Tags

Type your tag names separated by a space and hit enter

The leukotriene receptor antagonist zafirlukast inhibits sulfur dioxide-induced bronchoconstriction in patients with asthma.
Am J Respir Crit Care Med. 1997 Dec; 156(6):1725-30.AJ

Abstract

Inhalation of sulfur dioxide (SO2) causes bronchoconstriction in most people with asthma. To examine the role of leukotrienes in this response, the antagonism of SO2-induced bronchoconstriction by a single oral dose of the leukotriene receptor antagonist zafirlukast was assessed in a double-blind, placebo-controlled, two-period crossover trial in 12 subjects with mild-to-moderate asthma. Subjects had bronchial hyperresponsiveness, an FEV1 < or = 70% of predicted, and a positive response to inhaled SO2 (an 8-unit increase in specific airway resistance on inhaling an SO2 concentration of < or = 4 ppm (PC8SRaw). Subjects were treated with zafirlukast (20 mg) or placebo on two treatment days 5 to 14 d apart. Two and 10 hours after treatment, subjects inhaled SO2 (0.25, 0.5, 1.0, 2.0, 4.0, and 8.0 ppm) during eucapnic hyperventilation at 20 L/min. PC8SRaw was determined after each challenge. Blood samples were collected to assess zafirlukast plasma concentrations versus effect. PC8SRaw was significantly higher 2 h after zafirlukast compared with placebo (3.1 versus 1.5 ppm; p = 0.02) and remained higher 10 h after treatment with zafirlukast (2.7 versus 1.9 ppm; p = 0.09). An association was found between zafirlukast plasma concentrations and increases in PC8SRaw 10 h after treatment (p = 0.001). The safety profile of zafirlukast was not clinically different from placebo. A single 20-mg dose of zafirlukast attenuated SO2-induced bronchoconstriction. We conclude that S02-induced bronchoconstriction involves release of leukotrienes and that treatment with zafirlukast attenuates the bronchoconstrictor response.

Authors+Show Affiliations

Cardiovascular Research Institute, University of California, San Francisco, California 94143-0111, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Clinical Trial
Journal Article
Randomized Controlled Trial

Language

eng

PubMed ID

9412547

Citation

Lazarus, S C., et al. "The Leukotriene Receptor Antagonist Zafirlukast Inhibits Sulfur Dioxide-induced Bronchoconstriction in Patients With Asthma." American Journal of Respiratory and Critical Care Medicine, vol. 156, no. 6, 1997, pp. 1725-30.
Lazarus SC, Wong HH, Watts MJ, et al. The leukotriene receptor antagonist zafirlukast inhibits sulfur dioxide-induced bronchoconstriction in patients with asthma. Am J Respir Crit Care Med. 1997;156(6):1725-30.
Lazarus, S. C., Wong, H. H., Watts, M. J., Boushey, H. A., Lavins, B. J., & Minkwitz, M. C. (1997). The leukotriene receptor antagonist zafirlukast inhibits sulfur dioxide-induced bronchoconstriction in patients with asthma. American Journal of Respiratory and Critical Care Medicine, 156(6), 1725-30.
Lazarus SC, et al. The Leukotriene Receptor Antagonist Zafirlukast Inhibits Sulfur Dioxide-induced Bronchoconstriction in Patients With Asthma. Am J Respir Crit Care Med. 1997;156(6):1725-30. PubMed PMID: 9412547.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The leukotriene receptor antagonist zafirlukast inhibits sulfur dioxide-induced bronchoconstriction in patients with asthma. AU - Lazarus,S C, AU - Wong,H H, AU - Watts,M J, AU - Boushey,H A, AU - Lavins,B J, AU - Minkwitz,M C, PY - 1997/12/31/pubmed PY - 1997/12/31/medline PY - 1997/12/31/entrez SP - 1725 EP - 30 JF - American journal of respiratory and critical care medicine JO - Am J Respir Crit Care Med VL - 156 IS - 6 N2 - Inhalation of sulfur dioxide (SO2) causes bronchoconstriction in most people with asthma. To examine the role of leukotrienes in this response, the antagonism of SO2-induced bronchoconstriction by a single oral dose of the leukotriene receptor antagonist zafirlukast was assessed in a double-blind, placebo-controlled, two-period crossover trial in 12 subjects with mild-to-moderate asthma. Subjects had bronchial hyperresponsiveness, an FEV1 < or = 70% of predicted, and a positive response to inhaled SO2 (an 8-unit increase in specific airway resistance on inhaling an SO2 concentration of < or = 4 ppm (PC8SRaw). Subjects were treated with zafirlukast (20 mg) or placebo on two treatment days 5 to 14 d apart. Two and 10 hours after treatment, subjects inhaled SO2 (0.25, 0.5, 1.0, 2.0, 4.0, and 8.0 ppm) during eucapnic hyperventilation at 20 L/min. PC8SRaw was determined after each challenge. Blood samples were collected to assess zafirlukast plasma concentrations versus effect. PC8SRaw was significantly higher 2 h after zafirlukast compared with placebo (3.1 versus 1.5 ppm; p = 0.02) and remained higher 10 h after treatment with zafirlukast (2.7 versus 1.9 ppm; p = 0.09). An association was found between zafirlukast plasma concentrations and increases in PC8SRaw 10 h after treatment (p = 0.001). The safety profile of zafirlukast was not clinically different from placebo. A single 20-mg dose of zafirlukast attenuated SO2-induced bronchoconstriction. We conclude that S02-induced bronchoconstriction involves release of leukotrienes and that treatment with zafirlukast attenuates the bronchoconstrictor response. SN - 1073-449X UR - https://www.unboundmedicine.com/medline/citation/9412547/The_leukotriene_receptor_antagonist_zafirlukast_inhibits_sulfur_dioxide_induced_bronchoconstriction_in_patients_with_asthma_ L2 - https://www.atsjournals.org/doi/10.1164/ajrccm.156.6.9608006?url_ver=Z39.88-2003&amp;rfr_id=ori:rid:crossref.org&amp;rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -