Prostaglandin E in peptic ulcer disease

Prostaglandin E₁ and E₂ inhibit gastric secretion in vivo and in vitro under a variety of conditions. It is not known whether these compounds may play a role in normal gastric secretory physiology or in the pathophysiology of peptic ulcer disease. Six normal adults and six patients with documented duodenal ulcer disease were studied under basal conditions and during gastric secretory stimulation with betazole. Prostaglandin E in plasma and gastric juice was measured by radioimmunoassay. Prostaglandin E was significantly higher in the plasma of normal volunteers both in the basal state and during stimulation. Gastric juice prostaglandin E was also significantly higher in normal volunteers during the basal state but the difference disappeared during stimulation. The relative deficiency of prostaglandin E in the ulcer group may indicate a role for prostaglandins in the pathophysiology of gastric hypersecretion.     

Gastric emptying of liquids in patients with peptic ulcer disease

This study was designed to determine the rates of gastric emptying of water, saline and a 20% glucose solution in patients with gastric and duodenal ulcers. In all subjects, gastric emptying was fastest after administration of the saline, slower with water and the slowest with glucose. Significant statistical differences (p less than 0.05) in emptying rates between normal subjects and the group with duodenal ulcer were seen when water and saline but not glucose were used. We conclude that inhibitory effects of the osmotic receptors are not changed in gastric and duodenal ulcer patients. However, the emptying rates were higher when osmotic stimulus was withheld.