Protection of the rat gastric mucosa by prostaglandin E2: possible relation to stimulation of the alkaline secretion.
Exogenous prostaglandins have specific protective effects on the gastric mucosa called cytoprotection which is proposed to be connected to the stimulatory effects of prostaglandins on the gastric nonparietal secretions. The protection by oral prostaglandin E2 (PGE2) against indomethacin-induced gastric erosions was studied in the rat, as was the effect on the protection of blocking the gastric alkaline secretion by acetazolamide. PGE2 reduced dose-dependently the indomethacin gastric erosion formation, confirming previous results from others. Acetazolamide caused very little damage when given alone but potentiated the indomethacin erosion formation in a dose-related way. PGE2 was less protective or without effect against lesions caused by indomethacin when given together with acetazolamide, but protection could be obtained by increasing the doses of PGE2. Indomethacin and acetazolamide are both blockers of the gastric bicarbonate secretion, which is stimulated by PGE2. The potentiation of indomethacin induced lesions by acetazolamide and the antagonistic actions between acetazolamide and PGE2 on mucosal protection are compatible with the hypothesis that stimulation of the alkaline secretion is one mechanism of cytoprotection of the gastric mucosa by PGE2.
D000086:Acetazolamide / Q000494:pharmacology; D000818:Animals; D015237:Dinoprost; D004305:Dose-Response Relationship, Drug; D004347:Drug Interactions; D005750:Gastric Juice / Q000378:metabolism*; D005753:Gastric Mucosa / Q000187:drug effects*; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D011460:Prostaglandins F / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains
D011460:Prostaglandins F; D015237:Dinoprost; D000086:Acetazolamide; D007213:Indomethacin