Ippoliti A F, Isenberg J I, Hagie L
Gastroenterology. 1981 Jan;80(1):55-9.
Oral 16,16-dimethyl prostaglandin E2 is a potent inhibitor of meal-stimulated gastric acid secretion and gastrin release in humans. Experiments were performed in 5 patients with inactive duodenal ulcer to determine the effect of graded doses of intravenous 16,16-dimethyl PGE2 on meal-stimulated gastric acid secretion and gastrin release to demonstrate whether it is necessary for 16-16-dimethyl PGE2 to come into direct luminal contact with the oxyntic and antral gland portions of the stomach to produce its inhibitory effects. All doses of 16,16-dimethyl PGE2, between 0.01 and 0.1 microgram/kg i.v. and between 0.01 and 1.0 microgram/kg orally produced significant postprandial inhibitory effects on both gastric acid secretion and gastrin release as compared with saline control. 0.1 microgram/kg of intravenous of 1 microgram/kg of oral 16,16-dimethyl PGE2 inhibited meal-stimulated acid secretion and gastrin by 80-90%. In 6 unoperated Zollinger-Ellison syndrome patients, 1 microgram/kg of oral 16,16-dimethyl PGE2 significantly inhibited fasting gastric acid hypersecretion by approximately 85% without significantly altering serum gastrin. Each of the oral doses of 16,16-dimethyl PGE2 (0.01-1 microgram/kg) were without untoward effect, as were intravenous doses of 0.01-01 microgram/kg. Maximal inhibition of acid secretion was found with 0.1 microgram/kg 16,16-dimethyl PGE2 i.v. as compared with 1.0 microgram/kg orally. Since 16,16-dimethyl PGE2, whether given orally or intravenously, is a potent inhibitor of both gastric acid secretion and meal-stimulated gastrin release, without apparent untoward side effects, clinical trials with 16,16-dimethyl PGE2 are indicated in patients with acid peptic disease.
口服16,16 - 二甲基前列腺素E2是人体进餐刺激胃酸分泌和胃泌素释放的强效抑制剂。对5例非活动性十二指肠溃疡患者进行了实验，以确定静脉注射不同剂量的16,16 - 二甲基PGE2对进餐刺激胃酸分泌和胃泌素释放的影响，从而证明16,16 - 二甲基PGE2是否需要与胃的泌酸腺和胃窦腺部分直接腔面接触才能产生其抑制作用。静脉注射剂量在0.01至0.1微克/千克之间以及口服剂量在0.01至1.0微克/千克之间的所有16,16 - 二甲基PGE2剂量，与生理盐水对照相比，均对餐后胃酸分泌和胃泌素释放产生显著抑制作用。静脉注射0.1微克/千克或口服1微克/千克的16,16 - 二甲基PGE2可使进餐刺激的胃酸分泌和胃泌素释放抑制80 - 90%。在6例未经手术的佐林格 - 埃利森综合征患者中，口服1微克/千克的16,16 - 二甲基PGE2可使空腹胃酸分泌过多显著抑制约85%，而血清胃泌素无明显改变。16,16 - 二甲基PGE2的每个口服剂量（0.01 - 1微克/千克）均无不良反应，静脉注射剂量为0.01 - 0.1微克/千克时也无不良反应。与口服1.0微克/千克相比，静脉注射0.1微克/千克的16,16 - 二甲基PGE²对胃酸分泌的抑制作用最大。由于16,16 - 二甲基PGE2无论是口服还是静脉注射，都是胃酸分泌和进餐刺激胃泌素释放的强效抑制剂，且无明显不良反应，因此建议对消化性溃疡患者进行16,16 - 二甲基PGE2的临床试验。
