Effects of acetazolamide and metabolic acidosis and alkalosis upon gastric acid secretion

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Abstract
The gastric H+ secretory responses to i.v. HCl, NaHCO3, and acetazolamide were studied in Heidenhain-pouch dogs that had been stimulated to secrete by feeding. Acetazolamide in low doses (5 mg/kg) gave a 65% reduction in H+ output for 2–4 hr, after which H+ secretion increased above normal, coincident with renal HCO3– loss and metabolic acidosis. Higher doses produced a greater systemic acidosis and resulted in less initial reduction of H+ and greater augmentation. Doses of 75–100 mg/kg, given 17 hr before feeding to produce a systemic acidosis, resulted in increased secretion, even though sufficient drug remained in the plasma to inhibit tissue carbonic anhydrase. Metabolic acidosis (i.v. HCl) initially suppressed but later augmented gastric H+. Acetazolamide had no suppressive effect in the presence of either an HCl- or acetazolamide-induced acidosis. Metabolic alkalosis (i.v. NaHCO3) reduced gastric H+ in regular feeding experiments and in dogs made acidotic by acetazolamide.