Effect of the prostaglandin precursor, arachidonic acid, on histamine stimulated gastric secretion in the conscious dog, and observations on the effect of inhibiting endogenous prostaglandin synthesis.

The effects of intravenous infusions of prostaglandin E2 (PGE2) and arachidonic acid (AA) on histamine-stimulated gastric secretion have been studied in conscious dogs with either a simple gastric fistula or a denervated Heidenhain pouch. Both compounds produced a dose-related inhibition of acid secretion, though AA was 86-5 to 203-2 times less potent than PGE2. The maximal effect of AA was not achieved until 20 to 40 minutes after the infusion had ceased, suggesting that AA has to undergo some kinetic or metabolic process before it can act. Eicosatetraynoic acid (ETYN) 1-0 microgram.kg-1min-1, an inhibitor of PG biosynthesis, almost totally abolished the anti-secretory effect of AA up to 200 microgram.kg-1min-1. At 400 microgram AA.kg-1min-1, the antisecretory effect was reduced by about one half. The effect of PGE2 was not altered by ETYN. Furthermore, ETYN did not increase the response to histamine stimulation in control studies, which suggests that, in this model at least, prostaglandins are not involved in regulating gastric secretion.