Gastric secretory and motor inhibition induced by certain methyl analogues of prostaglandin E2 in healthy male volunteers and in patients with duodenal ulcer disease.
The present investigation shows that the 15(S)-15-methyl and 16,16-dimethyl analogues of PGE2 given orally are potent inhibitors of gastric acid secretion. The inhibition of acid output is mainly due to a reduction in volume output. The effect on acid secretion was shown to be less pronounced in a group of duodenal ulcer patients than among healthy volunteers. Only the 15-methyl analogue gave any significant secretory inhibition following intestinal administration. The results from the experiments in dogs indicate that a local action on the oxyntic glands could be the main reason for secretory inhibition following oral administration. The results from the studies on motor activity show that the prostaglandins inhibit both antral and duodenal pressure activity. However, with our experimental design, only with doses exceeding those required for secretory inhibition.
D000818:Animals; D004285:Dogs; D004305:Dose-Response Relationship, Drug; D004381:Duodenal Ulcer / Q000188:drug therapy; D005753:Gastric Mucosa / Q000187:drug effects* / Q000378:metabolism; D005769:Gastrointestinal Motility / Q000187:drug effects*; D006801:Humans; D008297:Male; D011458:Prostaglandins E / Q000494:pharmacology / Q000627:therapeutic use; D013329:Structure-Activity Relationship
D011458:Prostaglandins E