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Related Experiment Videos

Nonadrenergic bronchodilation in normal subjects.

M Ichinose1, H Inoue, M Miura

  • 1First Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.

The American Review of Respiratory Disease
|July 1, 1988
PubMed
Summary
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Capsaicin inhalation stimulates bronchial C-fibers, activating a nonadrenergic inhibitory (NAI) system that causes bronchodilation in humans. This reflex pathway is crucial for NAI system bronchodilation.

Area of Science:

  • Respiratory Physiology
  • Neuropharmacology

Background:

  • The nonadrenergic inhibitory (NAI) system's role in human bronchodilation is not fully understood.
  • Bronchial C-fibers are sensory nerves that can be stimulated by various agents.

Purpose of the Study:

  • To investigate if bronchial C-fiber stimulation via capsaicin inhalation triggers NAI system-mediated bronchodilation.
  • To explore the involvement of C-fiber receptors in the NAI reflex pathway for bronchodilation.

Main Methods:

  • Studied partial and maximal expiratory flow-volume curves in 5 healthy subjects.
  • Induced bronchoconstriction with PGF2 alpha, followed by capsaicin inhalation to stimulate C-fibers.
  • Administered oxitropium bromide, propranolol, and hexamethonium to assess drug effects.

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Main Results:

  • PGF2 alpha caused significant bronchoconstriction, decreasing FEV1 and V30p.
  • Capsaicin inhalation led to significant bronchodilation, increasing V30p and FEV1.
  • The bronchodilator response to capsaicin was abolished by hexamethonium, a ganglionic blocking agent.

Conclusions:

  • The NAI system exhibits a distinct bronchodilator action in humans in vivo.
  • Bronchial C-fiber receptors appear to be involved in the reflex pathway for NAI system bronchodilation in humans.