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

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Abstract
1 Intravenous and orally administered prostaglandin E2 (PGE2) and 16,16-dimethyl PGE2 (dm PGE2) 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. 2 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. 3 Intravenous pretreatment with dmPGE2 (20 μg kg−1) failed to prevent the gastric damage induced by the higher dose of Paf. Pretreatment with PGE2 (10–100 μg kg−1) or dmPGE2 (1–20 μg 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. 4 These studies demonstrate that the protective properties of PGE2 and dmPGE2 in the gastric mucosa do not extend to damage induced by Paf.