Airway effects of respiratory heat loss in normal subjects

O'Cain, C. F.; Dowling, N.; Slutsky, Arthur S.; Hensley, Michael; Strohl, Kingman P.; McFadden, E. R.; Ingram, R. H.

doi:10.1152/jappl.1980.49.5.875

Cited by 87 publications

(33 citation statements)

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“…This decrease is the consequence of a severe cold stimulus, since exposure to -10°C lasted more than 30 min and hyperventilation reached values up to 130 L·min -1 . These results are in agreement with previous experiments in which nonatopic subjects responded to extensive airway cooling by developing airway obstruction [4,5]. Airway cooling has been proposed as the key stimulus initiating events that lead to a bronchospasm [6] acting on thermosensitive receptors, and a parasympathetic reflex response, or directly on smooth muscle.…”

Section: Discussionsupporting

confidence: 92%

“…While these losses are known to induce airway obstruction in subjects with bronchial hyperresponsiveness, their effects are not well defined in normal nonatopic subjects. According to some authors, normal subjects do not develop measurable obstruction in response to airway cooling [1][2][3], whereas other authors claim that they respond by developing measurable obstruction when the stimulus is sufficiently great [4,5]. Under these conditions, the origin and mechanisms involved in the development of bronchial obstruction are still under debate [6][7][8].…”

Section: Bronchial Obstruction and Exhaled Nitric Oxide Response Durimentioning

confidence: 99%

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Bronchial obstruction and exhaled nitric oxide response during exercise in cold air

Therminarias

Oddou²,

Favre-Juvin³

et al. 1998

Eur Respir J

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aaMuscular exercise in a cold environment requires both the warming and the humidification of large amounts of inspired air, resulting in a loss of heat and water from the respiratory tract. While these losses are known to induce airway obstruction in subjects with bronchial hyperresponsiveness, their effects are not well defined in normal nonatopic subjects. According to some authors, normal subjects do not develop measurable obstruction in response to airway cooling [1][2][3], whereas other authors claim that they respond by developing measurable obstruction when the stimulus is sufficiently great [4,5]. Under these conditions, the origin and mechanisms involved in the development of bronchial obstruction are still under debate [6][7][8].Endogenous NO is produced in the lung by a family of NO synthases [9][10][11]. This NO is thought to be an important modulator of vascular tone and airway function in normal airways. Therefore, NO may be involved in several physiological mechanisms during airway cooling. Thus, in normal pulmonary circulation, NO mediates the vasodilation response to physical and chemical factors [9]. Moreover, NO mediates the nonadrenergic, noncholinergic neural inhibitory responses which represent the only neural bronchodilator mechanism in human airways [12,13]. In addition, NO may contribute to acute inflammation and host defence in the lung [14].NO may be detected in the air exhaled by humans and the amount of NO exhaled over time (V 'NO) may be measured accurately and continuously [15][16][17][18]. Although the NO detected at the mouth is the difference between what is produced in the respiratory system and what is transformed or eliminated continuously by other endogenous pathways, V 'NO is generally assumed to reflect the NO produced by cells within the respiratory tract. Therefore, if endogenous NO-production takes a part in the mechanisms involved during airway cooling, a change in exhaled [NO] may be expected during inhalation of cold air. The aim of the present study was: 1) to confirm that extensive airway cooling can induce detectable airway obstruction in nonatopic subjects, 2) to determine whether this cooling induces changes in the V 'NO response, and 3) to determine whether a relationship may be established between both of these observations. Methods SubjectsEight well-trained male subjects, engaged in various endurance activities (cross-country skiing, triathlon or running) for >8 h·week -1 , were studied. These subjects were selected because they were able to produce a high ventilatory response during exercise and, would therefore, need to warm up a large amount of air when they exercised in Thus, eight well-trained males performed two incremental exercise tests until exhaustion, followed by 5 min of recovery in temperate (22°C) and cold (-10°C) environments, at random. At -10°C, they were dressed in warm clothes. Ventilation (V'E), oxygen consumption (V'O 2 ), carbon dioxide production, cardiac frequency (fC), and [NO] and V'NO were measured continuously. Before and after...

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Section: Discussionsupporting

confidence: 92%

Section: Bronchial Obstruction and Exhaled Nitric Oxide Response Durimentioning

confidence: 99%

Bronchial obstruction and exhaled nitric oxide response during exercise in cold air

Therminarias

Oddou²,

Favre-Juvin³

et al. 1998

Eur Respir J

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“…Exercise-induced bronchoconstriction in asthmatics and bronchodilation in normal subjects correlate with inspired water content [73]. This confirms the tendency of normal human airways to narrow in response to hyperventilation [118][119][120]. The enhancement of AIB in asthmatic as compared to normal humans may reflect the presence of inflammatory mediators and an increased sensitivity to stimuli that are tolerated by normal airways during and after exposure to cool dry air.…”

supporting

confidence: 62%

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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“…Drug interaction with the response to CACh will have to be studied systematically together with the still controversial cellular, humoral, and neural mechanisms of the reaction (5,6,18,32).…”

Section: Resultsmentioning

confidence: 99%