Role of thromboxane-A2 and cholinergic mechanisms in bronchoconstriction induced by cigarette smoke in guinea-pigs

Matsumoto, Koichiro; Aizawa, Hisamichi; Inoue, Hiromasa; Takata, Shotaro; Shigyo, Mutsumi; Hara, N

doi:10.1183/09031936.96.09122468

Cited by 11 publications

(7 citation statements)

References 28 publications

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“…When anaesthetized guinea-pigs were acutely exposed to less diluted smoke through the tracheostomy tube for 10 min, marked bronchoconstriction occurred within a few minutes [41,42]. When exposing animals to more diluted smoke for only 3 min, it did not cause direct bronchoconstriction, but induced significant airway hyperresponsiveness to inhaled histamine [7].…”

Section: Discussionmentioning

confidence: 99%

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Eosinophilic airway inflammation induced by repeated exposure to cigarette smoke

et al. 1998

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Acute exposure to cigarette smoke causes airway hyperresponsiveness (AHR) in guinea-pigs, which resolves within a few hours. Repeated exposure may have a different effect on the airways. To address this question, guinea-pigs were repeatedly exposed to cigarette smoke (six cigarettes for 1 h x day(-1)) for 14 consecutive days. Airway responsiveness to inhaled histamine and differential cell counts in bronchoalveolar lavage fluid (BALF) were evaluated 1 day after the last exposure. Significant neutrophilia in BALF was observed after 3 days of smoke exposure. Significant eosinophilia in BALF and AHR were observed after 14 days of smoke exposure, but not after 3 or 7 days of smoke exposure. These changes persisted until 3 days after the last exposure and resolved 7 days afterwards. Histologically, the recruited eosinophils were observed predominantly in the airways, but not in the alveoli. Treatment with E-6123, a specific platelet-activating factor receptor antagonist (1 mg x kg(-1) x day(-1) p.o. during smoke exposure) significantly inhibited the eosinophil influx and AHR. Repeated exposure to cigarette smoke may induce prolonged airway inflammation and airway hyperresponsiveness in guinea-pigs. Platelet-activating factor or platelet-activating factor-like lipids may play a key role in airway hyperresponsiveness, presumably by the induction of eosinophilic airway inflammation.

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Section: Discussionmentioning

confidence: 99%

“…This study was started based on previous experience about acute exposure models [7,41,42]. When anaesthetized guinea-pigs were acutely exposed to less diluted smoke through the tracheostomy tube for 10 min, marked bronchoconstriction occurred within a few minutes [41,42].…”

Section: Discussionmentioning

confidence: 99%

Eosinophilic airway inflammation induced by repeated exposure to cigarette smoke

et al. 1998

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“…The most advanced theory is certainly that of bronchialinduced inflammation because of an irritant effect of ETS involving the parasympathic receptors or because of direct damage to the respiratory epithelium resulting in an inflammatory-immune process [27,28]. Some studies in vivo demonstrated, in exposed animals [29] or in human smokers [30], greater concentrations of thromboxane A # or neutrophils, macrophages, pro-inflammatory mediators (interleukin-1β and interleukin-6) and chemoattractants (the monocyte chemoattractant protein-1, MCP-1, and the neutrophil chemoattractant, interleukin-8) in the products of bronchoalveolar lavage. Additionally, the concentrations of macrophages, neutrophils, interleukin-1β and interleukin-8 are elevated in a cigarette dose-dependent manner [30].…”

Section: Discussionmentioning

confidence: 98%

Possible interaction between exposure to environmental tobacco smoke and therapy in children with asthma

DUBUS¹,

ODDOZE²,

BADIER³

et al. 1998

Clinical Science

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1. The aim of the study was to determine the carbachol and albuterol responsiveness in treated and untreated asthmatic and allergic children exposed to environmental tobacco smoke assessed by urinary cotinine measurements. 2. Forty-six asthmatic and allergic children with normal spirometric values were recruited. The doubling dose, concentration of carbachol producing a 2-fold increase in specific airway resistance (SRaw) was determined and 200 micrograms of albuterol were administered via a Volumatic(R) spacer. The percentage of bronchodilatation was defined as the difference between the largest obtained SRaw and the post-beta2 SRaw divided by the largest SRaw. Data were compared by a Mann-Whitney U-test. 3. The 23 children with a high urinary cotinine, compared with the 23 children without urinary cotinine, had a decreased doubling dose (108.2+/-14.7 micrograms versus 160.9+/-19.5 micrograms; P=0.04) and an increased percentage of bronchodilatation (74.8+/-1.4% versus 68.8+/-1.8%; P=0.03). A prophylactic anti-inflammatory treatment induced a weaker bronchial reactivity to carbachol and a slightly greater bronchodilatation in children exposed to environmental tobacco smoke. 4. Environmental tobacco smoke increases bronchial reactivity in asthmatic and allergic children. This effect might be reduced by anti-inflammatory therapy. The bronchodilator response may be enhanced in exposed children and may be caused by one or several direct interactions between tobacco smoke compounds and albuterol.

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“…Current smoking among males was associated with wheezing. Inhaling cigarette smoke for at least 15 years has been shown to be capable of inducing acute bronchoconstriction in both animals and humans [Hong et al, ; Hong and Lee, ; Matsumoto et al, ; Chiba et al, ]. Moreover, it has been suggested that simultaneous and persistent exposure to airborne allergens and to smoking may have an additional or synergetic effect on the occurrence of adult‐onset asthma [de Nijs et al, ].…”

Section: Discussionmentioning

confidence: 99%

“…The number of GTS episodes reported in the last year was linearly associated with wheezing in both genders. The action of nicotine inhaled through cigarette smoking on bronchoconstriction and increased mucous production have been widely described in the literature, either as direct action on the lungs or on the central nervous system [Hong et al, ; Hong and Lee, ; Matsumoto et al, ; Maouche et al, ]. However, respiratory risks when harvesting tobacco have not been investigated yet.…”

Section: Discussionmentioning

confidence: 99%

Wheezing in tobacco farm workers in Southern Brazil

Fiori

Fassa

Faria³

et al. 2015

American J Industrial Med

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Background Tobacco workers are exposed to several respiratory occupational sensitizers. Methods A representative cross-sectional study was carried out on 2469 tobacco family farming growers. Gender-stratified multivariate analyses evaluated the association between wheezing and socio-demographic, behavioral and occupational variables. Results Wheezing prevalence was 11.0% with no difference between genders. Among men, age, smoking, strenuous work, pesticide use, contact with vegetable dust and dried tobacco dust, lifting sticks with tobacco leaves to the curing barns and green tobacco sickness (GTS) were risk factors for wheezing. Among women, family history of asthma, tying hands of tobacco, strenuous work, contact with chemical disinfectants and GTS were positively associated with wheezing. Harvesting lower tobacco leaves was a protective factor for the outcome in both genders. Conclusions Pesticides, dusts exposure and GTS were risk factors for wheezing. The synergic effect of these factors needs to be better evaluated to improve prevention.

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Role of thromboxane-A2 and cholinergic mechanisms in bronchoconstriction induced by cigarette smoke in guinea-pigs

Abstract: R Ro ol le e o of f t th hr ro om mb bo ox xa an ne e--These results suggest that the bronchoconstriction induced by cigarette smoke is partially mediated by thromboxane A 2 , which is dependent on a cholinergic pathway.

Cited by 11 publications

References 28 publications

Eosinophilic airway inflammation induced by repeated exposure to cigarette smoke

Eosinophilic airway inflammation induced by repeated exposure to cigarette smoke

Possible interaction between exposure to environmental tobacco smoke and therapy in children with asthma

Wheezing in tobacco farm workers in Southern Brazil

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