The concept that gastric ulcers are usually caused by a hypersecretion of gastric juice of hormonal or gastrin origin due to stasis of food in the stomach1 of necessity assumes that food in contact with the antrum mucosa continues to stimulate the formation and release of gastrin and that this mechanism is not easily fatigued. Some existing evidence suggests that this assumption is correct. Thus, transplantation of the antrum as a diverticulum into the colon in experimental animals2 was found to produce a sustained hypersecretion of gastric juice and chronic peptic ulcers. The ulcerogenic effect of the isolated antrum in the Finsterer-Devine type of gastric resection probably represents an analogous situation when the antrum shielded from the inhibiting effect of the gastric acid continues to liberate gastrin in response to the presence of stagnant neutral food regurgitated from the duodenum. The present experiments were designed to test this