We studied the oral gastric antisecretory activity of prostaglandin E2 in three groups of six normal volunteers. Each volunteer was studied twice, once after receiving prostaglandin E2 (0.5, 1.0, or 2.0 mg) and the other time after receiving placebo administered in a double-blind, randomized fashion. Gastric acid secretion was stimulated with a liquid protein meal from 1/2 to 1 1/2 hr after drug administration. Acid secretion was quantitated using the technique of intragastric titration. Acid secretion after 0.5 mg of prostaglandin E2 was no different than after placebo administration, but 1.0 mg and 2.0 mg of prostaglandin E2 inhibited 58% (6.68 +/- 7.64 meq vs 14.67 +/- 6.75 meq, P less than 0.02) and 76% (2.38 +/- 2.38 meq vs 11.50 +/- 3.51, P less than 0.01) respectively, of gastric acid production compared to placebo therapy. After oral administration, prostaglandin E2 in man is antisecretory with an ED50 of 1.1 mg.
The gastric mucosa of animals and man can be damaged by noxious agents and protected by prostaglandins. We developed a Heidenhain pouch dog model which allows the study of multiple doses of the protective or noxious agent. Mucosal damage in the pouch caused by instillation of 160 mM aspirin suspended in 150 mM HCl for two 15-min periods was determined by measuring hemoglobin concentration in isotonic mannitol washes. Hemoglobin levels 24 h after the administration of the acid-aspirin suspension were significantly higher than basal levels. Pretreatment with oral doses of 0.3–3 µg/kg 16,16-dimethyl PGE2 at 24 and 18 h and 30 min before the acid-aspirin suspension decreased hemoglobin concentrations in the washes (p < 0.001).
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