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Related Experiment Videos

Calcium antagonists in exercise-induced asthma.

K R Patel

    British Medical Journal (Clinical Research Ed.)
    |March 21, 1981
    PubMed
    Summary

    Inhaled verapamil and sodium cromoglycate effectively protected against exercise-induced asthma by preventing bronchoconstriction. Both treatments showed comparable efficacy, suggesting calcium

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    Area of Science:

    • Pulmonary Medicine
    • Pharmacology

    Background:

    • Exercise-induced asthma (EIA) is a common condition characterized by bronchoconstriction following physical exertion.
    • The role of mediator release, particularly calcium-dependent pathways, in EIA pathophysiology is increasingly recognized.

    Purpose of the Study:

    • To compare the protective effects of inhaled verapamil and sodium cromoglycate against exercise-induced bronchoconstriction in patients with asthma.
    • To investigate the potential role of calcium channels in EIA by assessing the efficacy of a calcium antagonist.

    Main Methods:

    • A single-blind trial involving ten patients with EIA.
    • Comparison of inhaled verapamil (3 mg), sodium cromoglycate (12 mg), and saline (control).
    • Assessment of maximal percentage fall in forced expiratory volume in one second (FEV1) after standardized treadmill exercise.

    Main Results:

    • Saline inhalation resulted in a significant fall in FEV1 (45.4%).
    • Both sodium cromoglycate (18.4% fall) and verapamil (16.7% fall) significantly attenuated exercise-induced bronchoconstriction compared to saline.
    • The protective effects of verapamil and sodium cromoglycate were comparable and statistically significant (p<0.01 and p<0.02, respectively).

    Conclusions:

    • Inhaled verapamil and sodium cromoglycate demonstrate comparable efficacy in preventing exercise-induced bronchoconstriction.
    • The findings support the hypothesis that calcium-dependent mediator release plays a crucial role in EIA.
    • Calcium antagonists, like verapamil, may offer a therapeutic strategy for managing EIA by blocking calcium channels.

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