Abstracts
1999 Digestive Disease Week

# 2170 INCREASED GUT EPITHELIAL APOPTOSIS AND MUCOSAL ATROPHY AFTER BURN
S E Wolf, Shriners Burns Hosp-Galveston, Galveston, TX; M A DebRoy, M G Jeschke, S Rajaraman, J C Thompson, The Univ of Texas Med Branch & Shriners Hosp, Galveston, TX

We previously showed increased gut epithelial cell apoptosis at 12, 24, and 48 hours after burn in mice. These mice had different food intakes, with a 25% decrease found in the first 24 hours in the burned animals compared to controls. We wondered whether food intake was related to the stimulation of apoptosis and proliferation of the gut epithelial cells after burn. Methods: Twenty Fischer 344 rats underwent either a 60% full-thickness scald burn or sham burn, and the small bowel was collected at 6 and 12 hours (n=5 in each group) after injury. Gut epithelial cell apoptosis was quantified by TUNEL assay in paraffin-embedded sections of the proximal small bowel, and mucosal proliferation was determined by proliferative cell nuclear antigen immunostaining (PCNA). Mucosal weight and protein content were determined from scraped mucosa samples. Data are presented as means ± SEM; statistical analysis was done by t-test. Results: The % of apoptotic cells was not different between groups at 6 hours, however, apoptosis increased significantly at 12 hours following burn (p<0.02). There was no evidence of necrosis on histologic examination. Small bowel mucosal weight in the burned animals decreased significantly at 6 and 12 hours after burn compared to controls (25% and 35% respectively; p<0.05). Protein content of the proximal small bowel mucosa in burned animals also decreased significantly by 21% and 32% (p<0.05) respectively at 6 and 12 hours after burn. There were no differences in mucosal proliferation or villous height at any time point. Conclusion: Small bowel mucosal apoptosis increased after burn independent of dietary intake, which was associated with mucosal atrophy. Small bowel epithelial proliferation did not change. It is likely that a signal released in response to the burn wound causes an increase in gut epithelial apoptosis and gut mucosal atrophy.

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