1998 Abstract: EFFECTS OF BURN AND STARVATION ON SMALL BOWEL MUCOSAL APOPTOSIS IN RATS. M DebRoy, SE Wolf, H Ikeda, S Matin, S Rajaraman, DN Herndon and JC Thompson; Shriners Burns Institute, Galveston, Texas. 83
Abstracts 1998 Digestive Disease Week
#987
EFFECTS OF BURN AND STARVATION ON SMALL BOWEL MUCOSAL APOPTOSIS IN RATS. M DebRoy, SE Wolf, H Ikeda, S Matin, S Rajaraman, DN Herndon and JC Thompson; Shriners Burns Institute, Galveston, Texas.
The importance of apoptotic cell death in the maintenance of small bowel mucosal integrity has been demonstrated by the fact that injuries such as burn and starvation, which cause gut dysfunction, each induce epithelial cell apoptosis. We proposed to examine the simultaneous effects of burn and starvation on the rate of gut apoptosis, with the hypothesis that the two injuries would induce additive changes. Methods: Fifty male Fischer 344 rats (260-300 grams) were given a 60% full-thickness scald burn and divided into fed and starved groups. Small bowel was collected at 12, 24 and 48 hours after injury. All animals in the 12-hour group were starved while recovering from anesthesia. Sham burn rats served as controls. Apoptosis was quantified by immunohistochemical staining (TUNEL) in paraffin-embedded sections and mucosal proliferation was determined by either bromodeoxyuridine (BrdU) incorporation or proliferative cell nuclear antigen binding (PCNA). Results were analyzed by Wilcoxon's rank sum analysis and t-test. Results: The apoptotic index (TUNEL positive cells/100 villous epithelial cells) in burned rats was higher than controls at 12 hours. At 24 and 48 hours, apoptosis was highest in the starved groups, with no difference between sham and burn. Burn and starvation were not additive (see figure). Mucosal proliferation (BrdU incorporation positive cells/100 crypt cells) was not different between groups at any time point. Conclusion: Burn and starvation cause an increase in apoptosis in the small bowel mucosa, however, the effects are not additive. Starvation appears to be the greater stimulus of small bowel mucosal apoptosis. These results provide strong support for early enteral feeding after injury to maintain mucosal integrity.
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