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Inhibition of hypertonic saline-induced bronchoconstriction by terfenadine and flurbiprofen. Evidence for the predominant role of histamine.
Am Rev Respir Dis 1989; 140(3):593-7AR

Abstract

We investigated the possible inhibitory effects of terfenadine, a histamine H1-receptor antagonist, and flurbiprofen, a cyclooxygenase inhibitor, on the bronchoconstrictor effect of inhaled 3.6% hypertonic saline in a randomized, double-blind study. Nine mildly asthmatic subjects with a history of exercise-induced asthma took part. This was conducted, first as a dose-response study and, second, as a time-course study. In the dose-response study, the provocative dose of saline-laden air causing a 25% fall in FEV1 was calculated (PD25). Terfenadine (180 mg) and the combination of terfenadine (180 mg) plus flurbiprofen (100 mg) both protected significantly against hypertonic saline challenge, achieving increases in PD25 values by factors of 7.24 and 6.30, respectively. Flurbiprofen (100 mg) also displaced the dose-response to the right, increasing the PD25 by a factor of 1.92, but this protection was significantly less than that afforded by terfenadine. In the time-course studies, a single inhalation of hypertonic saline previously shown to cause at least a 25% fall in FEV1 was administered, and FEV1, was followed for 30 min. Preadministration of terfenadine reduced the mean area under the curve of percentage fall in FEV1-time response by 68.5%, with similar results obtained with the combination of terfenadine and flurbiprofen. We conclude that the bronchoconstriction in asthma provoked by inhaled hypertonic saline is mediated predominantly through the hyperosmolar release of histamine from airway mast cells, with a minor contribution being made by prostanoids.

Authors+Show Affiliations

Immunopharmacology Group, Southampton General Hospital, United Kingdom.No affiliation info availableNo affiliation info available

Pub Type(s)

Clinical Trial
Journal Article
Randomized Controlled Trial

Language

eng

PubMed ID

2571320

Citation

Finnerty, J P., et al. "Inhibition of Hypertonic Saline-induced Bronchoconstriction By Terfenadine and Flurbiprofen. Evidence for the Predominant Role of Histamine." The American Review of Respiratory Disease, vol. 140, no. 3, 1989, pp. 593-7.
Finnerty JP, Wilmot C, Holgate ST. Inhibition of hypertonic saline-induced bronchoconstriction by terfenadine and flurbiprofen. Evidence for the predominant role of histamine. Am Rev Respir Dis. 1989;140(3):593-7.
Finnerty, J. P., Wilmot, C., & Holgate, S. T. (1989). Inhibition of hypertonic saline-induced bronchoconstriction by terfenadine and flurbiprofen. Evidence for the predominant role of histamine. The American Review of Respiratory Disease, 140(3), pp. 593-7.
Finnerty JP, Wilmot C, Holgate ST. Inhibition of Hypertonic Saline-induced Bronchoconstriction By Terfenadine and Flurbiprofen. Evidence for the Predominant Role of Histamine. Am Rev Respir Dis. 1989;140(3):593-7. PubMed PMID: 2571320.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Inhibition of hypertonic saline-induced bronchoconstriction by terfenadine and flurbiprofen. Evidence for the predominant role of histamine. AU - Finnerty,J P, AU - Wilmot,C, AU - Holgate,S T, PY - 1989/9/1/pubmed PY - 1989/9/1/medline PY - 1989/9/1/entrez SP - 593 EP - 7 JF - The American review of respiratory disease JO - Am. Rev. Respir. Dis. VL - 140 IS - 3 N2 - We investigated the possible inhibitory effects of terfenadine, a histamine H1-receptor antagonist, and flurbiprofen, a cyclooxygenase inhibitor, on the bronchoconstrictor effect of inhaled 3.6% hypertonic saline in a randomized, double-blind study. Nine mildly asthmatic subjects with a history of exercise-induced asthma took part. This was conducted, first as a dose-response study and, second, as a time-course study. In the dose-response study, the provocative dose of saline-laden air causing a 25% fall in FEV1 was calculated (PD25). Terfenadine (180 mg) and the combination of terfenadine (180 mg) plus flurbiprofen (100 mg) both protected significantly against hypertonic saline challenge, achieving increases in PD25 values by factors of 7.24 and 6.30, respectively. Flurbiprofen (100 mg) also displaced the dose-response to the right, increasing the PD25 by a factor of 1.92, but this protection was significantly less than that afforded by terfenadine. In the time-course studies, a single inhalation of hypertonic saline previously shown to cause at least a 25% fall in FEV1 was administered, and FEV1, was followed for 30 min. Preadministration of terfenadine reduced the mean area under the curve of percentage fall in FEV1-time response by 68.5%, with similar results obtained with the combination of terfenadine and flurbiprofen. We conclude that the bronchoconstriction in asthma provoked by inhaled hypertonic saline is mediated predominantly through the hyperosmolar release of histamine from airway mast cells, with a minor contribution being made by prostanoids. SN - 0003-0805 UR - https://www.unboundmedicine.com/medline/citation/2571320/Inhibition_of_hypertonic_saline_induced_bronchoconstriction_by_terfenadine_and_flurbiprofen__Evidence_for_the_predominant_role_of_histamine_ L2 - http://www.atsjournals.org/doi/full/10.1164/ajrccm/140.3.593?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -