Stimulation by intragastrically administered E2 prostaglandins of human gastric mucus output

Abstract

Abstract. Prostaglandin E2 and 15(R)15 methyl prostaglandin E2 were instilled intragastrically to study gastric mucus output in healthy male subjects during an infusion of pentagastrin. Mucus was measured by determining total, free, and bound N‐acetyl neuraminic acid (NANA) in gastric recoveries. NANA is a sialic acid located at the end terminals on the carbohydrate chains of mucus glycoprotein. It contributes to viscosity and prevents enzymatic degradation of mucus.The methyl analogue of prostaglandin E2 increased the gastric output of NANA and inhibited gastric acid secretion in a dose‐dependent fashion. NANA produced in response to the analogue was bound to mucus glycoprotein. Prostaglandin E2 increased the output of NANA without affecting the gastric acid secretion. Both prostaglandin E2 and its methyl analogue increased volumes, pH, and NANA content of gastric aspirates withdrawn prior to start of the pentagastrin infusion, indicating a stimulation of the alkaline gastric secretion.The results show that oral E2 prostaglandins have dual effects on gastric secretion, and that their ability to stimulate mucus production is not secondary to gastric acid inhibition. Further studies are needed to examine whether their effect is mainly to increase the incorporation of NANA into mucus glycoproteins, or to stimulate the release and/or production of gastric mucus, and also to quantitate the gastric nonparietal secretion.The stimulatory properties of E2 prostaglandins on gastric mucus and alkaline secretion may be one mechanism by which they protect the gastric mucosa against experimentally induced damage.