Gastric acid and pepsin secretion after single oral doses of mifentidine in healthy subjects.

Mifentidine represents a potential improvement in the class of H2-receptor antagonists because of its long plasma half-life (10 h). The aim of this study was to evaluate the effects of mifentidine on pentagastrin-induced gastric pepsin and acid secretion in man. Nine healthy subjects participated in two separate sessions in which they were given randomly either a single oral dose of placebo or 10 or 20 mg of mifentidine, in accordance with an incomplete balanced block design. Basal secretion was measured 30 min before the administration of the drug, and 90 min later unstimulated gastric secretion was collected through a nasogastric tube for an additional 30 min. Then, 2 micrograms/kg/h pentagastrin were infused intravenously for 2 h, and gastric juice collected again in 15-min aliquots. Acid output was almost completely blocked by both doses of mifentidine during the unstimulated period (-99%). Pentagastrin infusion induced 10 times as much acid output as in the unstimulated phase. This dramatic increase was reduced by 32% with the low dose of mifentidine and to a major extent (-86%) with the high dose. The pepsin output was significantly inhibited by both doses of mifentidine during unstimulated (-83% and -82%) and stimulated (-49% and -71%) phases. Acid output correlated with the area under the mifentidine plasma levels (r = -0.69, p less than 0.05). It is concluded that mifentidine is a potent inhibitor of both acid and pepsin secretion in man.

RCT Entities:   Population Interventions Outcomes