Platelet-activating factor (PAF) is a potent chemical mediator of diverse physiological and pathological processes. In the present study, we examined the role of endogenous PAF in development of gastric ulcers. Water-immersion stress of rats induced proo nged decrease in endogenous PAF levels and altered the molecular heterogeneities of PAF in their corpus and antrum in early and late stages of development of gastric lesions. These alterations were suppressed by the antiulcer drugs, atropine and dopamine, concomitantly with suppression of ulcer development Vagal stimulation of rats by carbamylcholine transiently decreased endogenous gastric PAF level, which was not associated with ulcer development. Surprisingly, intraluminal administration of 1-hexadecyl-2-N-methylcarbamyl-sn-glycero-3-phosphocholine, a biologically potent and acetylhydrolase-resistant PAF analog, prevented the development of gastric lesions by water-immersion stress.
These observations indicate that endogeneous PAF is likely to function physiologically to prevent the initiation and development of gastric ulcers by water-immersion stress.
