In 1901 von Yzeren1 noticed the development of gastric ulcers in the stomachs of rabbits which had been submitted to vagotomy. Auer2 in 1909 made a similar observation during the course of some experiments on gastric motility, almost casually mentioning the likelihood of gastric ulcers developing in vagotomized rabbits. After these reports many workers confirmed this observation, and in 1936 Beazell and Ivy3 postulated the cause of gastric ulceration following complete vagotomy to be the stasis of acid and the mechanical trauma of rough food upon the gastric mucosa. They suggested an "unknown factor" responsible for the continued high acid production under these conditions.
In the early 1940's many clinical trials of vagotomy were started for the treatment of gastric4,5 and duodenal ulcer disease. It took only a few years of this type of treatment to prove that it was ineffective for the control of gastric