Mechanism of bronchoconstriction during inhalation of sulfur dioxide

Nadel, Jay A.; Salem, Harry; Tamplin, B.; Tokiwa, Y.

doi:10.1152/jappl.1965.20.1.164

Cited by 232 publications

(79 citation statements)

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“…Short-term exposure to NO2 could increase the bronchial tone by releasing histamine, as suggested by Nieding and Krekeler (16), or by stimulating the lung irritant receptors (17). Vagally mediated bronchoconstriction has been demonstrated for S02 (18), and the irritant receptors are thought to be hypersensitive in asthma (5). Such an increase in bronchial tone by N02 would explain the enhanced effect of carbachol since interaction between a bronchoconstrictor agent and increased airway tone would result in a potentiation of the effect of the bronchoconstrictor agent (19).…”

Section: Discussionmentioning

confidence: 89%

Effect of short-term, low-level nitrogen dioxide exposure on bronchial sensitivity of asthmatic patients.

Orehek¹,

Massari²,

Gayrard³

et al. 1976

J. Clin. Invest.

272

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A B S T R A C T Our purpose was to determine whether exposure to a realistic concentration of nitrogen dioxide (NO2) could increase the bronchial sensitivity of asthmatic patients to bronchoconstrictor agents. We established dose-response curves for changes in specific airway resistance (SRaw) in response to aerosolized carbachol in 20 asthmatics after each had spent 1 h in an exposure chamber breathing on one occasion unpolluted air and on a separate occasion 0.1 ppm N02: sequence of exposures to unpolluted air and to low levels of NO2 were randomized in a single-blind fashion. N02 induced a slight but significant increase in initial SRa. and enhanced the bronchoconstrictor effect of carbachol in 13 subjects: curves were shifted to the left and the mean dose of carbachol producing a twofold increase in initial SRaw was decreased from 0.66 mg to 0.36 mg (P < 0.001). In contrast, NO2 neither modified the initial SRaw nor the bronchoconstrictor effect of carbachol in seven subjects. In 4 out of the 20 subjects, exposure to a higher concentration of NO (0.2 ppm) yielded variable results.Potentiation of the carbachol bronchoconstrictor response by NO2 could not be related to any physical or clinical characteristics of the subjects tested. Although the mechanisms underlying the N02 effect remain controversial, the present results demonstrate that very low levels of NO. can adversely affect some asthmatics.

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Section: Discussionmentioning

confidence: 89%

Effect of short-term, low-level nitrogen dioxide exposure on bronchial sensitivity of asthmatic patients.

Orehek¹,

Massari²,

Gayrard³

et al. 1976

J. Clin. Invest.

272

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“…The mechanisms producing bronchoconstriction in humans are relatively poorly understood, but are thought to involve stimulation of irritant receptors in the upper airway [6]. Atropine has been shown to block SO 2 induced bronchoconstriction in normal adults [7], suggesting a cholinergic re¯ex, but this agent is only partially effective in subjects with asthma [8]. Neither the difference in the sensitivity between asthmatics and normals to SO 2 , nor the differing effects of atropine blockade in these groups have been adequately explained.…”

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confidence: 99%

The effect of sulphur dioxide exposure on indices of heart rate variability in normal and asthmatic adults

Tunnicliffe¹,

Hilton²,

Harrison³

et al. 2001

Eur Respir J

107

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Sulphur dioxide (SO2) is an important air pollutant and causes bronchoconstriction in normal and asthmatic adults. This paper has explored the autonomic consequences of SO2exposure using the spectral analysis of heart rate variability.Electrocardiogram recordings were made in 12 normal and 12 asthmatic adults undergoing pollutant exposures. Exposures were of a 1 h duration, double blind, in random order, ≥2 weeks apart and included air and 200 parts per billion SO2. Spectral analysis of R-R intervals was performed.SO2exposure was associated with an increase in total power (TP) and high (HF) and low frequency (LF) power in the normal subjects, and a reduction in these indices in the subjects with asthma. The difference in TP with SO2exposure compared to air was +1730 ms2in the normal group and −1021 ms2asthmatic group (p<0.003). For HF the respective values were +964 ms2and −539 ms2(p=0.02) and for LF, +43 7 ms2and −57 2 ms2(p=0.01). No change in lung function or symptoms was observed in either group.This suggests that SO2exposure at concentrations which are frequently encountered during air pollution episodes can influence the autonomic nervous system. This may be important in understanding the mechanisms involved in SO2induced bronchoconstriction, and of the cardiovascular effects of air pollution.

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“…The question of the potential roles of the airway epithelial surface in host defence occurred to us in 1960 when we found that cigarette smoke (an environmental pollutant) particles are deposited on the epithelial surface exerting deleterious effects on lung function [5]. The potential roles of the epithelial luminal surface in epithelial defence returned to us a decade later, when we discovered that the community pollutants sulfur dioxide [6] and ozone [7] cause airway narrowing due to smooth muscle contraction.…”

Section: @Erspublicationsmentioning

confidence: 99%

The CFTR and EGFR relationship in airway vascular growth, and its importance in cystic fibrosis

Nadel

2013

Eur Respir J

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Mechanism of bronchoconstriction during inhalation of sulfur dioxide

Cited by 232 publications

References 0 publications

Effect of short-term, low-level nitrogen dioxide exposure on bronchial sensitivity of asthmatic patients.

Effect of short-term, low-level nitrogen dioxide exposure on bronchial sensitivity of asthmatic patients.

The effect of sulphur dioxide exposure on indices of heart rate variability in normal and asthmatic adults

The CFTR and EGFR relationship in airway vascular growth, and its importance in cystic fibrosis

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