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Updated: Aug 7, 2026
Murine Model of Intestinal Ischemia-reperfusion Injury
Published on: May 11, 2016
Apoptosis after intestinal ischemia-reperfusion injury: a morphological study
K A Shah1, S Shurey, C J Green
1Department of Surgical Research, Northwick Park Institute for Medical Research, Northwick Park Hospital, Harrow, Middlesex, England. k.shah@ic.ac.uk
Background:
Apoptosis has been identified after ischemia-reperfusion (IR) injury to the brain, heart, kidney, retina, and the adrenals. Intestinal IR injury causes villous and crypt damage, which has so far been attributed to cellular necrosis. This study was undertaken to investigate the possible role of apoptosis after reperfusion of cold-stored small bowel grafts in syngeneic rats.
Methods:
Small intestinal grafts were stored at 4 degrees C for 24 hr in saline (n=6) or in modified University of Wisconsin solution (n=6), followed by reperfusion for 1 hr in syngeneic Lewis rats. Small bowel samples were obtained before storage, after preservation and after 1 hr of reperfusion. They were processed for light and electron microscopy and analyzed for cell death, with particular emphasis on apoptosis.
Results:
Less than one apoptotic event was seen per 10 crypts in normal and stored bowels. An occasional normal and some denuded villous epithelial cells of stored bowels exhibited apoptosis. After isotransplantation and 1 hr of reperfusion, marked increase in apoptosis was seen in the crypts and denuded villous epithelial cells of both saline- and modified University of Wisconsin-stored bowels. Secondary necrosis was seen in apoptotic cells, as were dark cells. Only a few cells showed signs of primary ischemic necrosis.
Conclusions:
Apoptosis occurs after intestinal IR injury. Modulation of its genetic regulatory and biochemical effector machinery might alleviate or even prevent IR injury in small bowel transplanted after similar periods of storage.
