Changes in neuroreceptor function of tracheal smooth muscle following acute ozone exposure of guinea pigs

Hoof, H.J.M. van; Voss, Hans–Peter; Krämer, K.; Boere, A. John F.; Dormans, J. A. M. A.; Bree, L. van; Bast, Aalt

doi:10.1016/s0300-483x(96)03603-7

Cited by 7 publications

(3 citation statements)

References 42 publications

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“…In cervical tracheas, the ic 50 and maximum relaxation caused by ISO were not affected by O 3 compared with air-exposed preparations (Fig. 1a).…”

Section: Resultsmentioning

confidence: 88%

“…Only a few of them try to explain the phenomenon through a derangement of relaxation pathways. [2][3][4] In guinea pig trachea, airway smooth-muscle relaxation is controlled by both adrenergic and non-adrenergic non-cholinergic pathways. 5 Mediators involved in these pathways include epinephrine and norepinephrine, as well as nitric oxide and vasoactive intestinal peptide, respectively.…”

Section: Introductionmentioning

confidence: 99%

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Ozone induces impairment of adrenergic relaxation in thoracic guinea pig tracheas

Sommer

Vargas

Campos

et al. 2001

J of Applied Toxicology

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The effect of ozone on airway relaxation mechanisms has been seldom studied. We exposed guinea pigs to ozone (0.3, 0.6 or 1.2 ppm for 4 h) and studied the in vitro tracheal responses to isoproterenol and nitroprusside, looking for differences between cervical and thoracic regions. We found that ozone did not alter responses to nitroprusside, whereas it produced a concentration-dependent decrease in the responses to isoproterenol in thoracic but not cervical tracheas. Thus, in isolated organ studies care should be taken to avoid mixing cervical and thoracic tracheal regions, at least when adrenergic responses are to be evaluated.

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“…In cervical tracheas, the ic 50 and maximum relaxation caused by ISO were not affected by O 3 compared with air-exposed preparations (Fig. 1a).…”

Section: Resultsmentioning

confidence: 88%

Section: Introductionmentioning

confidence: 99%

Ozone induces impairment of adrenergic relaxation in thoracic guinea pig tracheas

Sommer

Vargas

Campos

et al. 2001

J of Applied Toxicology

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“…The mechanisms underlying this phenomenon are also documented in the literature, including O 3 -induced elevated oxidative products (33,34); increased cholinergic neurotransmission (30,35); and direct stimulation of the airway sensory nerve (36). Although worldwide agreement has been reached in that O 3 can increase the airway smooth muscle contraction of various species (37)(38)(39), it is not clear whether O 3 can similarly influence an "irritated" airway smooth muscle in an experimental asthma model. Kierstein, S. and colleagues exposed their Aspergillus fumigatus-sensitized/-challenged mice to 3 ppm O 3 for 3 h, 82 h after the last challenge, and found that O 3 increased the P enh reaction to the agonist in both the control and asthma groups, but exclusively enhanced the contractility of the tracheal smooth muscle ring of the latter.…”

Section: Discussionmentioning

confidence: 99%

Consequences of acute ozone exposure imposed on the culminated allergic pulmonary inflammation in an established murine model of asthma

Bao

Li²,

Li³

et al. 2013

Front Biosci

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Asthma exacerbations are often triggered by air pollution, including O3, whereas how patients with asthma exacerbations react to high levels of ambient ozone remain unknown. Here, we investigated the manner in which acute ozone exposure affects the pathophysiological characteristics of an asthma model on the premise of culminated allergic airway inflammation. The asthma model was constructed in mice, and enhanced pause (Penh), total and differential cell number, soluble mediator concentration, histopathology, and Muc5ac mRNA expression in the mice were observed. The results showed that ozone could induce airway hyperresponsiveness (AHR) in controls and an additional enhancement of preexisting AHR in asthmatic mice. When exposed to ozone, the asthmatic mice expressed more neutrophils, TNF-α, IL-13, and hyaluronan in bronchoalveolar lavage than controls. The mice with asthma and the controls both showed decreased epithelial cell density in the proximal and distal airways. Ozone aggravated the increased mucus production and mucin gene expression in mice with asthma. These results show that subjects with asthma may react differently to the same high level of ambient ozone, especially for those with asthma exacerbations.

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Ozone Exposure may Enhance Airway Smooth Muscle Contraction by Increasing Ca2+ Refilling of Sarcoplasmic Reticulum in Guinea Pig

Yoshida

Aizawa

Inoue

et al. 2002

Pulmonary Pharmacology & Therapeutics

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Changes in neuroreceptor function of tracheal smooth muscle following acute ozone exposure of guinea pigs

Cited by 7 publications

References 42 publications

Ozone induces impairment of adrenergic relaxation in thoracic guinea pig tracheas

Ozone induces impairment of adrenergic relaxation in thoracic guinea pig tracheas

Consequences of acute ozone exposure imposed on the culminated allergic pulmonary inflammation in an established murine model of asthma

Ozone Exposure may Enhance Airway Smooth Muscle Contraction by Increasing Ca2+ Refilling of Sarcoplasmic Reticulum in Guinea Pig

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