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  Vol. 125 No. 4, April 1990 TABLE OF CONTENTS
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  PAPERS READ BEFORE THE 13TH ANNUAL MEETING OF THE ASSOCIATION OF VETERANS ADMINISTRATION SURGEONS, MAY 4 TO MAY 6, 1989, SAN ANTONIO, TEX
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Vagotomy Effect on Gastric Prostaglandins

Primarily Neural or Secondary to Hypoacidity?

Barry A. Levine, MD; Luke J. Curtsinger, MD; Kenneth R. Sirinek, MD, PhD

Arch Surg. 1990;125(4):457-459.


Abstract

• Prostaglandins have been implicated in gastric mucosal cytoprotection. Vagotomy results in both cytoprotection and increased mucosal prostaglandin concentrations. However, the mechanism by which vagotomy affects prostaglandin generation remains unknown. In this study we compared vagotomy with long-term acid suppression using anticholinergic (atropine sulfate) or histamine2-receptor antagonism (cimetidine) and assessed mucosal injury and prostaglandin generation during graded stress. Vagotomy correlated with decreases in injury only in severe stress, while both atropine and cimetidine decreased injury also during moderate stress. Prostaglandin generation decreased in all groups during severe stress. Compared with sham operation, vagotomy, atropine, and cimetidine were all associated with increased mucosal prostaglandin generation in all stress periods. During severe stress, both atropine and cimetidine also evidenced higher prostaglandin generation than did vagotomy. These results suggest that vagotomy primarily decreases acid secretion, which then secondarily results in increased mucosal generation.

(Arch Surg. 1990;125:457-459)



Author Affiliations

From the Department of Surgery, University of Texas Health Science Center and Audie L. Murphy Veterans Administration Hospital, San Antonio, Tex.


Footnotes

Accepted for publication August 14, 1989.

Read before the 13th Annual Meeting of the Association of Veterans Administration Surgeons, San Antonio, Tex, May 5, 1989.

Reprint requests to Department of Surgery, University of Texas Health Center, 7703 Floyd Curl Dr, San Antonio, TX 78284 (Dr Levine).



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