Determination of production of nitric oxide by lower airways of humans—theory

Hyde, Richard W.; Geigel, Edgar J.; Olszowka, Albert J.; Krasney, J. A.; Forster, R. E.; Utell, Mark J.; Frampton, Mark W.

doi:10.1152/jappl.1997.82.4.1290

Cited by 87 publications

(71 citation statements)

References 27 publications

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“…Thus, both haemodynamic alteration and hyperventilation have been suggested as being important stimuli for NO-production during exercise [15,18,19]. Moreover, it has been suggested recently that exercise does not necessarily increase V 'NO but only shifts the elimination of a proportion of the V 'NO from the blood to the airways, less NO diffusing into the blood and more being removed by ventilation [20]. In our study, the identical V 'O 2 values measured at -10 and 22°C at rest and during exercise shows an identical metabolic involvement.…”

Section: Discussionmentioning

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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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: Discussionmentioning

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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“…gas exchange; model; exhaled breath NITRIC OXIDE (NO) performs many important functions in the lungs and has been regarded as a potential noninvasive marker of lung inflammation (2). The characteristics of NO gas exchange are unique compared with other endogenous gases because exhaled NO is thought to have a significant alveolar and airway source (6,8,15,22). A two-compartment model is commonly used to characterize NO exchange dynamics for healthy and diseased lungs (9,11,13,20,21,23,24,27,29), by partitioning exhaled NO into airway and alveolar contributions using three flow-independent NO exchange parameters: maximum flux of NO from the airways (JЈaw NO ), the diffusing capacity of NO in the airways (Daw NO ), and the steady-state alveolar concentration (CA NO ).…”

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confidence: 99%

Probing the impact of axial diffusion on nitric oxide exchange dynamics with heliox

Shin

Condorelli

Rose-Gottron

et al. 2004

Journal of Applied Physiology

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Shin, Hye-Won, Peter Condorelli, Christine M. Rose-Gottron, Dan M. Cooper, and Steven C. George. Probing the impact of axial diffusion on nitric oxide exchange dynamics with heliox. J Appl Physiol 97: 874 -882, 2004. First published April 30, 2004 10.1152/ japplphysiol.01297.2003.-Exhaled nitric oxide (NO) is a potential noninvasive index of lung inflammation and is thought to arise from the alveolar and airway regions of the lungs. A two-compartment model has been used to describe NO exchange; however, the model neglects axial diffusion of NO in the gas phase, and recent theoretical studies suggest that this may introduce significant error. We used heliox (80% helium, 20% oxygen) as the insufflating gas to probe the impact of axial diffusion (molecular diffusivity of NO is increased 2.3-fold relative to air) in healthy adults (21-38 yr old, n ϭ 9). Heliox decreased the plateau concentration of exhaled NO by 45% (exhalation flow rate of 50 ml/s). In addition, the total mass of NO exhaled in phase I and II after a 20-s breath hold was reduced by 36%. A single-path trumpet model that considers axial diffusion predicts a 50% increase in the maximum airway flux of NO and a near-zero alveolar concentration (CA NO) and source. Furthermore, when NO elimination is plotted vs. constant exhalation flow rate (range 50 -500 ml/s), the slope has been previously interpreted as a nonzero CANO (range 1-5 ppb); however, the trumpet model predicts a positive slope of 0.4 -2.1 ppb despite a zero CANO because of a diminishing impact of axial diffusion as flow rate increases. We conclude that axial diffusion leads to a significant backdiffusion of NO from the airways to the alveolar region that significantly impacts the partitioning of airway and alveolar contributions to exhaled NO. gas exchange; model; exhaled breath NITRIC OXIDE (NO) performs many important functions in the lungs and has been regarded as a potential noninvasive marker of lung inflammation (2). The characteristics of NO gas exchange are unique compared with other endogenous gases because exhaled NO is thought to have a significant alveolar and airway source (6,8,15,22). A two-compartment model is commonly used to characterize NO exchange dynamics for healthy and diseased lungs (9,11,13,20,21,23,24,27,29), by partitioning exhaled NO into airway and alveolar contributions using three flow-independent NO exchange parameters: maximum flux of NO from the airways (JЈaw NO ), the diffusing capacity of NO in the airways (Daw NO ), and the steady-state alveolar concentration (CA NO ). However, the two-compartment model considers only convection of NO in the airways as a transport mechanism and has neglected axial diffusion of NO in the gas phase to preserve mathematical simplicity.Recently, our laboratory (17) and others (31) separately demonstrated theoretically that axial diffusion may play an important role in NO transport. During exhalation, the concentration of NO is higher in the airways compared with the alveoli, creating a gradient for diffusion of NO from the air...

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“…End tidal NO value was stable over many breaths and much easier to identify. When necessary, changes in minute ventilation, which can affect exhaled NO concentration, can be accounted for by calculating NO production [25]. The effect of nasal contamination [26] on NOet measurement is likely to be very small during normal breathing because most of the NO would have been washed away early during expiration, and can be further minimized by applying a small negative pressure at the nose [27].…”

Section: Discussionmentioning

confidence: 99%

“…Based on such evidence, it is reasonable to suggest that NOet represents alveolar NO and any changes in exhaled NO may reflect changes in NO diffusing into the blood. Indeed Hyde et al [25] suggested that changes in NO in the exhaled gas represents changes in diffusing capacity rather than changes in NO production in the airways. Clini et al [40] came to similar conclusions.…”

Section: Discussionmentioning

confidence: 99%

Measurement of Exhaled Nitric Oxide Using End Tidal Value during Normal Breathing

Hakim¹

2014

J Pulm Respir Med

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Increased nitric oxide (NO) production in the expired air has been associated with a number of disease conditions and may reflect the severity of inflammation in the lungs. Measurement of exhaled NO concentration has been proposed as a novel clinical tool for assessing airway inflammation and response to drug therapy. In spite of international guidelines aimed at standardizing the measurement of exhaled NO, clinicians remain skeptical due to the necessity of a significant degree of subject collaboration required by the procedure to obtain meaningful measurements. We hypothesized that exhaled NO concentration may be best measured by using end tidal NO concentration during a breath by breath monitoring. We tested laboratory staff and monitored their NO concentration online using a fast response chemiluminescence NO analyzer during normal breathing at rest for 5 minutes. First we confirmed that the NO analyzer was adequately fast to record fully the swings during normal breathing. We then compared the average end tidal NO value (NOet) from 6 to 10 breaths, to the NO value obtained from the plateau from a single slow vital capacity maneuver as recommended by the ATS guidelines (NOplat). End of exhalation was identified using end tidal carbon dioxide measurement. NOet while breathing room air was 24.3 ± 4.2 (SE) ppb and was not significantly different compared to 22.4 ± 2.8 (SE) ppb using NOplat. Additionally breathing high level of NO of up to 88 ppb did not affect either NOet or NOplat significantly suggesting that both measurements are independent of inhaled NO concentration. NO value at end of exhalation was very reproducible from breath to breath and did not require any special effort on the part of the subject. We recommend using NOet measurement instead of the NOplat value that is highly dependent on the exhalation rate and cooperation of the subject. NOet is much easier to record in children, elderly and patients with respiratory disease. The main requirement for measuring NOet is to have a fast response NO analyzer to record the full swings in NO concentration during normal breathing and to have a way of identifying end exhalation.

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Determination of production of nitric oxide by lower airways of humans—theory

Cited by 87 publications

References 27 publications

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

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

Probing the impact of axial diffusion on nitric oxide exchange dynamics with heliox

Measurement of Exhaled Nitric Oxide Using End Tidal Value during Normal Breathing

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