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Pathophysiology of adynamic ileus

J J Cullen1, D K Caropreso, L L Hemann

  • 1Department of Surgery and Internal Medicine, University of Iowa College of Medicine and VAMC, Iowa City 52242, USA.

Digestive Diseases and Sciences
|April 1, 1997
PubMed
Summary
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Endotoxemia disrupts gastrointestinal motility by delaying the migrating motor complex (MMC). This study found increased serum levels of vasoactive intestinal peptide (VIP) and nitrite/nitrate (NO(2)-/NO(3)-) following endotoxin administration.

Area of Science:

  • Gastroenterology
  • Neuroscience
  • Pharmacology

Background:

  • Endotoxemia is associated with disrupted gastrointestinal motility.
  • Nitric oxide (NO) and vasoactive intestinal peptide (VIP) are inhibitory neurotransmitters implicated in gastrointestinal function.

Purpose of the Study:

  • To investigate the role of NO and VIP in endotoxemia-induced gastrointestinal motility dysfunction.
  • To determine the effects of endotoxin on migrating motor complex (MMC) and serum/tissue levels of NO and VIP.

Main Methods:

  • Dogs were instrumented with strain gauge transducers to measure gastrointestinal motility.
  • Serum and tissue levels of NO synthase, VIP, and nitrite/nitrate (NO(2)-/NO(3)-) were measured.
  • A single intravenous dose of E. coli lipopolysaccharide was administered, and measurements were repeated for three days.

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Main Results:

  • Endotoxin administration delayed the MMC for two days.
  • Serum VIP levels increased on postendotoxin day 1, while serum NO(2)-/NO(3)- levels increased on postendotoxin day 2.
  • No significant changes were observed in gut smooth muscle levels of NO synthase or VIP.

Conclusions:

  • A single, sublethal dose of endotoxin prolongs the MMC in dogs.
  • Distinct and independent increases in serum VIP and NO(2)-/NO(3)- occur following endotoxin exposure.
  • These findings suggest a role for VIP and NO metabolites in the altered gastrointestinal motility during endotoxemia.