Failure of prostaglandin E₂ and its 16,16‐dimethyl analogue to prevent the gastric mucosal damage induced by Paf

Intravenous and orally administered prostaglandin E2 (PGE2) and 16,16-dimethyl PGE2 (dmPGE2) protect the rat gastric mucosa from injury induced by oral administration of acidified 40% ethanol. The effects of pretreatment with these prostaglandins on platelet activating factor (Paf)-induced gastric damage has now been investigated in the rat. A 10 min infusion of Paf (50 or 100 ng kg-1 min-1, i.v.) resulted in dose-related vasocongestion of the gastric mucosa. Intravenous pretreatment with dmPGE2 (20 micrograms kg-1) failed to prevent the gastric damage induced by the higher dose of Paf. Pretreatment with PGE2 (10-100 micrograms kg-1) or dmPGE2 (1-20 micrograms kg-1), either orally or intravenously, also failed to prevent the gastric vasocongestion induced by the lower dose of Paf. On the contrary, significant augmentation of Paf-induced damage was observed with several of the doses of PGE2 and dmPGE2. These studies demonstrate that the protective properties of PGE2 and dmPGE2 in the gastric mucosa do not extend to damage induced by Paf.