Vagal influence in gastric acid secretion in normals and in duodenal ulcer patients.

The nature of hypersecretion of gastric acid in duodenal ulcer subjects remains controversial. The duodenal ulcer patients, on an average, secrete more than twice the amount of acid secreted by normal persons. It is now known that the duodenal ulcer patients have an increased parietal cell population in the stomach. Whether this increased acid output is solely due to the increased parietal cell mass is uncertain. Dragstedt and his group has been actively propagating their view of 'vagal hypertonicity' in these patients for more than 20 years (Dragstedt, Harper, Tovee, and Woodward, 1947; Dragstedt, 1967). Grossman has, on the other hand, remained unconvinced of Dragstedt's arguments (Grossman, 1949; Grossman, 1967). Hunt and Kay (1954) and Card, Sircus, Kay, and Hunt (1962) have pleaded against the existence of a supranormal drive on the parietal cells in duodenal ulcer patients, whereas Baron (1963) has suggested that about half the duodenal ulcer patients have a supranormal drive to explain their basal hypersecretion. If duodenal ulcer patients do have vagal hypertonicity, blocking the vagal influence should reduce the gastric acid output to a greater degree in ulcer patients than in the normal person. There are many studies on the influence ofvagal transection (Waddell, 1957; Gillespie, Clark, Kay, and Tankel, 1960; Bachrach, 1962; Bell, 1964; Gelb, Baronofsky, and Janowitz, 1961; Barabas, Payne, Johnstone, and Burns, 1966; Bank, Marks, and Louw, 1967) and vagal block with drugs, 'medical vagotomy', (McArthur, Tankel, and Kay, 1960; Gillespie and Kay, 1961; Checketts, Gillespie, and Kay, 1966) upon gastric acid secretion in duodenal ulcer patients. Such data for normal healthy persons are not available. This study compares the results of the response of gastric acid secretion to vagal block with a combination of hexamethonium bromide and atropine sulphate in normal persons and in patients with duodenal ulcer.