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...
This study examines the response of exhaled nitric oxide (NO) concentration (ECNO) and quantity of exhaled NO over time (EVNO) in 10 healthy subjects breathing into five polyethylene bags, one in which synthetic air was free of NO and four in which NO was diluted to concentrations of 20 +/- 0.6, 49 +/- 0.8, 98 +/- 2, and 148 +/- 2 ppb, respectively. Each subject was connected to each bag for 10 min at random. Minute ventilation and ECNO were measured continuously, and EVNO was calculated continuously. ECNO and EVNO values were significantly higher for an inhaled NO concentration of 20 ppb than for NO-free air. Above 20 ppb, ECNO and EVNO increased linearly with inhaled NO concentration. It is reasonable to assume that a share of the quantity of inspired NO over time (InspVNO) because of air contamination by pollution is rejected by the ventilatory pathway. Insofar as InspVNO does not affect endogenous production or the metabolic fate of NO in the airway, this share may be estimated as being approximately one third of InspVNO, the remainder being taken by the endogenous pathway. Thus, air contamination by the NO resulting from pollution greatly increases the NO response in exhaled air.
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