British Journal of Surgery
Volume 83, Issue 11, pages 1537–1543, November 1996
How to Cite
Wang, X. D., Wang, Q., Andersson, R. and Ihse, I. (1996), Alterations in intestinal function in acute pancreatitis in an experimental model. Br J Surg, 83: 1537–1543. doi: 10.1002/bjs.1800831113
- Issue online: 8 DEC 2005
- Version of Record online: 8 DEC 2005
- Manuscript Accepted: 3 FEB 1996
- Swedish Medical Research Council. Grant Numbers: 17X-03012, B95–17X-11236
- Medical Faculty, Lund University, Sweden
Gastrointestinal tract failure may be involved in the development of systemic septic complications in acute pancreatitis. Systemic and intestinal circulation, intestinal permeability and absorptive function were evaluated in the early course of acute pancreatitis induced in rats by retrograde intraductal injection of 0·2 ml of 5 per cent sodium taurodeoxycholate and 0·4 nmol trypsin. A decrease in systemic arterial pressure and intestinal blood flow and an increase in intestinal permeability as measured by the leakage of 125I-labelled human serum albumin from blood to lumen were noted in the distal ileum and colon, reaching statistically significant differences 6 h after induction of pancreatitis. The transport of small molecular markers (sodium fluorescein and 51Cr-labelled ethylenediamine tetra-acetic acid) through the distal ileum and colon in vitro from the mucosal to the serosal site in Ussing chambers significantly increased in the early period (20–60 min) of incubation, while the passage of a macromolecular marker (ovalbumin) demonstrated a definite increase at 60–120 min of incubation. D-Xylose absorption from the gut lumen to the portal vein was significantly less in acute pancreatitis than after sham operation. Intravenous administration of the hydroxyl radical scavenger dimethylsulphoxide prevented the compromised intestinal permeability and gut absorptive capacity induced by acute pancreatitis, but did not affect the reduced arterial pressure and intestinal microcirculation. Cytotoxic oxygen-derived free radicals may contribute to the development of alterations in intestinal permeability and absorptive function found in the early stage of acute pancreatitis in the rat.