Assessment of changes in airway calibre I. Tests of forced expiration.

Pride, N. B.

doi:10.1111/j.1365-2125.1979.tb01002.x

Cited by 32 publications

(16 citation statements)

References 47 publications

(33 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This has become widely used as a proposed test of small airway function (McCarthy, Spencer, Greene & Milic-Emili, 1972;Collins, 1973) and can be measured either (a) as an extension of the single breath oxygen test or (b) by a bolus technique. The value of having such a test of the small airways lies in the difficulty of locating the main site of abnormality in patients with airways obstruction which was emphasized earlier in this series (Pride, 1979). There is some evidence that at least in chronic airways obstruction associated with bronchitis and emphysema the main pathological obstruction is situated peripherally (Hogg, Macklem & Thurlbeck, 1968;Niewoehner & Kleinerman, 1974).…”

Section: Distribution Of Ventilationmentioning

confidence: 97%

Ventilation.

Sterling¹

1979

Brit J Clinical Pharma

View full text Add to dashboard Cite

Section: Distribution Of Ventilationmentioning

confidence: 97%

Ventilation.

Sterling¹

1979

Brit J Clinical Pharma

View full text Add to dashboard Cite

“…Those who had quit smoking o12 months prior to the study Exposure to ETS The subjects were asked three separate questions about ETS: ''Have you ever been exposed to environmental tobacco smoke at home/at work/ generally in the surroundings?'' The answer alternatives of all three questions were: ''never'', ''yes previously, not any more'' and ''yes, currently'' ETS exposure ever ETS at home or at work, or both, currently or previously ETS exposure present ETS currently at the time of the study at home, at work, or both BHR: bronchial hyperresponsiveness; FEV1: forced expiratory volume in 1 s; FVC: forced vital capacity; MEF50: maximal expiratory flow at 50% of FVC [21]; ETS: environmental tobacco smoke; PD15: provocative dose of histamine inducing a 15% fall in FEV1; % pred: % predicted. In the multivariate analysis, smoking remained as an independent determinant of BHR and marked BHR when co-variates, including impaired lung function and other determinants of BHR that were significant in the univariate analysis, were taken into account ( …”

Section: Definitionsmentioning

confidence: 99%

Dose-dependent association of smoking and bronchial hyperresponsiveness

et al. 2013

View full text Add to dashboard Cite

Our aim was to study the association of smoking habits and environmental tobacco smoke (ETS) exposure with bronchial hyperresponsiveness (BHR).A random sample of 292 adults was examined using a structured interview, spirometry, skin prick tests, exhaled nitric oxide fraction (FeNO) and bronchial histamine challenge.A large majority of subjects with BHR were smokers or ex-smokers. Starting to smoke before 20 years of age was significantly associated with BHR, as was current smoking, quantity of smoking and ETS exposure. The severity of BHR increased significantly with increasing pack-years of exposure (p,0.001). Current smokers with decreased lung function were at a particularly high risk of BHR. Impaired forced expiratory volume in 1 s and mean maximal expiratory flow were independent determinants for more severe BHR, regardless of age. In multivariate analysis, smoking remained an independent determinant for BHR after adjustment for impaired lung function and other covariates: o15 pack-years yielded an odds ratio of 3.00 (95% CI 1.33-6.76) for BHR. The association between BHR and FeNO was dependent on smoking habits.The results indicate that smoking is a significant risk factor for BHR, with a dose-dependent pattern, and that the severity of BHR increases with pack-years. The findings strongly suggest assessment of smoking habits in subjects with BHR. @ERSpublications Bronchial hyperresponsiveness is dose-dependently linked to smoking; severity increases with pack-years

show abstract

“…It has been suggested that the measurements Vmax30 and sGaw reflect dimensions of the airways at different levels in the bronchial tree, Vmax3o comprising a major small airway component (17) and sGaw a large component being derived from the more proximal airways (18). The greater potency of inhaled 9a,1 Ij3-PGF2 and PGD2, when compared with histamine was of similar magnitude irrespective of whether sGaw, FEVy, or Vmax3o were used to measure airway caliber.…”

Section: Discussionmentioning

confidence: 99%

9 alpha,11 beta-prostaglandin F2, a novel metabolite of prostaglandin D2 is a potent contractile agonist of human and guinea pig airways.

Beasley¹,

Robinson²,

Featherstone³

et al. 1987

J. Clin. Invest.

View full text Add to dashboard Cite

Prostaglandin (PG) D2, the predominant prostanoid released from activated mast cells in humans is initially metabolized by reduction of the C-1l keto function to yield 9a,11,6-PGF2. In this study the airway effects of 9a,11t-PGF2 were compared with those of its epimer 9a,11a-PGF2 (PGF2.) and PGD2.9a,11( -PGF2 was a potent contractile agonist of isolated guinea pig trachea and 4-mm human airways in vitro; the potencies of the PMs relative to PGD2 (= 1.00) being 0.65 (NS) and 4.08-(P < 0.001) for 9a,11ft-PGF2, and 0.52 (P < 0.01) and 2.40 (P < 0.001) for PGF2., respectively. When inhaled by asthmatic subjects, 9a,1fj-PGF2 was a potent bronchoconstrictor agent, being approximately equipotent with PGD2 and 28-32 times more potent than histamine (P < 0.01). These studies suggest that 9a,11B-PGF2 is at least equipotent with PGD2 as a bronchoconstrictor agonist, and in being a major metabolite of PGD2, could contribute to the bronchoconstrictor effect of this mast cell-derived mediator in asthma.

show abstract

Assessment of changes in airway calibre I. Tests of forced expiration.

Cited by 32 publications

References 47 publications

Ventilation.

Ventilation.

Dose-dependent association of smoking and bronchial hyperresponsiveness

9 alpha,11 beta-prostaglandin F2, a novel metabolite of prostaglandin D2 is a potent contractile agonist of human and guinea pig airways.

Contact Info

Product

Resources

About