From the Gastrointestinal Unit, Groote Schuur Hospital, and the Departments ofMedicine and

Gastric ulceration was recognized as an occasional complication of vagotomy soon after Dragstedt championed the operation for the treatment of duodenal ulceration (Dragstedt and Owens, 1943). Gastric atony and antral stasis were to be expected after vagotomy without adequate drainage of the gastric contents and it was perhaps not surprising that a number of patients should have developed lesser curve gastric ulceration after vagotomy alone. The mechanism responsible for the development of gastric ulceration in these circumstances was later considered to be due to gastric retention, antral stasis and alkalinization, and gastrin release, with the resulting continual gastric acid stimulation (Drag-stedt, 1953; Burge, 1964; Oberhelman, 1964). The occurrence of gastric ulceration after vagotomy lent further support to Dragstedt's well known postulate that all gastric ulceration was dependent on the hormonal phase of gastric secretion consequent upon antral stasis and 'hyperfunction or dysfunction of the gastric antrum ' (Dragstedt, 1953, 1956). Other workers have not noted a significant difference in gastric emptying between duodenal and gastric ulce