AJP - Gastrointestinal and Liver Physiology, Vol 250, Issue 6 830-G835, Copyright © 1986 by American Physiological Society
Indomethacin and turnover of gastric mucosal cells in the rat
A. Baumgartner, H. R. Koelz and F. Halter
Mucosal morphology and the balance between cell loss and cell renewal were
analyzed during treatment with a non-ulcerative dose of indomethacin. All
rats were treated twice daily by subcutaneous injection of 2 mg/kg
indomethacin or the solvent. The following parameters were assessed: cell
proliferation on day 3 (determination of in vitro [3H]thymidine
incorporation), cell migration on days 1 and 3 (autoradiography), cell
shedding on days 7 and 14 (measurement of the remaining DNA-bound mucosal
radioactivity after in vivo labeling with [3H]thymidine prior to
treatment), mucosal morphology on day 14 (light microscopy), ex vivo
mucosal prostaglandin E2 on day 14, and serum gastrin on days 0, 7, and 14.
Indomethacin treatment had no effect on serum gastrin levels but reduced
mucosal prostaglandin E2. Indomethacin produced a significant increase of
[3H]thymidine incorporation, cell migration, and loss of mucosal DNA-bound
radioactivity in the corpus and, to a lesser degree, in the antrum.
Morphologically, this led to a hyperplasia of parietal cells (+15%, P less
than 0.05) and chief cells (+45%, P less than 0.01) in the corpus, but
antral morphology remained unchanged. We conclude that indomethacin
stimulates the turnover of gastric mucosal cells. In the corpus, but not in
the antrum, proliferation exceeds shedding, thus leading to increased
mucosal volume.
