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Increased intragallbladder pressure stimulates gallbladder eicosanoid release

S I Myers1, L R Inman, B Kalley-Taylor

  • 1Department of Surgery, University of Texas Southwestern Medical Center, Dallas 75235-9031.

Prostaglandins
|July 1, 1994
PubMed
Summary

Increased gallbladder pressure during cholecystitis stimulates eicosanoid release. This physical force on the gallbladder mucosa may contribute to early cholecystitis inflammation.

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Area of Science:

  • Gastroenterology
  • Physiology
  • Pathology

Background:

  • The triggers for elevated gallbladder eicosanoid synthesis in cholecystitis remain unclear.
  • Eicosanoids play a role in inflammatory processes within the gallbladder.

Purpose of the Study:

  • To investigate the hypothesis that elevated intraluminal gallbladder pressure stimulates endogenous eicosanoid release.
  • To determine the relationship between intraluminal pressure and gallbladder eicosanoid production.

Main Methods:

  • Rabbit gallbladders were perfused in vitro with Krebs-Henseleit buffer.
  • Gallbladders were subjected to varying intraluminal pressures (0, 12, 24 mm Hg).
  • Eicosanoid release (6-keto-PGF1α, PGE2, thromboxane B2) was measured using enzyme immunoassay; histological examination was performed.

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Main Results:

  • Increased intraluminal pressure significantly elevated gallbladder 6-keto-PGF1α release.
  • Histological analysis revealed increased basolateral edema in the submucosal space with higher pressures.
  • Indomethacin administration reduced 6-keto-PGF1α release by 70% at 24 mm Hg.

Conclusions:

  • Elevated intraluminal gallbladder pressure is a stimulus for increased gallbladder eicosanoid release.
  • The physical force exerted by increased pressure on the gallbladder mucosa may contribute to early cholecystitis.
  • These findings suggest a mechanical component in the pathogenesis of cholecystitis-associated inflammation.