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Effect on Gastric Secretion

HERBERT B. GREENLEE, M.D.; ALSTRUP N. JOHNSON, JR., M.D.; THOMAS S. NELSEN, M.D.; LESTER R. DRAGSTEDT, M.D.

AMA Arch Surg. 1961;83(6):872-877.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Experimental as well as clinical studies have demonstrated an interrelationship between the pancreas and gastric secretion. Dragstedt in 1942 reported that 100% of dogs with external total pancreatic fistulae developed duodenal ulcer, whereas dogs in whom the pancreatic ducts had been ligated had only a 33% incidence.¹ Previous experimental work in our laboratory demonstrated a marked increase in gastric secretory output after construction of total external pancreatic fistulae.² Clinically, instances of recurrent peptic ulceration associated with islet cell tumors of the pancreas are known.^3,4

The purpose of the present experiments is to determine quantitatively the effect of total pancreatic duct ligation on gastric secretory output in previously controlled Heidenhain pouch dogs. Initially, these experiments were conducted in animals whose gastric antrums were in normal continuity. Subsequent studies were done in antrectomized Heidenhain pouch dogs in order to determine whether or not the gastric antrum is a factor . . . [Full Text PDF of this Article]

Author Affiliations
CHICAGO; PALO ALTO, CALIF.; GAINESVILLE, FLA.

From the Department of Surgery of the University of Chicago.; Residents in Surgery, University of Chicago (Dr. Greenlee, Dr. Johnson); Assistant Professor of Surgery, Stanford University (Dr. Nelsen); Research Professor of Surgery, University of Florida (Dr. Dragstedt).

Footnotes
Submitted for publication Feb. 17, 1961.

This work has been aided by grants from the Otho S. A. Sprague Memorial Institute and from the Division of Research Grants and Fellowships, National Institutes of Health.

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