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Characterisation of bronchoconstrictor responses to sodium metabisulphite aerosol in atopic subjects with and without asthma.
Thorax. 1989 Dec; 44(12):1009-14.T

Abstract

Inhalation of sodium metabisulphite is thought to induce bronchoconstriction by release of sulphur dioxide. We sought to establish the reproducibility of the airway response to inhaled sodium metabisulphite given in increasing doubling concentrations (0.3 to 160 mg/ml) to 13 asthmatic and five atopic non-asthmatic subjects and the contribution of cholinergic mechanisms to this response. In 15 of the 18 subjects bronchoconstriction was sufficient to allow calculation of the dose of metabisulphite causing a 20% reduction in the forced expiratory volume in one second (FEV1) from baseline values (PD20 metabisulphite). The 95% confidence limit for the difference between this and a second PD20 metabisulphite determined 2-14 days later was 2.5 doubling doses. The difference between repeat PD20 metabisulphite measurements was unrelated to the number of days between challenges or change in baseline FEV1. Ten subjects returned for a third study 3-120 days after the second challenge; variability in PD20 metabisulphite did not differ from that seen between the first and second challenges. PD20 methacholine was determined between the two metabisulphite challenges and found to correlate with PD20 metabisulphite (r = 0.71). Inhaled ipratropium bromide 200 micrograms given in a randomised, placebo controlled, crossover study to 10 subjects increased PD20 methacholine 42 fold but had no significant effect on the response to metabisulphite. A single inhalation of the PD20 metabisulphite in five subjects induced maximal bronchoconstriction 2-3 minutes after inhalation, with a plateau in FEV1 lasting a further four minutes before recovery. A further single inhalation of the same PD20 dose 43 minutes later produced a 27% (SEM 4%) smaller fall in FEV1 than the first inhalation. These results show that metabisulphite PD20 values measured over days and weeks show similar reproducibility to those reported for histamine inhalation and that PD20 metabisulphite correlates with methacholine responsiveness. Most of the bronchoconstriction is not inhibited by antimuscarinic agents; the underlying mechanisms require further investigation.

Authors+Show Affiliations

Department of Thoracic Medicine, National Heart and Lung Institute, Brompton Hospital, London.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Clinical Trial
Journal Article
Randomized Controlled Trial

Language

eng

PubMed ID

2533410

Citation

Nichol, G M., et al. "Characterisation of Bronchoconstrictor Responses to Sodium Metabisulphite Aerosol in Atopic Subjects With and Without Asthma." Thorax, vol. 44, no. 12, 1989, pp. 1009-14.
Nichol GM, Nix A, Chung KF, et al. Characterisation of bronchoconstrictor responses to sodium metabisulphite aerosol in atopic subjects with and without asthma. Thorax. 1989;44(12):1009-14.
Nichol, G. M., Nix, A., Chung, K. F., & Barnes, P. J. (1989). Characterisation of bronchoconstrictor responses to sodium metabisulphite aerosol in atopic subjects with and without asthma. Thorax, 44(12), 1009-14.
Nichol GM, et al. Characterisation of Bronchoconstrictor Responses to Sodium Metabisulphite Aerosol in Atopic Subjects With and Without Asthma. Thorax. 1989;44(12):1009-14. PubMed PMID: 2533410.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Characterisation of bronchoconstrictor responses to sodium metabisulphite aerosol in atopic subjects with and without asthma. AU - Nichol,G M, AU - Nix,A, AU - Chung,K F, AU - Barnes,P J, PY - 1989/12/1/pubmed PY - 1989/12/1/medline PY - 1989/12/1/entrez SP - 1009 EP - 14 JF - Thorax JO - Thorax VL - 44 IS - 12 N2 - Inhalation of sodium metabisulphite is thought to induce bronchoconstriction by release of sulphur dioxide. We sought to establish the reproducibility of the airway response to inhaled sodium metabisulphite given in increasing doubling concentrations (0.3 to 160 mg/ml) to 13 asthmatic and five atopic non-asthmatic subjects and the contribution of cholinergic mechanisms to this response. In 15 of the 18 subjects bronchoconstriction was sufficient to allow calculation of the dose of metabisulphite causing a 20% reduction in the forced expiratory volume in one second (FEV1) from baseline values (PD20 metabisulphite). The 95% confidence limit for the difference between this and a second PD20 metabisulphite determined 2-14 days later was 2.5 doubling doses. The difference between repeat PD20 metabisulphite measurements was unrelated to the number of days between challenges or change in baseline FEV1. Ten subjects returned for a third study 3-120 days after the second challenge; variability in PD20 metabisulphite did not differ from that seen between the first and second challenges. PD20 methacholine was determined between the two metabisulphite challenges and found to correlate with PD20 metabisulphite (r = 0.71). Inhaled ipratropium bromide 200 micrograms given in a randomised, placebo controlled, crossover study to 10 subjects increased PD20 methacholine 42 fold but had no significant effect on the response to metabisulphite. A single inhalation of the PD20 metabisulphite in five subjects induced maximal bronchoconstriction 2-3 minutes after inhalation, with a plateau in FEV1 lasting a further four minutes before recovery. A further single inhalation of the same PD20 dose 43 minutes later produced a 27% (SEM 4%) smaller fall in FEV1 than the first inhalation. These results show that metabisulphite PD20 values measured over days and weeks show similar reproducibility to those reported for histamine inhalation and that PD20 metabisulphite correlates with methacholine responsiveness. Most of the bronchoconstriction is not inhibited by antimuscarinic agents; the underlying mechanisms require further investigation. SN - 0040-6376 UR - https://www.unboundmedicine.com/medline/citation/2533410/Characterisation_of_bronchoconstrictor_responses_to_sodium_metabisulphite_aerosol_in_atopic_subjects_with_and_without_asthma_ L2 - https://thorax.bmj.com/lookup/pmidlookup?view=long&pmid=2533410 DB - PRIME DP - Unbound Medicine ER -