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Ethionine-Induced Alteration in Gastric Secretion

G. ROBERT MASON, MD; EDWIN H. EIGENBRODT, MD; HARRY A. OBERHELMAN JR., MD; THOMAS S. NELSEN, MD
Arch Surg. 1964;88(6):1063-1069. doi:10.1001/archsurg.1964.01310240159027.
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The pancreas has been shown to be capable of influencing gastric hydrochloric acid secretion, both clinically and experimentally. Clinically, the Zollinger-Ellison type of pancreatic islet-cell tumor is associated with gastric hypersecretion and intractable peptic ulceration.2 Experimentally, such procedures as total pancreatic duct ligation,9 total pancreatic fistula,8 and pancreatitis17 have been shown to elevate acid secretion from an isolated denervated gastric pouch. The relative influence of endocrine and exocrine portions of the pancreas in these secretory interrelationships is difficult to assess. It would be of value to be able to distinguish the gastric secretory response by functional alteration of either the endocrine or exocrine portion of the pancreas. Various toxic substances have been reported to destroy the β-cells of the pancreatic islet (alloxan)4 and α-cells (cobaltous chloride and guanidine [Synthalin]).6 None of these compounds will destroy all cellular components of the pancreatic islet. DL-Ethionine

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