The Mechanism of the Inhibition of Gastric Secretion Produced by Esophageal Ligation in the Pylorus-Ligated Rat

Abstract

Esophageal ligation in the pylorus-ligated rat significantly inhibited volume, titratable acidity, and titratable acid output and reduced the incidence of ulcers, perforations, and death of 18-hr pylorus-ligated rats. Draining the saliva outside the body of the rat by esophageal cannulation produced a significant increase in volume and gastric acidity over the esophagus-ligated preparation. A method for collection of saliva in the unanesthetized unstimulated rat was developed, and basal salivary flow was found to be 0.84 ml/4 hr. Administration of 1.0 ml of freshly collected saliva to esophagus + pylorus-ligated rats increased titratable acidity, but not volume of secretion, to the level found in the pylorus-ligated rat. A similar effect was obtained with administration of 1.0 ml of a phosphate buffer. Removal of the salivary glands had no significant effect on gastric acidity in the pylorus-ligated rat and the reduction in volume could be accounted for by the lack of saliva. Gastric secretion in the esophagus + pylorus-ligated rat was stimulated by histamine, carbachol, insulin, and 2-deoxyglucose. When the vagus nerves were cut, stimulation was still obtained with carbachol but not with insulin or 2-deoxyglucose. The data indicated that rat saliva did not contain a specific gastric stimulant material, and esophageal ligation depressed gastric secretion in the pylorus-ligated rat by inhibition of the central vagal activity.