Central Deposition of Aerosols as a Detemining Factor in Bronchial Responsiveness

Gillett, M K; Briggs, B A; Snashall, P. D.

doi:10.1042/cs071082p

Cited by 2 publications

(2 citation statements)

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“…Thus, WANNER et al [19] showed that some of the inter-subject variability in bronchial responsiveness to inhaled histamine was accounted for by differences in the dose of histamine retained in the airways. With inhaled atropine we have recently demonstrated that the amount of central airway deposition (which is largely determined by the total pulmonary deposition) is a major factor determining the degree of muscarinic antagonism produced by inhaled atropine [20].…”

Section: Discussionmentioning

confidence: 99%

Influence of airway calibre on the intrapulmonary dose and distribution of inhaled aerosol in normal and asthmatic subjects

Chung

Jeyasingh²,

Snashall³

1988

Eur Respir J

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We investigated the relationship between airway calibre and the dose and distribution of inhaled aerosol in ten normal and six asthmatic subjects. Subjects inhaled saline aerosol containing 99mTcO4 delivered from a nebulizer connected to a dosimeter, and the lung fields were scanned with a gamma-camera. Right lung dose (RLD) was calculated as percentage of total dose. Intrapulmonary distribution was measured as penetration index (PI) (peripheral zone counts/central zone counts). Asthmatics had a significantly lower PI than normal subjects and there was a linear relationship between PI and baseline specific airway conductance (sGaw, p less than 0.001), and forced expiratory volume in one second (FEV1, p less than 0.05). After bronchodilatation with salbutamol (delta sGaw 101 +/- 31%, mean +/- SEM), PI increased from 0.73 +/- 0.11 to 1.09 +/- 0.15 (p less than 0.05); after bronchoconstriction with methacholine (delta sGaw 62.6 +/- 2.9%), PI decreased from 1.42 +/- 0.24 to 1.06 +/- 0.22 (p less than 0.05). Changes of PI were correlated with changes in sGaw and FEV1 (n = 20, p less than 0.001) but changes of RLD and changes in airway calibre were not. The distribution of inhaled aerosol, but not the dose, is largely dependent on airway calibre. The differences in PI between normal and asthmatic subjects may at best be explained by the differences in central airway calibre.

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Section: Discussionmentioning

confidence: 99%

Influence of airway calibre on the intrapulmonary dose and distribution of inhaled aerosol in normal and asthmatic subjects

Chung

Jeyasingh²,

Snashall³

1988

Eur Respir J

View full text Add to dashboard Cite

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“…Our subsequent studies have quantified aerosol deposition in the bronchi using the same apparatus and inhalation technique as in the present experiments. In normal and asthmatic subjects similar proportions of inhaled drug reach the tracheobronchial tree but in asthma deposition tends to be patchy and more central [13]. The degree of uneveness of deposition correlated positively with atropine (DR -1).…”

Section: Discussionmentioning

confidence: 94%

Measurement of pharmacological antagonism produced by atropine in bronchi of normal and asthmatic subjects

Gillett¹,

Snashall²

1988

Eur Respir J

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The bronchial response of six normal and six asthmatic subjects to increasing concentrations of methacholine aerosol was measured by serial measurements of specific airways conductance (sGaw) in a body plethysmograph. On separate days, the subjects were premedicated with 0.9% NaCl, inhaled atropine at four different doses, or intravenous atropine at two different doses. Cumulative log dose-response curves were constructed. The provocative dose of methacholine needed to cause a 35% fall in sGaw was measured from each curve (PD35). The antagonism produced by a given atropine dose was quantified as the dose ratio, which was defined as the ratio of PD35 after atropine to PD35 after saline. In normal subjects, approximately equal amounts of atropine given by the inhaled or intravenous routes produced mean dose ratios of almost identical value. However, in asthmatic subjects inhaled atropine (1.28 mg, 4.4 mumol) produced a mean dose ratio 7.5 times greater than the mean value seen with intravenous atropine (1.0 mg, 3.46 mumol). Intravenous atropine (1.0 mg, 3.46 mumol) produced a mean dose ratio of 18.3 for all subjects, compared to a value of 26 predicted from in vitro experiments. The slope of the regression line for the relationship of log (dose ratio -1) vs -log atropine dose (Schild plot) for all subjects was -0.99. The actions we have observed are compatible with the main actions of atropine being that of a competitive antagonist at the muscarinic receptor. The greater blocking effect of inhaled atropine in some asthmatics suggests that a higher concentration of atropine is achieved at the muscarinic receptor by the inhaled route in these subjects.

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Central Deposition of Aerosols as a Detemining Factor in Bronchial Responsiveness

Cited by 2 publications

References 0 publications

Influence of airway calibre on the intrapulmonary dose and distribution of inhaled aerosol in normal and asthmatic subjects

Influence of airway calibre on the intrapulmonary dose and distribution of inhaled aerosol in normal and asthmatic subjects

Measurement of pharmacological antagonism produced by atropine in bronchi of normal and asthmatic subjects

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