Methylated analogues of prostaglandin E2 and the gastric mucosal barrier.
15(R)-methyl PGE2 methyl ester (15MPG) and 16,16-dimethyl PGE2 methyl ester (16DMPG) were assessed for their effect on gastric mucosal permeability to Na+ and H+ in dogs prepared by antrectomy and vagally-denervated fundic pouches. 15MPG did not increase mucosal permeability to either ion when given topically (18.75-300 microgram) or parenterally (30 microgram), and did not affect permeability increases induced by topical 5mM sodium taurocholate in acid solution. 16DMPG caused significant increases in net Na+ gain when given topically (18.75-75 microgram) but did not affect net H+ loss from the pouch lumen. Attempts to use higher doses of 16DMPG were abandoned because of bleeding from the pouch, and perforation in one animal. It is conceivable that 16DMPG could cause adverse effects on the gastric mucosal barrier if used to suppress gastric secretion therapeutically. 15MPG does not share this potentially harmful property and remains worthy of further study as an inhibitor of gastric secretion with therapeutic promise.[1]References
- Methylated analogues of prostaglandin E2 and the gastric mucosal barrier. Kenyon, G.S., Ansell, I.F., Carter, D.C. Prostaglandins (1978) [Pubmed]
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