Indomethacin does not alter the effect of pentagastrin on rat gastric defense mechanisms

Abstract

We studied the effect of the prostaglandin synthesis inhibitor, indomethacin, on pentagastrin-associated enhancements of gastric mucosal defense mechanisms, using a microfluorometric technique in which mucus gel thickness, intracellular pH (pHi), gastric mucosal blood flow, and acid secretion were measured simultaneously in vivo. Intravenous infusion with pentagastrin (80 micrograms/kg/h) increased mucus gel thickness, induced a hyperemic response to luminal acid, and enhanced pHi homeostasis during acid superfusion. Indomethacin, (5 mg/kg, IP) did not alter the effects of pentagastrin on acid output, mucus gel thickness, mucosal blood flow, and pHi homeostasis. Indomethacin alone did not affect any of these measures. We conclude that the enhancement of gastric defense mechanisms due to pentagastrin is independent of prostaglandin synthesis.