Chest · 2001
Anti-inflammatory and lung function effects of montelukast in asthmatic volunteers exposed to sulfur dioxide.
Клиническое исследованиеСтатьяРандомизированное исследованиеПоддержка исследования: вне правительства СШАПоддержка правительства СШАПоддержка службы здравоохранения СШАНазвание и аннотация: Перевод в очереди
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Gong H, Linn W S, Terrell S L, Anderson K R, Clark K W
Аннотация
BACKGROUND: Sulfur dioxide (SO(2)) gas may induce acute asthmatic responses when inhaled by individuals in the setting of community or occupational air pollution during exercise. Some asthma medications mitigate the SO(2) response, which is not fully understood but appears to involve multiple mechanisms.
OBJECTIVE: We tested the hypothesis that pretreatment with the cysteinyl-leukotriene inhibitor montelukast sodium protects against the inflammatory and bronchoconstrictive effects of SO(2) in the airways of asthmatic subjects.
METHODS: Asthmatic volunteers (enrolled, 12 subjects; completed study, 11 subjects) were exposed to 0.75 ppm SO(2) for 10-min periods during exercise (mean ventilation, 35 L/min) and were exposed similarly to filtered air (control condition) after double-blinded pretreatments with montelukast (10 mg/d for 3 days) and placebo.
RESULTS: After montelukast pretreatment, specific airways resistance, FEV(1), symptoms, and eosinophil counts in induced sputum showed statistically and clinically significant improvements in preexposure measurements and/or decreased responses to SO(2) exposure or exercise. The mean FEV(1) immediately after exposure was 95% of baseline FEV(1) with montelukast pretreatment vs 82% with placebo.
CONCLUSION: Montelukast significantly protects against airways eosinophilic inflammation and bronchoconstriction from SO(2) exposure during exercise. This implies a role for leukotrienes in SO(2)-induced lung effects.
OBJECTIVE: We tested the hypothesis that pretreatment with the cysteinyl-leukotriene inhibitor montelukast sodium protects against the inflammatory and bronchoconstrictive effects of SO(2) in the airways of asthmatic subjects.
METHODS: Asthmatic volunteers (enrolled, 12 subjects; completed study, 11 subjects) were exposed to 0.75 ppm SO(2) for 10-min periods during exercise (mean ventilation, 35 L/min) and were exposed similarly to filtered air (control condition) after double-blinded pretreatments with montelukast (10 mg/d for 3 days) and placebo.
RESULTS: After montelukast pretreatment, specific airways resistance, FEV(1), symptoms, and eosinophil counts in induced sputum showed statistically and clinically significant improvements in preexposure measurements and/or decreased responses to SO(2) exposure or exercise. The mean FEV(1) immediately after exposure was 95% of baseline FEV(1) with montelukast pretreatment vs 82% with placebo.
CONCLUSION: Montelukast significantly protects against airways eosinophilic inflammation and bronchoconstriction from SO(2) exposure during exercise. This implies a role for leukotrienes in SO(2)-induced lung effects.