The vagus nerves play a dominant role in the stimulation of gastric secretion. The basal or continuous secretion of gastric juice in normal man and animals is almost entirely caused by tonic impulses in the vagus nerves. The hormonal mechanism for the stimulation of gastric secretion is almost entirely quiescent when there is no food in the stomach or duodenum. Food taking causes an immediate and profound stimulation of gastric secretion. Impulses in the vagus nerves are aroused reflexly by the sight, odor, and taste of palatable food. These impulses release acetylcholine at the endings of the vagus fibers in the stomach wall and the transmission of the nervous impulse to the acid- and pepsin-producing cells is probably done by this humoral agent. If the gastric content in contact with the antral mucosa is not acid in reaction, the vagus impulses also cause a small release of gastrin into the circulation which is sufficient to potentiate the stimulating effect of the vagus impulses on the parietal and chief cells. The suggestion that both gastrin and vagus impulses release histamine and that histamine serves as a final common pathway for both of these types of stimulation seems improbable. Gastric juice secreted in response to vagus stimulation is rich in pepsin, that secreted in response to histamine stimulation is poor in pepsin, and that secreted in response to gastrin is intermediary in compositon. If the final agent for all three is assumed to be histamine, these differences in the composition of the gastric secretion should not occur. A profound increase in the basal or continuous secretion of gastric juice occurs regularly in patients with duodenal ulcer. This is of sufficient magnitude so that if a comparable hypersecretion is induced in animals, chronic peptic ulcers are produced. The basal hypersecretion is of vagus origin and is abolished if all or nearly all of the vagus fibers to the stomach are divided. Failure to divide all of the vagus fibers may result in persistence of hypersecretion and failure of the ulcer to heal. This suggests that some intermediary mechanism, possibly Meissner's plexus, exists between the efferent vagus fibers and the parietal cells so that even a small vagus branch can activate the entire glandular apparatus. In long-standing duodenal ulcers the number of acid-secreting cells in the stomach may be twice or more the normal amount. This increase in the parietal cell mass probably accounts for the increased secretory response of the duodenal ulcer patient to the augmented histamine test as well as to the increased response to the test meals of the early gastroenterologists. There is still some difference of opinion with respect to the cause of basal hypersecretion of gastric juice in duodenal ulcer patients. I believe it is due to a secretory hypertonus in the vagus nerves in turn produced in some way by the tensions, emotional strains, and competitive efforts of modern life. It is in this way that the central nervous system plays its role in the pathogenesis of the disease and in this sense duodenal ulcer may be considered a psychosomatic disease. Evidence for this hyperactivity in the vagus secretory apparatus is entirely indirect. We have observed that basal secretion in duodenal ulcer patients on the night before a surgical operation is almost always twice as much as that during other periods. This could be caused by anxiety and apprehension of the approaching surgical ordeal. It could not be caused by an increase in the parietal cell mass developing in such a short time. Exacerbation of duodenal ulcer symptoms with hemorrhage and perforation reported from English cities during the bombing raids in World War II are also in harmony with this view. Similar exacerbation of symptoms in duodenal ulcer patients during periods of emotional conflict and stress has for a long time been commented upon in the literature. In my experience determination of the basal secretion has been useful in selecting patients for surgical versus medical treatment and in determining the prognosis after surgery. When the basal secretion exceeds three to four times the normal values, the prospect for permanent cure of a duodenal ulcer by medical treatment is remote and surgery should be advised. If basal hypersecretion persists after surgery, recurrence of the ulcer should be anticipated.
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