I can perhaps best summarize this discussion by referring to Figures 18, 19, and 20. I am persuaded that duodenal ulcers are usually caused by a hypersecretion of gastric juice of nervous origin brought about in some way by the tensions, strains, and competitive efforts of modern life. These factors, increasing gradually over the years, produce an increase in the tonus of the vagus nerves which involves both motor and secretory fibers. The long-continued vagal stimulation of the gastric glands produces hyperplasia and hypertrophy with resultant increase in the parietal cell mass. The secretory hypertonus of the vagi causes a marked increase in the basal gastric secretion. This large secretion in the empty stomach without the buffering effect of food makes the gastric content very corrosive and, when it is hurried onward into the duodenum by the gastric hypermotility, produces the chronic progressive ulcer in the less resistant duodenal mucosa. Gastric ulcers on the other hand are usually caused by hypersecretion of gastric juice of humoral or gastrin origin caused by stasis of food in the stomach in contact with the gastric antrum. This stasis may be due to pyloric stenosis from an accompanying duodenal ulcer or to defective gastric tonus and motility. Patients with gastric ulcers and an accompanying duodenal ulcer display the nervous hypersecretion characteristic of the duodenal ulcer patient and also an excessive secretion of humoral origin due to prolonged contact of food with the antrum mucosa. Patients with gastric ulcers without organic obstruction at the pylorus usually display subnormal basal gastric secretion and a dilated poorly emptying stomach. Many patients secrete little or even no free hydrochloric acid in the basal secretions, indicating that the nervous phase of gastric secretion is markedly reduced. This is probably an indication of decreased tonus in the secretory fibers in the vagi and the stasis of food in the stomach suggests an accompanying decrease also in the tonus of the motor fibers. Stasis in gastric ulcer patients may not be revealed by the usual liquid barium meal of the roentgenologist but becomes evident when the patient eats a large meal of customary food. The gradually increasing acidity of the gastric content eight to twelve hours after eating testifies to the continuing secretion of gastric juice caused by gastrin and to the increase in the corrosive properties of the gastric content as the buffering effect of the food becomes exhausted. © 1969.
