Stimulation by intragastrically administered E₂ prostaglandins of human gastric mucus output

Abstract

Abstract. Prostaglandin E 2 and 15(R)15 methyl prostaglandin E 2 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 E 2 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 E 2 increased the output of NANA without affecting the gastric acid secretion. Both prostaglandin E 2 and its methyl analogue increased volumes, pH, and NANA content of gastric aspirates withdrawn prior to start of the pentagastrin infusion, indicating a stimulation of the alkaline gastric secretion.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 E 2 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 E 2 prostaglandins on gastric mucus and alkaline secretion may be one mechanism by which they protect the gastric mucosa against experimentally induced damage.