Lack of effect from a single cigarette challenge on bronchial responsiveness in healthy non-smoking subjects.

Suzuki, Shunsuke; Sano, F; Suzuki, Junnichi; Numata, Hiroaki; Ōkubo, Takao

doi:10.1136/thx.43.5.401

Cited by 4 publications

(2 citation statements)

References 18 publications

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“…In human nonsmokers, smoking a single cigarette will not increase airway responsiveness [15,25], and airway hyperresponsiveness is not a significant feature in young Fig. 3.…”

Section: Figmentioning

confidence: 99%

Long Term Cigarette Smoke Exposure Does Not Increase Airway Responsiveness in Rats

Wright

Sun

Vedal

1998

Lung

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To ascertain whether chronic cigarette smoke exposure induces increased airway responsiveness, we performed methacholine response tests in Sprague-Dawley rats by calculating pulmonary resistance after nebulization of saline followed by an increasing concentration of methacholine. We also calculated the concentration of methacholine which doubled the baseline resistance (R200). Tests were performed at baseline and after 2, 4, 8, and 12 months of exposure to the smoke of seven cigarettes per day, 5 days each week; control animals were exposed to room air. At the completion of the study, there were 13 rats in the smoke-exposed group and 7 rats remaining in the control group. Airway morphology was assessed using a point counting technique. We found that (1) chronic exposure to cigarette smoke did not alter either the baseline resistance or the R200; (2) the saline baseline resistance decreased over time in the control animals; and (3) at the 12-month time point, smokers with increased baseline airway resistance had greater amounts of airway smooth muscle compared with the smoke-exposed animals without increased resistance. We conclude that in this animal model, long term exposure to cigarette smoke did not alter the response to methacholine but did increase airway smooth muscle and baseline resistance in some but not all animals.

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“…In human nonsmokers, smoking a single cigarette will not increase airway responsiveness [15,25], and airway hyperresponsiveness is not a significant feature in young Fig. 3.…”

Section: Figmentioning

confidence: 99%

Long Term Cigarette Smoke Exposure Does Not Increase Airway Responsiveness in Rats

Wright

Sun

Vedal

1998

Lung

View full text Add to dashboard Cite

show abstract

“…Chronic smokers with mild-tomoderate airflow limitation demonstrate an increased airway responsiveness to inhaled methacholine (33). However, in asymptomatic nonsmokers, smoking a single cigarette does not increase airway responsiveness to methacholine (15,32). In patients with asthma, studies of the effect of acute exposure to passive environmental cigarette smoke have produced conflicting results.…”

mentioning

confidence: 98%

Acute cigarette smoke inhalation blunts lung responsiveness to methacholine and allergen in rabbit: differentiation of central and peripheral effects

Porra

Peták

Strengell

et al. 2010

American Journal of Physiology-Lung Cellular and Molecular Phys

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Despite the prevalence of active smoking in asthmatics, data on the short-term effect of acute mainstream tobacco smoke exposure on airway responsiveness are very scarce. The aim of this study was to assess the immediate effect of acute exposure to mainstream cigarette smoke on airway reactivity to subsequent nonspecific and allergenic challenges in healthy control (n = 5) and ovalbumin-sensitized rabbits (n = 6). We combined low-frequency forced oscillations and synchrotron radiation CT imaging to differentiate central airway and peripheral airway and lung parenchymal components of the response to airway provocation. Acute exposure to smoke generated by four successive cigarettes (CS) strongly inhibited the central airway response to subsequent IV methacholine (MCh) challenge. In the sensitized animals, although the response to ovalbumin was also inhibited in the central airways, mainstream CS did not blunt the peripheral airway response in this group. In additional groups of experiments, exposure to HEPA-filtered CS (n = 6) similarly inhibited the MCh response, whereas CO (10,000 ppm for 4 min, n = 6) or nitric oxide inhalation instead of CS (240 ppm, 4 x 7 min, n = 5) failed to blunt nonspecific airway responsiveness. Pretreatment with alpha-chymotrypsin to inhibit endogenous VIP before CS exposure had no effect (n = 4). Based on these observations, the gas phase of mainstream cigarette smoke may contain one or more short-term inhibitory components acting primarily on central airways and inhibiting the response to both specific and nonspecific airway provocation, but not on the lung periphery where both lung mechanical parameters, and synchrotron-imaging derived parameters, showed large changes in response to allergen challenge in sensitized animals.

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Acute Exposure to Cigarette Smoke Induces Airway Hyperresponsiveness without Airway Inflammation in Guinea Pigs: Dose-Response Characteristics

Nishikawa¹,

Ikeda²,

Fukuda³

et al. 1990

Am Rev Respir Dis

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We examined whether acute exposure to a low dose of cigarette smoke causes an increase in airway responsiveness in guinea pigs and whether the changes in airway responsiveness are accompanied by increased vascular permeability or neutrophil influx in the trachea. Animals were divided into four groups: groups exposed to 5, 10, or 20 puffs of cigarette smoke and a control group. Airway responsiveness was assessed by measuring specific airway resistance (SRaw) as a function of increasing concentration of inhaled methacholine (Mch) aerosol immediately, 5 h, and 24 h after exposure. In parallel studies, tracheal vascular permeability was quantified by measuring the tracheal extravasation of intravenously administered Evans blue dye, and neutrophil influx into the tracheal mucosa was quantified by counting cells within whole mounts of tracheas that were stained with Giemsa. Exposure to 5 puffs of cigarette smoke caused no changes in airway responsiveness. Exposure to 10 puffs induced airway hyperresponsiveness only immediately after exposure. Exposure to 20 puffs induced airway hyperresponsiveness not only immediately but also 5 h after exposure. There was a significant correlation between the dose (puffs) of cigarette smoke and increase in airway responsiveness immediately after exposure (r = 0.77; p less than 0.001). The tracheal extravasation of intravenously administered Evans blue dye and the number of neutrophils in the tracheal mucosa did not differ significantly from the corresponding control values at any time or in any exposed group. Furthermore, none of these changes was observed in the airways distal to the trachea of any animal immediately after exposure to 20 puffs of cigarette smoke.(ABSTRACT TRUNCATED AT 250 WORDS)

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Lack of effect from a single cigarette challenge on bronchial responsiveness in healthy non-smoking subjects.

Cited by 4 publications

References 18 publications

Long Term Cigarette Smoke Exposure Does Not Increase Airway Responsiveness in Rats

Long Term Cigarette Smoke Exposure Does Not Increase Airway Responsiveness in Rats

Acute cigarette smoke inhalation blunts lung responsiveness to methacholine and allergen in rabbit: differentiation of central and peripheral effects

Acute Exposure to Cigarette Smoke Induces Airway Hyperresponsiveness without Airway Inflammation in Guinea Pigs: Dose-Response Characteristics

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