Elevated nitric oxide concentrations in isolated lower airway gas of asthmatic subjects.

Massaro, Anthony F.; Mehta, Sanjay; Lilly, Craig M.; Kobzik, Lester; Reilly, JJ; Drazen, Jeffrey M.

doi:10.1164/ajrccm.153.5.8630594

Cited by 169 publications

(128 citation statements)

References 20 publications

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“…In agreement with our findings during IMV in healthy rabbits, they documented slightly increasing intratracheal COµ concentrations with increasing distance into the lung (Eckmann & Gavriely, 1996). Measurement in premixed intratracheal gas samples distinguishes our study from previous work (Eckmann & Gavriely, 1996;Kharitonov et al 1996;Massaro et al 1996) and was chosen for two reasons. Firstly the determination of NO and COµ concentrations fluctuating at the frequency of HFOV (9 Hz in this study) is imprecise due to insufficient response times of even the fastest available equipment (Fig.…”

Section: ------------------------------------------------------------supporting

confidence: 88%

“…Data on measurements of NO and COµ concentrations at different positions in the tracheobronchial system are sparse (Eckmann & Gavriely, 1996;Kharitonov et al 1996;Massaro et al 1996). Eckmann & Gavriely (1996) measured COµ concentrations at various levels in the tracheobronchial system during intermittent positive pressure ventilation in healthy dogs.…”

Section: ------------------------------------------------------------mentioning

confidence: 99%

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Exhaled Nitric Oxide Increases During High Frequency Oscillatory Ventilation in Rabbits

Artlich¹,

Adding²,

Agvald³

et al. 1999

Exp. Physiol.

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summaryThis study compared the effects of high frequency oscillatory ventilation (HFOV) and intermittent mandatory ventilation (IMV) on the homeostasis of nitric oxide (NO) in the lower respiratory tract of healthy rabbits. The mechanisms underlying a putative stretch response of NO formation in the airways were further elucidated. Male New Zealand White rabbits were anaesthetized, tracheotomized and ventilated with IMV or HFOV in random order. Total NO excretion increased from 9·6 ± 0·8 nl min¢ (mean ± s.e.m.) during IMV to 22·6 ± 2·7 nl min¢ during HFOV (P < 0·001). This increase was not explained by changes of functional residual capacity (ÄFRC). A similar increase in NO excretion during HFOV was seen in isolated buffer-perfused lungs under constant circulatory conditions (P < 0·05, n = 4). Intratracheal mean COµ and NO concentrations, measured at 2·5, 5, 7·5 and 10 cm below tracheostomy, increased significantly with increasing distance into the lung during both IMV and HFOV (P < 0·001 for each comparison). At every intratracheal location of the sampling catheter, particularly low in the airways, both COµ and NO concentrations were significantly higher during HFOV than during IMV (P < 0·01 for each comparison). We conclude that HFOV increases pulmonary NO production in healthy rabbits. Increased stretch activation of the respiratory system during HFOV is suggested as a possible underlying mechanism. The increase in mean airway NO concentrations may have biological effects in the respiratory tract. Whether it can account for some of the benefits of HFOV treatment needs to be considered. introduction NO, which is continuously produced within the lower respiratory tract (Gustafsson et al. 1991;Persson et al. 1993), can be detected in the exhaled gas of most mammalian species, offering a unique possibility to study features of NO metabolism non-invasively (Gustafsson, 1997). However, the anatomic site and main cell type producing those NO molecules detected in exhaled gas is still a matter of debate (Gustafsson, 1997). Thus the extent to which the various biological functions of NO are reflected in the concentration of NO in exhaled gas merits further study. Moreover, factors influencing the amount of NO detected in exhaled gas are only beginning to evolve. We have recently shown in rabbits and guinea-pigs that lower airway NO formation is suppressed by high airway concentrations of COµ Str omberg et al. 1997;Adding et al. 1999). This rapid effect is also present in isolated buffer-perfused rabbit lungs and cannot be explained by either altered sympathetic outflow or changes of extracellular pH (Adding et al. 1999). Another mechanism to increase lower airway NO formation is revealed during increases of positive end-expiratory pressure (PEEP)

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Section: ------------------------------------------------------------supporting

confidence: 88%

Section: ------------------------------------------------------------mentioning

confidence: 99%

Exhaled Nitric Oxide Increases During High Frequency Oscillatory Ventilation in Rabbits

Artlich¹,

Adding²,

Agvald³

et al. 1999

Exp. Physiol.

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“…The strength of the evidence, and hence the validity of the finding, is based on both practical and theoretical grounds. Higher levels of exhaled NO in asthma have been consistently found by several independent investigators using different techniques of measurement [18,22,23]. Theoretical considerations are also consistent with the raw data.…”

supporting

confidence: 78%

Measuring exhaled nitric oxide: not only a matter of how--but also why--should we do it?

Dinh-Xuan¹,

Texereau²

1998

Eur Respir J

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The biological functions of nitric oxide are so diverse and complex that it is now becoming increasingly difficult to delineate briefly the physiological roles and pathophysiological implications of this seemingly simple messenger molecule [1]. In respiratory medicine, NO can either be viewed as a paracrine factor (derived from endothelium, epithelium, nerves, inflammatory cells, etc), a therapeutic gas or a marker of inflammation [2]. Amongst other paracrine factors, the endothelium-derived NO has, in its own right, a central role to play in the modulation of pulmonary vascular tone [3]. As a gaseous molecule, NO has been extensively investigated in clinical settings and used as inhalational therapy to relieve pulmonary hypertension and/or refractory hypoxaemia in adults and infants [4]. Although there are many questions that still remain to be properly answered [5], the use of inhaled NO has undoubtedly revived interest in molecules that can selectively reduce both pulmonary vascular resistance and intrapulmonary shunt. As a radical molecule, NO is highly reactive and readily combines with an array of biological molecules, ranging from reactive oxygen species to haeme moiety containing proteins [6]. This explains why measurement of NO in biological systems was often fraught with difficulties in the early days [7]. Since 1991, however, measurement of in vivo NO production in humans have been proven to be technically feasible by means of ex vivo manoeuvres, i.e. by sampling the exhaled breath and analysing it for NO content using a chemiluminescent NO analyser [8]. As the technique is noninvasive, it was immediately applied to patients, especially those with bronchial asthma, to assess endogenous production of NO by the lung [9][10][11]. Soon, the accumulating evidence suggested that measurement of exhaled NO could be viewed as a new lung function test [12] to monitor airway inflammation in asthma [13] and other conditions associated with inflammation of the respiratory tract [14]. It is still difficult to know the actual source of the endogenous NO that is detected in the exhaled air [15]. As NO is synthesized by many lung cells, it could originate from virtually anywhere in the respiratory tract, from alveolar space to the nose. Several recent and carefully conducted studies have clearly shown how the techniques of measurement are likely to affect the amount and origin of exhaled NO [16][17][18][19][20]. This prompted the European Respiratory Society, in 1997, to issue specific recommendations for the measurement of exhaled and nasal NO [21], an initiative which was followed in 1998 by the American Thoracic Society.In contrast with the ongoing technical debate on how to measure exhaled NO, it seems that a consensus has been reached on the diagnostic value of NO measurement in asthma. Compelling evidence clearly demonstrates that asthmatic subjects who are not treated with inhaled glucocorticoids have on average higher amounts of exhaled NO as compared with healthy controls [9-14, 18, 21]. The strength of the e...

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“…This peak was followed by a plateau, associated with the last part of exhalation, which represented the NO levels derived from the lower respiratory tract [24,25]. Three successive reproducible recordings were made at 2-min intervals.…”

Section: Detection Of No Levels In Orally Exhaled Airmentioning

confidence: 99%

Orally exhaled nitric oxide levels are related to the degree of blood eosinophilia in atopic children with mild-intermittent asthma

et al. 1999

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Orally exhaled nitric oxide levels are related to the degree of blood eosinophilia in atopic children with mild-intermittent asthma. M. Silvestri, D. Spallarossa, V. Frangova Yourukova, E. Battistini, B. Fregonese, G.A. Rossi. #ERS Journals Ltd 1999. ABSTRACT: Increased levels of nitric oxide have been found in expired air of patients with asthma, and these are thought to be related to the airway inflammatory events that characterize this disorder. Since, in adults, bronchial inflammatory changes are present even in mild disease, the present study was designed to evaluate whether a significant proportion of children with mild-intermittent asthma could have increased exhaled air NO concentrations.Twenty-two atopic children (aged 11.1 0.8 yrs) with mild-intermittent asthma, treated only with inhaled b 2 -adrenoreceptor agonists on demand and 22 age-matched controls were studied.NO concentrations in orally exhaled air, measured by chemiluminescence, were significantly higher in asthmatics, as compared to controls (19.4 3.3 parts per billion (ppb) and 4.0 0.5 ppb, respectively; p<0.01). Interestingly, 14 out of 22 asthmatic children had NO levels >8.8 ppb (i.e. >2 standard deviations of the mean in controls). In asthmatic patients, but not in control subjects, statistically significant correlations were found between exhaled NO levels and absolute number or percentage of blood eosinophils (r=0.63 and 0.56, respectively; p<0.01, each comparison). In contrast, exhaled NO levels were not correlated with forced expiratory volume in one second (FEV1) or forced expiratory flows at 25±75% of vital capacity (FEF25±75%) or forced vital capacity (FVC), either in control subjects, or in asthmatic patients (p>0.1, each correlation).These results suggest that a significant proportion of children with mild-intermittent asthma may have airway inflammation, as shown by the presence of elevated levels of nitric oxide in the exhaled air. The clinical relevance of this observation remains to be established. Eur Respir J 1999; 13: 321±326.

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Elevated nitric oxide concentrations in isolated lower airway gas of asthmatic subjects.

Cited by 169 publications

References 20 publications

Exhaled Nitric Oxide Increases During High Frequency Oscillatory Ventilation in Rabbits

Exhaled Nitric Oxide Increases During High Frequency Oscillatory Ventilation in Rabbits

Measuring exhaled nitric oxide: not only a matter of how--but also why--should we do it?

Orally exhaled nitric oxide levels are related to the degree of blood eosinophilia in atopic children with mild-intermittent asthma

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