The Inhibitory Effect of 15(R) 15 Methyl Prostaglandin E2and the Interaction with Atropine on Stimulated Gastric Acid Secretion in Man

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Abstract
The inhibitory effect of 15(R)15 methyl prostaglandin E2 (Me PGE2) on the gastric acid response to pentagastrin stimulation, 0.6 .mu.g .cntdot. kg-1 .cntdot. h-1, was examined in healthy male volunteers. Each subject underwent a control test and tests with intragastrically administered graded doses of 15(R)15 Me PGE2 as free acid (80, 140, 200 and 400 .mu.g, n = 5) and as methylester (80, 140 and 200 .mu.g, n = 6). The percentage inhibition of the acid output during 2 h after increasing doses of the free acid was 24 .+-. 11, 49 .+-. 7, 44 .+-. 9, and 76 .+-. 12%. Corresponding figures for the methylester were 35 .+-. 2, 54 .+-. 5, and 64 .+-. 8%. Both volume and acidity were reduced. Side effects did not occur, except for moderate diarrhea in 1 subject after 400 .mu.g of the free acid. In a 3rd series (n = 6) the combined effect of 80 .mu.g methyl ester (44 .+-. 5% inhibition) and 1.5 mg atropine sulfate was studied. Atropine alone gave a 43 .+-. 6% inhibition by lowering the secreted volumes. For the combination the inhibition was 82 .+-. 3%. Intragastric 15(R)15 Me PGE2 inhibited dose-dependently the pentagastrin-stimulated gastric acid response. Differences between the free acid and methyl ester of the analog were not significant. Compared with other methyl PGE2 compounds, 15(R)15 Me PGE2 was less effective per dose but the dose range was broader and side effects were slight. Concomitantly given atropine had a significant additive inhibitory effect.