Abstract

The role of alkaline secretion in the protection against acid-induced (50 mM HCl) damage was investigated in the perfused rabbit duodenum. Basal alkaline secretion was 3.86 +/- 0.23 mu Eq/cm2 . 10 min (pH-stat method). Perfusion with HCl increased alkaline secretion to 4.39 +/- 0.17 mu Eq/cm2 . 10 min and led to superficial damage of 51.8% of the villi. Intravenous treatment with NaHCO3 and glucagon increased alkaline secretion (+25% and +37%, respectively) and decreased damage (-27.7% and -25.3%, respectively), whereas mucosal blood flow as assessed by radioactive microspheres was stimulated only by glucagon. Intravenous treatment with NH4Cl, vasopressin, and furosemide decreased alkaline secretion (-31%, -52%, and -50%, respectively) and led to increased damage (+18.5%, +19.3%, and +19.6% superficial and 30%-50% deep lesions), and mucosal blood flow was decreased (vasopressin) or unchanged. There was a direct linear relationship (r = 0.88, y = 103-15.8x) between the degree of damage and alkaline secretion. These results support the hypothesis that duodenal alkaline secretion is indeed a protective factor against acid damage.