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Vagotomy effect on gastric prostaglandins. Primarily neural or secondary to hypoacidity?

Authors
  • Levine, B A
  • Curtsinger, L J
  • Sirinek, K R
Type
Published Article
Journal
Archives of Surgery
Publisher
American Medical Association
Publication Date
Apr 01, 1990
Volume
125
Issue
4
Pages
457–459
Identifiers
PMID: 2108654
Source
Medline
License
Unknown

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.

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