Pyloric Stenosis and Gastric Ulcer

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Abstract
In 1953, L. R. Dragstedt1 developed 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 Smith2 found 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.3 Obstruction to the isolated colon containing the antrum transplant produced a hypersecretion

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