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Related Experiment Videos

Interaction between SO2 and cold-induced bronchospasm in anesthetized rabbits.

P Barthélemy1, M Badier, Y Jammes

  • 1Laboratoire de Médecine Expérimentale, GS 15 (CNRS), Faculté de Médecine, Marseille, France.

Respiration Physiology
|January 1, 1988
PubMed
Summary

Sulfur dioxide (SO2) exposure in rabbits increases lung resistance and suppresses cold-induced bronchospasm. These effects suggest SO2 causes transient airway changes, reducing nerve receptor accessibility.

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Area of Science:

  • Respiratory Physiology
  • Environmental Toxicology

Background:

  • Sulfur dioxide (SO2) is an environmental pollutant known to affect respiratory function.
  • Airway hyperresponsiveness to cold air is a common phenomenon.
  • The role of vagal reflexes in SO2-induced airway changes requires further elucidation.

Purpose of the Study:

  • To investigate the effects of SO2 exposure on reflex and non-reflex bronchoconstriction in rabbits.
  • To determine if SO2-induced changes in lung resistance are mediated by vagal reflexes.
  • To assess the impact of SO2 on cold-induced bronchospasm and responses to other stimuli.

Main Methods:

  • Anesthetized, paralyzed, and ventilated rabbits were exposed to 0.5 or 5 ppm SO2 for 45 minutes.
  • Lung resistance (RL) was measured before and after SO2 exposure.

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  • Cold-induced bronchospasm was elicited by cooling inspired air.
  • Vagotomy was performed in some animals.
  • Responses to intravenous phenyldiguanide (PDG) and histamine were also assessed.
  • Main Results:

    • Both 0.5 and 5 ppm SO2 significantly increased RL in intact rabbits.
    • The increase in RL after 5 ppm SO2 persisted after vagotomy.
    • Cold-induced bronchospasm was significantly reduced after SO2 exposure.
    • The reflex bronchoconstrictor response to PDG disappeared after 5 ppm SO2 exposure.
    • Histamine-induced bronchomotor responses remained unaltered.

    Conclusions:

    • Prolonged increase in lung resistance following SO2 exposure is not mediated by vagal reflexes.
    • SO2 exposure transiently alters the tracheobronchial wall, reducing accessibility to nervous receptors.
    • These alterations suppress cold-induced bronchospasm and reflex responses to PDG, indicating a modulation of airway sensory pathways.