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TNF-alpha induced bronchial vasoconstriction.

E M Wagner1

  • 1Department of Medicine, Johns Hopkins University, Baltimore, Maryland 21224, USA. wagnerem@jhmi.edu

American Journal of Physiology. Heart and Circulatory Physiology
|September 20, 2000
PubMed
Summary
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Tumor necrosis factor-alpha (TNF-alpha) initially dilates, then constricts bronchial vasculature in sheep. This constriction is mediated by endothelin-1 (ET-1), contributing to airway inflammation.

Area of Science:

  • Pulmonary Medicine
  • Immunology
  • Vascular Biology

Background:

  • Tumor necrosis factor-alpha (TNF-alpha) is a pro-inflammatory cytokine implicated in asthma.
  • Airway vasculature is crucial for inflammatory cell trafficking.

Purpose of the Study:

  • To investigate the effects of TNF-alpha on bronchial vascular resistance (BVR).
  • To elucidate the mechanism behind TNF-alpha-induced changes in BVR.

Main Methods:

  • Anesthetized, ventilated sheep were used.
  • The bronchial artery (BA) was cannulated and perfused.
  • TNF-alpha was infused into the BA, and BVR was measured.
  • An endothelin-1 (ET-1) antagonist (BQ-123) was used to block ET(A) receptors.

Related Experiment Videos

Main Results:

  • TNF-alpha infusion initially decreased BVR (vasodilation) but later increased BVR (vasoconstriction).
  • The late-phase vasoconstriction was significantly attenuated by the ET(A) receptor antagonist BQ-123.
  • These findings suggest TNF-alpha induces bronchial vasoconstriction via secondary ET-1 release.

Conclusions:

  • TNF-alpha exerts vasoactive effects on the bronchial vasculature.
  • The mechanism involves the release of ET-1, contributing to airway inflammation.
  • These vascular effects may exacerbate the inflammatory status of the airways.