Digestive Diseases and Sciences

, Volume 51, Issue 4, pp 754–765

Effects of Lipopolysaccharide on Gastric Stasis: Role of Cyclooxygenase

  • Sonlee D. West
  • James W. Suliburk
  • Gregory S. Smith
  • David W. Mercer
Esophageal, Gastric, and Duodenal Disorders

DOI: 10.1007/s10620-006-3203-2

Cite this article as:
West, S.D., Suliburk, J.W., Smith, G.S. et al. Dig Dis Sci (2006) 51: 754. doi:10.1007/s10620-006-3203-2

Abstract

This study was done to examine the role of cyclooxygenase (COX) in lipopolysaccharide (LPS)-induced gastroprotection and gastric stasis. In conscious rats, LPS dose and time dependently increased gastric luminal fluid accumulation. LPS decreased blood flow (laser Doppler) and prevented gastric injury from acidified ethanol at time points before significant fluid accumulation occurred. LPS increased COX-2 but not COX-1 expression. In contrast, LPS decreased gastric mucosal prostaglandin synthesis. LPS-induced gastric luminal fluid accumulation was negated by both nonselective COX inhibition with salicylate and selective COX-2 inhibition with NS-398 but not by selective COX-1 inhibition with SC-560. Neither salicylate nor NS-398 blocked LPS-induced gastroprotection. LPS-induced gastroprotection does not depend entirely on accumulation of luminal fluid and is independent of COX-1 and COX-2. However, the ability of LPS to cause gastric stasis and increase gastric luminal fluid accumulation involves COX-2.

Key Words

gastroprotectionlipopolysaccharideNS-398salicylateSC-560

Copyright information

© Springer Science + Business Media, Inc. 2006

Authors and Affiliations

  • Sonlee D. West
    • 1
  • James W. Suliburk
    • 1
  • Gregory S. Smith
    • 2
  • David W. Mercer
    • 1
    • 3
  1. 1.Department of SurgeryUniversity of Texas Medical SchoolHouston
  2. 2.Department of SurgerySt. Louis University School of MedicineSt. LouisUSA
  3. 3.UT—Houston Medical School/LBJ General HospitalHoustonUSA