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H2‐receptor blockade and exercise‐induced asthma.
Author(s) -
Nogrady SG,
Hahn AG
Publication year - 1984
Publication title -
british journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.216
H-Index - 146
eISSN - 1365-2125
pISSN - 0306-5251
DOI - 10.1111/j.1365-2125.1984.tb02545.x
Subject(s) - bronchoconstriction , cimetidine , placebo , medicine , exercise induced asthma , asthma , blockade , anesthesia , vital capacity , ventilation (architecture) , lung function , receptor , lung , mechanical engineering , alternative medicine , pathology , diffusing capacity , engineering
While in vitro studies suggest that H2‐receptor blockade enhances mediator release from bronchial mast cells and leads to bronchoconstriction, in vivo studies have given conflicting results. Eight asthmatic subjects were given cimetidine 800 mg and placebo double‐blind on different days. Baseline values of forced expiratory volume in one second (FEV1) were obtained before an 8 min standardized exercise test using a bicycle ergometer. Subjects inhaled cold, dry air and exercise on cimetidine and placebo days was matched for ventilation and thermal load. FEV1 was measured immediately, 5, 10, 15, and 20 min after exercise. No significant differences were observed between mean baseline FEV1, immediate post exercise FEV1, or maximum percentage fall from baseline after exercise on cimetidine or placebo days. Cimetidine does not appear to effect lung function or bronchial responses to cold air exercise challenge.