AJP - Gastrointestinal and Liver Physiology, Vol 241, Issue 6 509-G515, Copyright © 1981 by American Physiological Society
Gastric alkaline response to mucosa-damaging agents: effect of 16,16-dimethyl prostaglandin E2
J. S. Swierczek and S. J. Konturek
We investigated the effects of luminal application of graded concentrations
of conventional mucosal barrier breakers such as ethanol, aspirin (ASA),
and sodium taurocholate (TCh), as well as 16,16-dimethyl prostaglandin E2
(DMPGE2) on gastric alkaline output (GAO) and transmucosal potential
difference (PD). The Lucite chamber stomach-flap preparation was used in 50
dogs whose basal H+ secretion was inhibited by intravenous cimetidine.
Graded concentrations of ethanol, and TCh at pH 5.0, and acidified
solutions of ASA (at pH 5.0--2.0) were found to produce a dose-dependent
increase in GAO accompanied by a stepwise decline in PD. Increasing
concentrations of DMPGE2 above 1.0 microgram/ml caused a dose-related
increase in GAO and a reduction in PD. The combination of DMPGE2 with
ethanol aggravated the PD changes, whereas GAO induced by these agents was
decreased. Alterations in GAO and PD evoked by the ASA solutions varying in
pH were not significantly affected by the addition of 1.0 microgram/ml
DMPGE2 to the bathing fluid. These results indicate that stimulation of
gastric alkalinization with concomitant fall in PD is a common feature for
various mucosa-irritant substances, and pretreatment with DMPGE2 does not
prevent these effects.
