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The antrum of the stomach in dogs was excluded by constructing a membrane of gastric mucosa separating the cavity of the antrum from that of the corpus. A fistula was made of the pylorus and intestinal continuity re-established by anastomosing the corpus of the stomach to the open end of the duodenum. A vagus denervated Heidenhain pouch was also prepared. With this type of preparation it was found that insulin hypoglycemia produced a marked stimulation of gastric secretion from the Heidenhain pouch. Furthermore, with the antrum excluded from contact with the gastric contents but with its innervation preserved, the secretory response of the Heidenhain pouch to the ingestion of food was not only not reduced but was actually prolonged. These effects can be accounted for by peristaltic activity in the antrum induced by the peristalsis of digestion in the main stomach and enhanced by the absence of the usual inhibitory effect of acid gastric content on the release of gastrin. Insulin hypoglycemia produced vigorous contractions in the isolated antrum with intact vagus innervation.

In 1953, L. R. Dragstedt1developed the concept that gastric ulcers are usually due to a hypersecretion of gastric juice of humoral or hormonal origin dependent upon hyperfunction or dysfunction of the gastric antrum, whereas duodenal ulcers are usually due to a hypersecretion of gastric juice of nervous origin. In previous experiments, Dragstedt, Oberhelman, and Smith2found that transplantation of the antrum of the stomach into the colon as a diverticulum caused a long-continued hypersecretion of gastric juice with the formation of chronic progressive ulcers in dogs. This hyperfunction of the gastric antrum when transplanted into the colon was abolished when the portion of colon containing the antrum transplant was excluded from intestinal continuity by means of a Thiry-Vella fistula and the isolated colon was washed clean of all traces of fecal material and food.3Obstruction to the isolated colon containing the antrum transplant produced a hypersecretion

The current surgical treatment of duodenal ulcer emphasizes subtotal gastric resection. The aim of this operation is the reduction of the acid-secreting capacity of the stomach, and, indeed, a large experience has shown that following subtotal resection the vast majority of duodenal ulcers heal. A quantitative relationship, however, between the amount of stomach removed and the secretion of acid gastric juice has never been shown. Histologic studies of the stomach have revealed a decrease in the number of parietal cells in the upper part of the fundus and in the cardiac region. 1 Common practice is to remove the lower 75% of the stomach, but does this result in a 75% drop in secretion? Evidence against such a direct relationship is the very high fasting gastric secretion occasionally seen in duodenal ulcer patients who have previously been subjected to subtotal gastrectomy and have subsequently developed stomach ulcers. This hypersecretion of

The identification and measurement of uropepsin, a substance found in the urine which is thought to be identical with pepsinogen, has prompted the idea that uropepsin determinations may be a simple and accurate index of gastric secretory activity. Available evidence indicates that pepsinogen present in gastric glands is secreted by two routes: directly into the lumen of the stomach, where it is converted to pepsin, and into the blood stream, whereby it is carried to the kidneys and excreted as uropepsin.* Gray and co-workers have demonstrated the importance of the hypothalamic-pituitaryadrenal axis in the control of uropepsin excretion.† Administration of corticotropin (ACTH), cortisone, or hydrocortisone (Compound F) to patients produces an average increase in uropepsin excretion of almost 200%, paralleled by an equal increase in gastric pepsin and HCl output. That this increase is mediated by the adrenals is shown by the fact that patients with Addison's disease have very