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Inhibition of sodium metabisulphite induced bronchoconstriction by frusemide in asthma: role of cyclooxygenase products.
Thorax. 1994 Apr; 49(4):307-11.T

Abstract

BACKGROUND

Inhaled frusemide inhibits airway responses to sodium metabisulphite and other indirect bronchial challenges in asthma by undetermined mechanisms which may relate to its ability to stimulate prostaglandin release. Inhalation of sodium metabisulphite provokes indirect bronchoconstriction, possibly by activating sensory nerves. To investigate the role of cyclooxygenase products in the airway actions of frusemide and sodium metabisulphite, the effects of a potent cyclooxygenase inhibitor, flurbiprofen, alone and in combination with frusemide were investigated against airway responsiveness to sodium metabisulphite.

METHODS

In a double blind double placebo controlled study, 12 mild asthmatic subjects attended on four occasions to undergo three inhalation challenges with sodium metabisulphite. A baseline challenge was performed one hour before oral intake of flurbiprofen 200 mg or matched placebo, and two hours before inhalation of frusemide 40 mg or matched placebo. A second challenge was performed immediately after inhalation of frusemide (two hours after flurbiprofen) with a further challenge three hours later. The log concentration provoking a 20% fall in FEV1 (log PC20) was used to assess airway responsiveness to sodium metabisulphite.

RESULTS

Frusemide caused an immediate 1.9 doubling dose protection and a lesser 0.7 doubling dose protection at three hours. This protection was enhanced by flurbiprofen at both time points to 2.7 (early) and 1.9 (late) doubling doses. In addition, flurbiprofen alone significantly reduced airway responsiveness to sodium metabisulphite by 1.1 doubling doses at both two and five hours.

CONCLUSIONS

The generation of bronchoprotective prostaglandins is unlikely to underlie the inhibitory action of frusemide against airway responsiveness to sodium metabisulphite. Endogenous contractile prostaglandins within the airways may be involved in the bronchoconstrictor response to sodium metabisulphite.

Authors+Show Affiliations

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

Pub Type(s)

Clinical Trial
Comparative Study
Journal Article
Randomized Controlled Trial
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

8202898

Citation

O'Connor, B J., et al. "Inhibition of Sodium Metabisulphite Induced Bronchoconstriction By Frusemide in Asthma: Role of Cyclooxygenase Products." Thorax, vol. 49, no. 4, 1994, pp. 307-11.
O'Connor BJ, Barnes PJ, Chung KF. Inhibition of sodium metabisulphite induced bronchoconstriction by frusemide in asthma: role of cyclooxygenase products. Thorax. 1994;49(4):307-11.
O'Connor, B. J., Barnes, P. J., & Chung, K. F. (1994). Inhibition of sodium metabisulphite induced bronchoconstriction by frusemide in asthma: role of cyclooxygenase products. Thorax, 49(4), 307-11.
O'Connor BJ, Barnes PJ, Chung KF. Inhibition of Sodium Metabisulphite Induced Bronchoconstriction By Frusemide in Asthma: Role of Cyclooxygenase Products. Thorax. 1994;49(4):307-11. PubMed PMID: 8202898.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Inhibition of sodium metabisulphite induced bronchoconstriction by frusemide in asthma: role of cyclooxygenase products. AU - O'Connor,B J, AU - Barnes,P J, AU - Chung,K F, PY - 1994/4/1/pubmed PY - 1994/4/1/medline PY - 1994/4/1/entrez SP - 307 EP - 11 JF - Thorax JO - Thorax VL - 49 IS - 4 N2 - BACKGROUND: Inhaled frusemide inhibits airway responses to sodium metabisulphite and other indirect bronchial challenges in asthma by undetermined mechanisms which may relate to its ability to stimulate prostaglandin release. Inhalation of sodium metabisulphite provokes indirect bronchoconstriction, possibly by activating sensory nerves. To investigate the role of cyclooxygenase products in the airway actions of frusemide and sodium metabisulphite, the effects of a potent cyclooxygenase inhibitor, flurbiprofen, alone and in combination with frusemide were investigated against airway responsiveness to sodium metabisulphite. METHODS: In a double blind double placebo controlled study, 12 mild asthmatic subjects attended on four occasions to undergo three inhalation challenges with sodium metabisulphite. A baseline challenge was performed one hour before oral intake of flurbiprofen 200 mg or matched placebo, and two hours before inhalation of frusemide 40 mg or matched placebo. A second challenge was performed immediately after inhalation of frusemide (two hours after flurbiprofen) with a further challenge three hours later. The log concentration provoking a 20% fall in FEV1 (log PC20) was used to assess airway responsiveness to sodium metabisulphite. RESULTS: Frusemide caused an immediate 1.9 doubling dose protection and a lesser 0.7 doubling dose protection at three hours. This protection was enhanced by flurbiprofen at both time points to 2.7 (early) and 1.9 (late) doubling doses. In addition, flurbiprofen alone significantly reduced airway responsiveness to sodium metabisulphite by 1.1 doubling doses at both two and five hours. CONCLUSIONS: The generation of bronchoprotective prostaglandins is unlikely to underlie the inhibitory action of frusemide against airway responsiveness to sodium metabisulphite. Endogenous contractile prostaglandins within the airways may be involved in the bronchoconstrictor response to sodium metabisulphite. SN - 0040-6376 UR - https://www.unboundmedicine.com/medline/citation/8202898/Inhibition_of_sodium_metabisulphite_induced_bronchoconstriction_by_frusemide_in_asthma:_role_of_cyclooxygenase_products_ L2 - https://thorax.bmj.com/lookup/pmidlookup?view=long&pmid=8202898 DB - PRIME DP - Unbound Medicine ER -