Acid secretion and serum gastrin at graded intragasric pressures in man.
In 16 healthy subjects, gastric distention was produced by infusion of 5% mannitol solution, pH 5.5. Constant intragastric pressure was maintained by use of a barostat. Over successive 1-hr periods the head of pressure was raised in 5-cm increments from an arbitrary zero point to 15 cm. Gastric acid secretion was measured by constant intragastric titration. Blood samples were obtained throughout the study for measurement of serum gastrin concentrations. When intragastric pressure was raised from zero to 5 cm H2O, gastric acid secretion increased significantly (24% of peak acid response to pentagastrin). Acid responses at 10 and 15 cm pressure were lower. Serum gastrin concentrations increased slightly at 15 cm pressure but not at 5 or 10 cm. There was no correlation between increments in serum gastrin and acid secretory rates. We conclude that gastric distention at low pressures stimulated acid secretion by a mechanism and did not involve increases in circulating gastrin concentrations. Slight increases in serum gastrin observed at the highest distending pressure were not associated with further increases in acid secretion.
Acid secretion and serum gastrin at graded intragasric pressures in man. In 16 healthy subjects, gastric distention was produced by infusion of 5% mannitol solution, pH 5.5. Constant intragastric pressure was maintained by use of a barostat. Over successive 1-hr periods the head of pressure was raised in 5-cm increments from an arbitrary zero point to 15 cm. Gastric acid secretion was measured by constant intragastric titration. Blood samples were obtained throughout the study for measurement of serum gastrin concentrations. When intragastric pressure was raised from zero to 5 cm H2O, gastric acid secretion increased significantly (24% of peak acid response to pentagastrin). Acid responses at 10 and 15 cm pressure were lower. Serum gastrin concentrations increased slightly at 15 cm pressure but not at 5 or 10 cm. There was no correlation between increments in serum gastrin and acid secretory rates. We conclude that gastric distention at low pressures stimulated acid secretion by a mechanism and did not involve increases in circulating gastrin concentrations. Slight increases in serum gastrin observed at the highest distending pressure were not associated with further increases in acid secretion.