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Abstract
Significant gastric acid hypersecretion from Heidenhain pouches follows conversion
of the upper half of the small bowel below the pancreatic ducts into a defunctionalized
Thiry fistula, or excision of this segment. Since comparable hypersecretion is produced
by both procedures, this hyperacidity is probably due to the removal of a gastric
acid inhibitor normally released by this segment of the bowel.
Antrectomy with Billroth I type reconstruction radically reduces this acid hypersecretion
well below base line controls, suggesting that the normal intestinal inhibition of
acid is directed against antial gastrin.
If the antrectomy is performed first, and the Thiry fistula formed later, the fistula
induces a modest increase in acid, and subsequent excision of the fistula lowers acid
levels to those expected after antrectomy alone. This reaction after antrectomy suggests
that significant lengths of defunctionalized bowel also have the potential of releasing
an acid-stimulating hormone.
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References
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Article info
Footnotes
☆This work was supported by U.S.P.H.S. Research Grants AM-05138 and AM-07864, National Institutes of Health, Bethesda, Maryland.
☆☆Presented at the Eighth Annual Meeting of the Society for Surgery of the Alimentary Tract, Atlantic City, New Jersey, June 17 and 18, 1967.
Identification
Copyright
© 1968 Published by Elsevier Inc.
