Acute gastric ulceration occurred within 2 days of highly selective vagotomy (HSV) or truncal vagotomy and pyloroplasty (VP) in 24 of 38 piglets (63%). Twenty-three control animals with gastric and nongastric sham operations or anesthesia alone had normal stomachs when examined after 2 days. Microspheres labeled with various isotopes were injected sequentially to study a possible hemodynamic etiology of postvagotomy ulceration. At intervals of 1, 3, and 5 hours after vagotomy or a control operation, mierospheres were injected into the left atrium. Animals were sacrificed 48 hours later and stomachs excised, inspected, divided into 1-2 cm squares and counted for radioactivity. Blood flow to squares, gastric regions, and total stomach was calculated for each isotope (time interval). Total flow in squares with and without ulcers was similar, but the distribution of flow between mucosa and muscle varied. In HSV piglets, mucosal perfusion decreased 41% in ulcerated squares and 21% in normal areas. Muscle flow was increased 95% in ulcerated squares and 177% in normal areas. In VP piglets, mucosal perfusion was reduced 45% in squares with ulcers and 21% in normal squares, while muscle flow increased 18% in ulcerated samples and 194% in normal areas. Vagotomy appears to cause acute gastric ulceration in piglets by diverting gastric blood flow from mucosa to muscle.Acute gastric ulceration in piglets follows both hemorrhagic [1, 2] and endotoxic shock [3]. Gastric lesions in each instance are similar histologically and occur within 2 days of shock. This ulceration can be prevented by exclusion of bile [4] and by pretreatment with cholestyramine or methylpredniso-