Effect of airways constriction on exhaled nitric oxide

Verbanck, Sylvia; Kerckx, Yannick; Schuermans, Daniël; Vincken, Walter; Paiva, Manuel; Muylem, Alain Van

doi:10.1152/japplphysiol.01019.2007

Cited by 44 publications

(44 citation statements)

References 21 publications

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“…C A NO is normally low and close to zero because of its fast reaction rate with haemoglobin. It may be increased due to increased alveolar dead space and with increased axial diffusion of NO into the alveoli due to bronchoconstriction (31). A reduced FE NO and C A NO are associated with primary pulmonary hypertension (12).…”

Section: Introductionmentioning

confidence: 99%

Bronchial Nitric Oxide Flux and Alveolar Nitric Oxide Concentration After Exposure to Hyperoxia

Caspersen¹,

Stensrud²,

Thorsen³

2011

aviat space environ med

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Section: Introductionmentioning

confidence: 99%

Bronchial Nitric Oxide Flux and Alveolar Nitric Oxide Concentration After Exposure to Hyperoxia

Caspersen¹,

Stensrud²,

Thorsen³

2011

aviat space environ med

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“…The current American Thoracic Society/European Respiratory Society guidelines recommend measuring the exhaled concentration at a single constant flow of 50 ml/s (i.e., FE NO,50 ), a remarkably simple protocol, and thus easily translatable to the clinic, but may be limiting the potential to utilize exhaled NO as an inflammatory marker. While we understand that exhaled NO is predominantly from the airways at this flow, Verbanck and colleagues (24) suggest that we might more precisely locate the airway source of NO with an accurate mathematical model. Similarly, Kerckx and colleagues (10) use the same model to enhance our understanding of how to accurately determine the small, but potentially important, alveolar concentration.…”

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confidence: 99%

“…We recently quantified this potential effect and presented a simple method to account for axial diffusion of NO on the estimation of the alveolar concentration (4); however, we only tested the model in healthy subjects. Two new studies (10,24) are presented in the Journal of Applied Physiology, both of which elegantly combine experimental measurements and a mathematical model of NO exchange that advance our knowledge and understanding of NO gas exchange and thus our interpretation of the exhaled NO signal.Kerckx and colleagues (10) have independently developed a similar method to account for axial diffusion of NO into the …”

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confidence: 99%

How accurately should we estimate the anatomical source of exhaled nitric oxide?

George

2008

Journal of Applied Physiology

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FOR MORE THAN A DECADE it has been recognized that nitric oxide (NO) appears in the exhaled breath and the level is altered in numerous pulmonary diseases in which inflammation plays an integral role (e.g., asthma) (1,8). Thus the exhaled NO signal has the potential to uniquely delineate the contribution of inflammatory processes to lung disease in a noninvasive manner complementing more traditional measurements of lung function, namely, lung volumes and expiratory airflow that focus solely on structural properties of the respiratory system. This potential, combined with the relative ease with which it can be detected and the serious and ongoing epidemic of asthma and other chronic lung diseases, has imbued the measurement of exhaled NO with the promise of becoming a useful clinical tool. However, this promise has not yet been fulfilled. Skepticism regarding the measurement of exhaled NO persists due to both its variability among clinically similar subjects and the inconsistent correlations with other indexes of lung function and symptoms. This skepticism is appropriate and stems both from the relatively crude techniques currently employed to characterize exhaled NO and from our still incomplete understanding of the fundamental biological mechanisms that determine the appearance of NO in the exhaled breath.Since the initial observation that NO appears in the exhaled breath, several research groups have made seminal contributions toward our understanding of the unique features of NO exchange in the lungs. In particular, exhaled NO has sources from both the airway and alveolar regions, which has been determined from a combined approach implementing experimental observations (5,7,15,19) and "two-compartment" mathematical models (9,14,20,21). The present clinical approach for exhaled NO measures the concentration during a vital capacity maneuver while holding expiratory flow and pressure constant (2). The recommended exhalation flow is low enough (50 ml/s) to cause the concentration to be predominantly of airway origin and is thus ineffective at describing the lower alveolar concentration of NO, ignoring this potentially important signal.Although asthma is traditionally thought to be an inflammatory disease of the airways, several groups have employed the two-compartment model of NO exchange and reported an elevated alveolar concentration of NO during periods of enhanced symptoms (11, 13), or in patients who are refractory to inhaled corticosteroids and bronchodilators (3,6,12). The observations of increased alveolar NO are particularly relevant as these patients have proven to be difficult to manage, are hospitalized more frequently, and could well benefit from early detection of disease exacerbation and alternate therapeutic regimens.Since the alveolar concentration cannot be directly measured, estimating the alveolar concentration requires a model of NO exchange in the lungs that, when combined with experimental measurements, can partition the exhaled NO signal into proximal and peripheral contributions. This fea...

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“…Other studies using multiple breath nitrogen washout and imaging [32] have shown an increase in ventilation heterogeneity in individuals with hyper reactivity to methacholine which appeared to be independent of changes in airway resistance [33]. Modelling studies indicate that the most marked effect of airways constriction on FeNO50 is most likely to occur in generations 10-15 and that constriction in smaller airways is likely to increase FeNO50 due to interference with the NO back diffusion effect [34]. Ventilation heterogeneity has been reported as a major predictor of airway reactivity independently of the degree of inflammation [35], while airway smooth muscle contraction may be the major cause of airway reactivity [36].…”

Section: Discussionmentioning

confidence: 93%

Untitled

2015

JLPRR

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Increased nitric oxide in exhaled gas in patients with asthma is thought to reflect the severity of airway inflammation and perhaps airway reactivity. Several studies attempted to identify a relationship between exhaled NO levels and airway reactivity or severity of airway inflammation for the purpose of finding out if exhaled NO could be used in place of pulmonary function testing and airway provocation test. Unfortunately, the relationship is not always evident. In recent years, it has become clearer that exhaled NO becomes elevated primarily in atopic asthma patients. All previous studies have used the single vital capacity slow exhalation maneuver to measure ENO (FeNO50). This method is subject to errors because it requires patient cooperation, is flow rate dependent and adds more stress on the patient. Recently, we showed that end tidal NO concentration (NOet) is clinically relevant, is much easier to measure and is not subject to flow variation or patient cooperation. We used NOet (ppb) measurement before and during methacholine challenge in patients with symptoms of mild, persistent asthma. In addition we calculated NO production (NOpr) (nmole/ min) to correct for possible changes in ventilation. Eleven patients exhibited hyper-responsiveness to methacholine (responders) and 17 exhibited negative response (non-responders). The responders had a slightly higher NO level than the non-responders whether expressed in ppb or in nmol/min but did not reach statistical significance: NOet values were 15.1±2.4 ppb (±SE) and 11.7±2.3 ppb respectively and NOpr values were 5.83±0.86 nmol/min and 5.12±1.13 nmol/min respectively.There was no correlation between baseline NOet levels and the change in FEV1 in the responders. Furthermore, there was no consistent change in NOet or NOpr levels during broncho-constriction with methacholine. We conclude that although exhaled NO levels may serve as a helpful adjunct in treatment of asthma, its level alone does not reflect severity of the disease in mild asthmatics nor the airway responsiveness to methacholine. Exhaled NO was estimated using the average NO value at end expiration during normal tidal breathing. This method was quicker, repeatable and much easier on the patients and none of the patients objected to doing the measurement. There was no need to put patients through the complicated single full vital capacity slow exhaled maneuver to obtain this information.

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Effect of airways constriction on exhaled nitric oxide

Cited by 44 publications

References 21 publications

Bronchial Nitric Oxide Flux and Alveolar Nitric Oxide Concentration After Exposure to Hyperoxia

Bronchial Nitric Oxide Flux and Alveolar Nitric Oxide Concentration After Exposure to Hyperoxia

How accurately should we estimate the anatomical source of exhaled nitric oxide?

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