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AJP - Gastrointestinal and Liver Physiology, Vol 260, Issue 4 610-G614, Copyright © 1991 by American Physiological Society
ARTICLES |
K. R. Larsen, J. G. Moore and M. T. Dayton
Department of Medicine, Salt Lake Veterans Affairs Medical Center 84148.
One model of gastric ulcerogenesis implicates a disruption of complementary circadian rhythms between protective and destructive factors. The purpose of this study was to compare circadian rhythms in gastric production of H+ and HCO3- in fasted rats. Sprague-Dawley rats were acclimatized in sound-attenuating, light-proof chambers for 3 wk on a 12:12-h light-dark schedule. Eighteen-hour fasted rats were studied at each of eight sampling times. After anesthesia, the stomachs were cannulated and filled with test solution. Thirty-minute gastric samples were titrated for H+ or assayed for HCO3-. Cosinor analysis of the data showed significant (P less than 0.05) circadian rhythms for both H+ and HCO3-. Peak times were 22:45 HALO (hours after lights on) (4:45 A.M.) for H+ and 05:41 HALO (11:41 A.M.) for HCO3-. These data demonstrate that H+ and HCO3- secretion in the fasting rat gastric lumen follow circadian rhythms with different peak times. Theoretically, this may result in circadian rhythmicity of relative mucosal vulnerability to injury.
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