Cold-induced bronchospasm in normal and sensitized rabbits

Jammes, Yves; Barthélémy, Pierre; Fornaris, M; Grimaud, C

doi:10.1016/0034-5687(86)90101-5

Cited by 23 publications

(8 citation statements)

References 26 publications

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“…In the esophagus and stomach, these receptors are well suited for monitoring the temperature of ingested materials. Furthermore, breathing cold air can also trigger protective vagal reflexes, such as cold-induced bronchospasm, cough, and hypoapnea (Jammes et al, 1986;Orani et al, 1991). Visceral thermoreceptors are also thought to play an important role in the regulation of body temperature (Steiner et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

TRPA1 Channels Mediate Cold Temperature Sensing in Mammalian Vagal Sensory Neurons: Pharmacological and Genetic Evidence

Fajardo

Meseguer²,

Belmonte³

et al. 2008

J. Neurosci.

146

118

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Section: Introductionmentioning

confidence: 99%

TRPA1 Channels Mediate Cold Temperature Sensing in Mammalian Vagal Sensory Neurons: Pharmacological and Genetic Evidence

Fajardo

Meseguer²,

Belmonte³

et al. 2008

J. Neurosci.

146

118

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“…The fact that NK-receptor antagonists do not abolish AIB in guinea-pigs [69] suggests that other mediators or mechanisms account for the residual component in this model. The magnitude of AIB (measured as an increase over baseline resistance) elicited from guinea-pigs hyperventilated with hyperoxic gas [6,15] tends to be markedly greater than that reported for either this species [7,52], or other species [8,9,12,13], hyperventilated with normoxic gas ( fig. 1).…”

Section: Calcium Antagonistsmentioning

confidence: 73%

Models and mechanisms of exercise-induced asthma

An¹

1995

Eur Respir J

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M Mo od de el ls s a an nd d m me ec ch ha an ni is sm ms s o of f e ex xe er rc ci is se e--i in nd du uc ce ed d a as st th hm ma a A.N. FreedModels and mechanisms of exercise-induced asthma. A.N. Freed. ERS Journals Ltd 1995. ABSTRACT: Airflow-induced bronchoconstriction (AIB) in mammals can be broadly categorized as either vagal-dependent or vagal-independent. Among mammals, rabbits and cats belong to the former and guinea-pigs belong to the latter categories. Although insufficient data are available to classify monkeys, dogs and man appear to occupy the middle ground in which a small but significant parasympathetic component modulates airflow-induced bronchoconstriction. The fact that vagal activity can only partially account for airflow-induced bronchoconstriction in some asthmatic subjects suggests that vagal-dependent models may be of limited value in studying the human condition, but should prove valuable in elucidating the parasympathetic component of this mechanism. Although airflow-induced bronchoconstriction appears to be remarkably similar in guinea-pigs, dogs and humans, there are important differences concerning the potential role of specific mediators in producing airflow limitation. Concordant data from animal models and man suggest that: 1) airflow-induced bronchoconstriction is a basic mammalian response to airway desiccation; 2) airway drying stimulates and cooling inhibits this response; 3) hyperpnoea with dry air may damage the bronchial mucosa and contribute to this response; 4) biochemical mediators contribute to the development of this response; 5) vascular engorgement and airway oedema do not appear to be the primary effectors of this response, and in fact may antagonize it; 6) airway smooth muscle constriction is involved in the production of airflow-induced bronchoconstriction, and airway oedema may enhance its effect; and 7) airway and vascular responses to dehydration may protect against acute dry air-induced mucosal injury.Finally, although one must be cautious in extrapolating results from animals to humans, the similarities that do exist suggest that the investigation of airflow-induced bronchoconstriction in carefully selected animal models will continue to provide new insights concerning its development in humans.

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“…In animal models, there are a number of studies focused on eucapnic hyperventilation and airway drying (possible associated triggers of EIB) and AHR (e.g., 18,28,34). However, this is one of the few studies to examine clinically detectable airway responses and lung cytokine, leukocyte, and mediator responses to a brief exercise or allergic challenge in rats at a time interval (10 min postchallenge) that mimics the phenomenon of EIB in humans (59).…”

Section: Discussionmentioning

confidence: 97%

A rat model of exercise-induced asthma: a nonspecific response to a specific immunogen

Kodesh¹,

Zaldivar²,

Schwindt³

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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Exercise-induced bronchoconstriction (EIB) is common; however, key aspects of its pathogenesis are still unclear. We investigated the feasibility of adapting an established animal model of asthma to investigate the earliest stages of EIB. The hypothesis was that a single exposure to a normally innocuous, and brief, exercise challenge could trigger EIB symptoms in rats previously sensitized to ovalbumin (OVA) but otherwise unchallenged. Brown-Norway rats were sensitized by intraperitoneal injection of OVA at 0 and 2 wk. At week 3, animals were exposed to either aerosolized OVA (SS) or exercise (EXS). A trained, blinded, clinical observer graded EIB by respiratory sounds. Plasma and lung cytokine levels were analyzed. No control rats with or without exercise (EX, CON) showed evidence of EIB. Eighty percent of the SS group demonstrated abnormal breath sounds upon exposure to aerosolized OVA. Approximately 30% of EXS rats sensitized to OVA but exposed only to exercise had abnormal breath sounds. Lung tissue levels of TNF-α, IL-1α, growth-related oncogene/keratinocyte/chemoattractant, and IFN-γ were significantly higher (P < 0.001) in the SS group, relative to all other groups. Changes in most of these cytokines were not notable in the EXS rats, suggesting a different mechanism of EIB. Remarkably, IFN-γ, but not the other cytokines measured, was significantly elevated following brief exercise in both sensitized and unsensitized rats. Exercise led to detectable breathing sound abnormalities in sensitized rats, but less severe than those observed following classical OVA challenge. Precisely how this immune crossover occurs is not known, but this model may be useful in elucidating essential mechanisms of EIB.

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Cold-induced bronchospasm in normal and sensitized rabbits

Cited by 23 publications

References 26 publications

TRPA1 Channels Mediate Cold Temperature Sensing in Mammalian Vagal Sensory Neurons: Pharmacological and Genetic Evidence

TRPA1 Channels Mediate Cold Temperature Sensing in Mammalian Vagal Sensory Neurons: Pharmacological and Genetic Evidence

Models and mechanisms of exercise-induced asthma

A rat model of exercise-induced asthma: a nonspecific response to a specific immunogen

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