Many factors all sharing in common predisposing damage of the gastric mucosal barrier in the presence of acid have been implicated in the pathogenesis of gastric ulcerations [3, 4, 6, 71. Shock and/or anemia with resultant ischemia of the mucosa, in the experimental animal, appears to be a potent causal factor. Such a mechanism can be implicated in man, if for no other reason than that the clinical setting in which stress ulceration occurs is often characterized by both hypotension and anemia, but direct measurements of mucosal blood flow have not been made because of a lack of a technique which allows for repeated determinations under various conditions. Laboratory techniques usually employed are not directly applicable to man. A method to evaluate gastric mucosal blood flow in the intact, physiologically unaltered state, would be an important tool in both man and animal for demonstrating the nature of the relationship between blood flow and breakdown of the mucosal barrier. Secondly, it is appreciated that the stomach may be thought of as essentially two distinct organs, the antrum (control) and the corpus (secretion), each with a potent influence over the other. The interrelationship between the function of the glandular elements, located in the mucosa, and the blood flow to that particular mucosa is unknown. If blood flow is important in this interrelationship, and on the basis of a demonstrated increase in metabolic activity