Protective action of endogenous prostacyclin (PGI2) and prostaglandin E2 (PGE2) in endoscopic polypectomy-induced human ulcers.
To assess how endogenous prostaglandin (PG) in gastric mucosa acts against ulcer formation, we determined the mucosal prostacyclin (PGI2), PGE2, PGF2 alpha, and thromboxane A2(TXA2) concentrations before and after polypectomy in 6 patients in whom gastric ulcers were produced by electric burning resection of gastric polyps. These artificially induced ulcers all healed within short periods (25.7 +/- 7.4 days, mean +/- SE). Of the PGs assayed, the level of PGI2 was highest. The pG levels were increased at 4 and 7 days post-polypectomy; the most remarkable increase took place in the mucosa along the ulcer margin rather than the mucosa far from the ulcer site. We suggest that the observed increase in endogenous PGs represents a physiological response against polypectomy-induced ulcer formation.
D000527:Alprostadil; D015237:Dinoprost; D015232:Dinoprostone; D004564:Electrocoagulation; D011464:Epoprostenol / Q000502:physiology*; D005260:Female; D005753:Gastric Mucosa / Q000378:metabolism; D005773:Gastroscopy; D006801:Humans; D007417:Intestinal Polyps / Q000601:surgery; D008297:Male; D008875:Middle Aged; D011453:Prostaglandins / Q000502:physiology*; D011458:Prostaglandins E / Q000502:physiology*; D011460:Prostaglandins F / Q000502:physiology; D013274:Stomach Neoplasms / Q000601:surgery; D013276:Stomach Ulcer / Q000209:etiology / Q000503:physiopathology*; D013928:Thromboxane A2 / Q000502:physiology
D011453:Prostaglandins; D011458:Prostaglandins E; D011460:Prostaglandins F; D013928:Thromboxane A2; D015237:Dinoprost; D011464:Epoprostenol; D000527:Alprostadil; D015232:Dinoprostone