Effect of airways constriction on exhaled nitric oxide

2008 ◽  
Vol 104 (4) ◽  
pp. 925-930 ◽  
Author(s):  
Sylvia Verbanck ◽  
Yannick Kerckx ◽  
Daniel Schuermans ◽  
Walter Vincken ◽  
Manuel Paiva ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Vital Capacity ◽  
Normal Subjects ◽  
Forced Expiratory Volume ◽  
Exhaled Nitric Oxide ◽  
Lung Model ◽  
Airway Constriction ◽  
Exhaled No ◽  
Ventilation Heterogeneity ◽  
Mechanical Factors

While airway constriction has been shown to affect exhaled nitric oxide (NO), the mechanisms and location of constricted airways most likely to affect exhaled NO remain obscure. We studied the effects of histamine-induced airway constriction and ventilation heterogeneity on exhaled NO at 50 ml/s (FeNO,50) and combined this with model simulations of FeNO,50 changes due to constriction of airways at various depths of the lung model. In 20 normal subjects, histamine induced a 26 ± 15(SD)% FeNO,50 decrease, a 9 ± 6% forced expiratory volume in 1 s (FEV1) decrease, a 19 ± 9% mean forced midexpiratory flow between 25% and 75% forced vital capacity (FEF25–75) decrease, and a 94 ± 119% increase in conductive ventilation heterogeneity. There was a significant correlation of FeNO,50 decrease with FEF25–75 decrease ( P = 0.006) but not with FEV1 decrease or with increased ventilation heterogeneity. Simulations confirmed the negligible effect of ventilation heterogeneity on FeNO,50 and showed that the histamine-induced FeNO,50 decrease was due to constriction, with associated reduction in NO flux, of airways located proximal to generation 15. The model also indicated that the most marked effect of airways constriction on FeNO,50 is situated in generations 10–15 and that airway constriction beyond generation 15 markedly increases FeNO,50 due to interference with the NO backdiffusion effect. These mechanical factors should be considered when interpreting exhaled NO in lung disease.

scholarly journals Effects of Exposure to New Car Interiors in Patients With Asthma and Allergic Rhinitis

2018 ◽  
Vol 9 ◽  
pp. 215265671880006
Author(s):  
Amber N. Pepper ◽  
Adeeb Bulkhi ◽  
Catherine R. Smith ◽  
Matthias Colli ◽  
Karl-Christian Bergmann ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Allergic Rhinitis ◽  
Vital Capacity ◽  
Linear Mixed Model ◽  
Forced Expiratory Volume ◽  
Exhaled Nitric Oxide ◽  
Inspiratory Flow ◽  
Clinical Effects ◽  
Fractional Exhaled Nitric Oxide ◽  
Peak Nasal Inspiratory Flow

Rationale Vehicle interiors are an important microenvironment for atopic subjects. This study evaluated the subjective and objective physiologic and clinical effects of exposing subjects with asthma and allergic rhinitis to new 2017 Mercedes vehicles during 90-minute rides. Methods Ten adult asthmatics with allergic rhinitis were assessed before and 45 and 90 minutes into rides in a 2017 Mercedes-Benz S-Class sedan and GLE-Class SUV on 2 separate days. Assessments included spirometry, fractional exhaled nitric oxide, peak nasal inspiratory flow, asthma symptom scores, and physical examinations. Results Of the 10 subjects, 6 were women, mean age was 32 years, and 6 and 4 were using chronic asthma controllers or intranasal corticosteroids, respectively. None of the subjects had worsening of asthma or rhinitis symptoms during the rides. There were no statistically significant changes from baseline in forced expiratory volume in 1 second, forced expiratory volume in 1 second:forced vital capacity ratio, forced expiratory flow at 25%–75% of vital capacity, fractional exhaled nitric oxide, or peak nasal inspiratory flow at 45 or 90 minutes into the rides with either Mercedes vehicle (all P values > .1 using generalized linear mixed model). Conclusion The interior environment of the tested Mercedes vehicles did not cause changes in subjective or objective measures of asthma and allergic rhinitis. We suggest that this model system can be used to test other vehicles for putatively adverse effects on patients with allergic respiratory disorders.

The effect of conductive ventilation heterogeneity on diffusing capacity measurement

2008 ◽  
Vol 104 (4) ◽  
pp. 1094-1100 ◽  
Author(s):  
Sylvia Verbanck ◽  
Daniel Schuermans ◽  
Sophie Van Malderen ◽  
Walter Vincken ◽  
Bruce Thompson
Keyword(s):  
Carbon Monoxide ◽  
Vital Capacity ◽  
Experimental Situation ◽  
Normal Subjects ◽  
Diffusing Capacity ◽  
Capacity Measurement ◽  
Alveolar Volume ◽  
Estimation Errors ◽  
Single Breath ◽  
Ventilation Heterogeneity

It has long been assumed that the ventilation heterogeneity associated with lung disease could, in itself, affect the measurement of carbon monoxide transfer factor. The aim of this study was to investigate the potential estimation errors of carbon monoxide diffusing capacity (DlCO) measurement that are specifically due to conductive ventilation heterogeneity, i.e., due to a combination of ventilation heterogeneity and flow asynchrony between lung units larger than acini. We induced conductive airway ventilation heterogeneity in 35 never-smoker normal subjects by histamine provocation and related the resulting changes in conductive ventilation heterogeneity (derived from the multiple-breath washout test) to corresponding changes in diffusing capacity, alveolar volume, and inspired vital capacity (derived from the single-breath DlCO method). Average conductive ventilation heterogeneity doubled ( P < 0.001), whereas DlCO decreased by 6% ( P < 0.001), with no correlation between individual data ( P > 0.1). Average inspired vital capacity and alveolar volume both decreased significantly by, respectively, 6 and 3%, and the individual changes in alveolar volume and in conductive ventilation heterogeneity were correlated ( r = −0.46; P = 0.006). These findings can be brought in agreement with recent modeling work, where specific ventilation heterogeneity resulting from different distributions of either inspired volume or end-expiratory lung volume have been shown to affect DlCO estimation errors in opposite ways. Even in the presence of flow asynchrony, these errors appear to largely cancel out in our experimental situation of histamine-induced conductive ventilation heterogeneity. Finally, we also predicted which alternative combination of specific ventilation heterogeneity and flow asynchrony could affect DlCO estimate in a more substantial fashion in diseased lungs, irrespective of any diffusion-dependent effects.

Pattern and mechanism of airway response to hypocapnia in normal subjects

1979 ◽  
Vol 47 (1) ◽  
pp. 8-12 ◽  
Author(s):  
C. F. O'Cain ◽  
M. J. Hensley ◽  
E. R. McFadden ◽  
R. H. Ingram
Keyword(s):  
Vital Capacity ◽  
Normal Subjects ◽  
Oxygen Mixture ◽  
Flow Volume ◽  
Mixture Density ◽  
Lung Capacity ◽  
Airway Constriction ◽  
Maximal Expiratory Flow ◽  
Airway Response ◽  
Expiratory Flow

We examined the bronchoconstriction produced by airway hypocapnia in normal subjects. Maximal expiratory flow at 25% vital capacity on partial expiratory flow-volume (PEFV) curves fell during hypocapnia both on air and on an 80% helium- 20% oxygen mixture. Density dependence also fell, suggesting predominantly small airway constriction. The changes seen on PEFV curves were not found on maximal expiratory flow-volume curves, indicating the inhalation to total lung capacity substantially reversed the constriction. Pretreatment with a beta-sympathomimetic agent blocked the response, whereas atropine pretreatment did not, suggesting that hypocapnia affects airway smooth muscle directly, not via cholinergic efferents.

Evaluation of pulmonary resistance and maximal expiratory flow measurements during exercise in humans

1999 ◽  
Vol 86 (4) ◽  
pp. 1388-1395 ◽  
Author(s):  
Kenneth C. Beck ◽  
Robert E. Hyatt ◽  
Panagiotis Mpougas ◽  
Paul D. Scanlon
Keyword(s):  
Vital Capacity ◽  
Normal Subjects ◽  
Forced Expiratory Volume ◽  
Pulmonary Resistance ◽  
Tidal Breathing ◽  
Flow Measurements ◽  
Airway Function ◽  
Minor Influence ◽  
Exercise Induced ◽  
Exercise In Humans

To evaluate methods used to document changes in airway function during and after exercise, we studied nine subjects with exercise-induced asthma and five subjects without asthma. Airway function was assessed from measurements of pulmonary resistance (Rl) and forced expiratory vital capacity maneuvers. In the asthmatic subjects, forced expiratory volume in 1 s (FEV1) fell 24 ± 14% and Rl increased 176 ± 153% after exercise, whereas normal subjects experienced no change in airway function (Rl−3 ± 8% and FEV1−4 ± 5%). During exercise, there was a tendency for FEV1 to increase in the asthmatic subjects but not in the normal subjects. Rl, however, showed a slight increase during exercise in both groups. Changes in lung volumes encountered during exercise were small and had no consistent effect on Rl. The small increases in Rl during exercise could be explained by the nonlinearity of the pressure-flow relationship and the increased tidal breathing flows associated with exercise. In the asthmatic subjects, a deep inspiration (DI) caused a small, significant, transient decrease in Rl 15 min after exercise. There was no change in Rl in response to DI during exercise in either asthmatic or nonasthmatic subjects. When percent changes in Rl and FEV1 during and after exercise were compared, there was close agreement between the two measurements of change in airway function. In the groups of normal and mildly asthmatic subjects, we conclude that changes in lung volume and DIs had no influence on Rl during exercise. Increases in tidal breathing flows had only minor influence on measurements of Rl during exercise. Furthermore, changes in Rl and in FEV1 produce equivalent indexes of the variations in airway function during and after exercise.

scholarly journals Regional airflow obstruction after bronchoconstriction and subsequent bronchodilation in subjects without pulmonary disease

2019 ◽  
Vol 127 (1) ◽  
pp. 31-39 ◽  
Author(s):  
E. T. Geier ◽  
R. J. Theilmann ◽  
G. K. Prisk ◽  
R. C. Sá
Keyword(s):  
Healthy Subjects ◽  
Standard Dose ◽  
Airway Remodeling ◽  
Airflow Obstruction ◽  
Normal Subjects ◽  
Forced Expiratory Volume ◽  
Bronchodilator Therapy ◽  
Ventilation Imaging ◽  
Ventilation Heterogeneity ◽  
Healthy Lung

Some subjects with asthma have ventilation defects that are resistant to bronchodilator therapy, and it is thought that these resistant defects may be due to ongoing inflammation or chronic airway remodeling. However, it is unclear whether regional obstruction due to bronchospasm alone persists after bronchodilator therapy. To investigate this, six young, healthy subjects, in whom inflammation and remodeling were assumed to be absent, were bronchoconstricted with a PC20 [the concentration of methacholine that elicits a 20% drop in forced expiratory volume in 1 s (FEV1)] dose of methacholine and subsequently bronchodilated with a standard dose of albuterol on three separate occasions. Specific ventilation imaging, a proton MRI technique, was used to spatially map specific ventilation across 80% of each subject’s right lung in each condition. The ratio between regional specific ventilation at baseline and after intervention was used to classify areas that had constricted. After albuterol rescue from methacholine bronchoconstriction, 12% (SD 9) of the lung was classified as constricted. Of the 12% of lung units that were classified as constricted after albuterol, approximately half [7% (SD 7)] had constricted after methacholine and failed to recover, whereas half [6% (SD 4)] had remained open after methacholine but became constricted after albuterol. The incomplete regional recovery was not reflected in the subjects’ FEV1 measurements, which did not decrease from baseline ( P = 0.97), nor was it detectable as an increase in specific ventilation heterogeneity ( P = 0.78). NEW & NOTEWORTHY In normal subjects bronchoconstricted with methacholine and subsequently treated with albuterol, not all regions of the healthy lung returned to their prebronchoconstricted specific ventilation after albuterol, despite full recovery of integrative lung indexes (forced expiratory volume in 1 s and specific ventilation heterogeneity). The regions that remained bronchoconstricted following albuterol were those with the highest specific ventilation at baseline, which suggests that they may have received the highest methacholine dose.

Exhaled nitric oxide during exercise: site of release and modulation by ventilation and blood flow

1996 ◽  
Vol 80 (6) ◽  
pp. 1865-1871 ◽  
Author(s):  
C. R. Phillips ◽  
G. D. Giraud ◽  
W. E. Holden
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Exhaled Nitric Oxide ◽  
Balloon Occlusion ◽  
Dobutamine Infusion ◽  
Exhaled No ◽  
Increased Blood Flow ◽  
Exercise In Humans

To define the site of release and factors modulating exhaled nitric oxide (NO) during exercise in humans, we measured exhaled NO output during exercise, during exercise after balloon occlusion of the nasopharynx (to exclude nasal NO), and at rest with isocapneic hyperventilation or dobutamine infusion. Exhaled NO output increased from rest to exercise (57 +/- 10 to 171 +/- 30 nl.min-1.m-2; P < 0.003; n = 8). Exclusion of nasal NO reduced exhaled NO at rest and during exercise. Calculated nasal contribution at rest (53 +/- 5%) decreased during exercise (29 +/- 6%; P < 0.05), whereas nonnasal contribution increased (47 +/- 5 to 71 +/- 6%; P < 0.05). Isocapneic hyperventilation at rest increased exhaled NO output (51 +/- 8 to 94 +/- 22 nl.min-1.m-2; P = 0.05). Dobutamine infusion did not increase exhaled NO output. We conclude that nasal exhaled NO decreases (and nonnasal exhaled NO increases) with exercise. We also conclude that, under the conditions of this study, increased exhaled NO output during exercise is more closely related to increased ventilation than to increased blood flow.

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