AJP - Gastrointestinal and Liver Physiology, Vol 257, Issue 2 259-G265, Copyright © 1989 by American Physiological Society

ARTICLES

Induction of gastric and duodenal mucosal ornithine decarboxylase during stress

J. Y. Wang and L. R. Johnson
Department of Physiology and Cell Biology, University of Texas Medical School, Houston 77030.

The purpose of this study was to determine whether gastric and duodenal mucosal ornithine decarboxylase (ODC) activity increased during a period of ulcer-producing stress and whether changes in enzyme activity altered the severity of damage. Rats were fasted for 22 h, placed in a restraint cage, and immersed in water to the xiphoid process for different times lasting from 2 to 8 h. After 6 h, stress slightly increased gastric mucosal ODC and caused a sevenfold increase in duodenal mucosal ODC activity. Macroscopic ulcers developed in the oxyntic gland mucosa but not duodenal mucosa. Interestingly, however, after 6 h microscopic inspection showed an absence of most villi from the duodenum. DNA, RNA, and protein content of both tissues decreased over the time rats were exposed to stress. DL-alpha-Difluoromethylornithine (DFMO, a specific ODC inhibitor) prevented the increase in ODC in both tissues and increased the loss of DNA and RNA from duodenal mucosa. The degree of damage was not altered by DFMO in either tissue in response to 6 h of stress. These results show that 1) stress causes microscopic damage to the duodenum, 2) stress increases ODC in both gastric and duodenal mucosa, and 3) the inhibition of ODC during 6 h of stress does not alter the severity of damage.

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