BACKGROUND: Interdigestive pain relieved by food is a common feature of ulcer disease. We tested the hypothesis that the duodenal bulb is intermittently acidified in association with phase III of the interdigestive motility cycle, and tried to quantify the balance between acid and duodenal bicarbonate secretion during this particular period. METHODS: The experiments were performed in Helicobacter-negative healthy volunteers. Gastric and duodenal luminal pH was measured with a triple antimon electrode before, during, and after phase III of the migrating motor complex. Gastric acid secretion rate was measured in real time with a perfusion system and duodenal bicarbonate secretion was estimated from a continuous recording of the transmucosal potential difference (PD) in the duodenal bulb. RESULTS: No significant changes in bulb pH occurred before, during, or after phase III. During the studied time window, the stomach produced 2.24 +/- 0.55 mmol of acid at a peak pH of 1.74 +/- 0.10. Basal HCO3- secretion calculated from bulb PD was 0.82 +/- 0.12 mmol x 30 min(-1) to which was added 0.47 +/- 0.07 mmol of HCO3- during duodenal phase III. The contribution of retroperistalsis-driven HCO3- reflux was small (0.08 +/- 0.02 mmol). CONCLUSIONS: Both the pH recording and the quantitative assessment of secretion rates show that in healthy subjects, fasting gastric acid production and duodenal bicarbonate secretion are of similar magnitude and dynamically coordinated. The mechanism behind the linkage may be reflex activation by motor activity, or a luminal PCO2 rise during phase III activity.
BACKGROUND: Interdigestive pain relieved by food is a common feature of ulcer disease. We tested the hypothesis that the duodenal bulb is intermittently acidified in association with phase III of the interdigestive motility cycle, and tried to quantify the balance between acid and duodenal bicarbonate secretion during this particular period. METHODS: The experiments were performed in Helicobacter-negative healthy volunteers. Gastric and duodenal luminal pH was measured with a triple antimon electrode before, during, and after phase III of the migrating motor complex. Gastric acid secretion rate was measured in real time with a perfusion system and duodenal bicarbonate secretion was estimated from a continuous recording of the transmucosal potential difference (PD) in the duodenal bulb. RESULTS: No significant changes in bulb pH occurred before, during, or after phase III. During the studied time window, the stomach produced 2.24 +/- 0.55 mmol of acid at a peak pH of 1.74 +/- 0.10. Basal HCO3- secretion calculated from bulb PD was 0.82 +/- 0.12 mmol x 30 min(-1) to which was added 0.47 +/- 0.07 mmol of HCO3- during duodenal phase III. The contribution of retroperistalsis-driven HCO3- reflux was small (0.08 +/- 0.02 mmol). CONCLUSIONS: Both the pH recording and the quantitative assessment of secretion rates show that in healthy subjects, fasting gastric acid production and duodenal bicarbonate secretion are of similar magnitude and dynamically coordinated. The mechanism behind the linkage may be reflex activation by motor activity, or a luminal PCO2 rise during phase III activity.