Gastric acid secretion stimulated by modified sham-feeding, and the effects of histamine H2-antagonist and anti-muscarinic agent in patients with duodenal ulcer.

Patients with duodenal ulcer (DU) were classified into responders to H2-antagonist and non-responders in whom DU did not heal within 3 months with the antagonist. In these patients and healthy controls, a modified sham-feeding (MSF) test was performed to elucidate the pathogenesis of resistance to H2-antagonist. By MSF stimulation, gastric acid secretion significantly increased in all subjects. The mean acid output by MSF amounted to about 52 of the tetra-gastrin maximum in controls (12 cases), 46% in responders (12 cases) and 72% in non-responders (14 cases). The mean acid output in non-responders was significantly higher than in controls under baseline conditions, MSF and gastrin stimulations, but was higher than in responders during MSF stimulation. The effects of H2-antagonist (cimetidine 1mg/kg/h), anti-muscarinic agent (pirenzepine 0.3mg/kg/h), or both on the acid secretion were examined on non-responders (6 cases), responders (6 cases) and healthy controls (6 cases). The acid secretion stimulated by MSF was significantly inhibited by pirenzepine in responders and controls, but not in non-responders. With cimetidine, the acid output was significantly inhibited in all groups, but was still higher in non-responders than in controls and responders, indicating that the reduction of acid output by a H2-antagonist is significantly less in non-responders than in other groups. The combined use of pirenzepine and cimetidine almost completely inhibited the acid output in all groups. These data suggest that the vagal activity in non-responders to H2-antagonist is higher than in responders and healthy subjects, and H2-antagonist combined with anti-muscarinic agent is more effective in reducing the gastric acid secretion in non-responders.