Markers of Lung Disease in Exhaled Breath: Nitric Oxide

2006 ◽  
Vol 7 (4) ◽  
pp. 241-255 ◽  
Author(s):  
JiYeon Choi ◽  
Leslie A. Hoffman ◽  
George W. Rodway ◽  
Jigme M. Sethi
Keyword(s):  
Nitric Oxide ◽  
Clinical Practice ◽  
Airway Inflammation ◽  
Measurement Techniques ◽  
Historical Background ◽  
Future Application ◽  
Exhaled Breath ◽  
Physiological Importance ◽  
Exhaled No

Management of airway inflammation requires proper monitoring and treatment to improve long-term outcomes. However, achieving this goal is difficult, as current methods have limitations. Although nitric oxide (NO) was first identified 200 years ago, its physiological importance was not recognized until the early 1980s. Many studies have established the role of NO as an essential messenger molecule in body systems. In addition, studies have demonstrated a significant relationship between changes in exhaled NO levels and other markers of airway inflammation. The technique used to measure NO in exhaled breath is noninvasive, reproducible, sensitive, and easy to perform. Consequently, there is growing interest in the use of exhaled NO in the management of asthma and other pulmonary conditions. The purpose of this review is to promote a basic understanding of the physiologic actions of NO, measurement techniques, and ways that research findings might translate to future application in clinical practice. Specifically, the article will review the role of exhaled NO in regard to its historical background, mechanisms of action, measurement techniques, and implications for clinical practice and research.

A two-compartment model of pulmonary nitric oxide exchange dynamics

1998 ◽  
Vol 85 (2) ◽  
pp. 653-666 ◽  
Author(s):  
Nikolaos M. Tsoukias ◽  
Steven C. George
Keyword(s):  
Nitric Oxide ◽  
Elimination Rate ◽  
Compartment Model ◽  
Phase Iii ◽  
Exhaled Breath ◽  
Dynamic Relationship ◽  
Exhaled No ◽  
Two Compartment Model ◽  
Conducting Airways ◽  
The Relationship

The relatively recent detection of nitric oxide (NO) in the exhaled breath has prompted a great deal of experimentation in an effort to understand the pulmonary exchange dynamics. There has been very little progress in theoretical studies to assist in the interpretation of the experimental results. We have developed a two-compartment model of the lungs in an effort to explain several fundamental experimental observations. The model consists of a nonexpansile compartment representing the conducting airways and an expansile compartment representing the alveolar region of the lungs. Each compartment is surrounded by a layer of tissue that is capable of producing and consuming NO. Beyond the tissue barrier in each compartment is a layer of blood representing the bronchial circulation or the pulmonary circulation, which are both considered an infinite sink for NO. All parameters were estimated from data in the literature, including the production rates of NO in the tissue layers, which were estimated from experimental plots of the elimination rate of NO at end exhalation (ENO) vs. the exhalation flow rate (V˙E). The model is able to simulate the shape of the NO exhalation profile and to successfully simulate the following experimental features of endogenous NO exchange: 1) an inverse relationship between exhaled NO concentration and V˙E, 2) the dynamic relationship between the phase III slope andV˙E, and 3) the positive relationship between ENO andV˙E. The model predicts that these relationships can be explained by significant contributions of NO in the exhaled breath from the nonexpansile airways and the expansile alveoli. In addition, the model predicts that the relationship between ENO and V˙E can be used as an index of the relative contributions of the airways and the alveoli to exhaled NO.

scholarly journals Nitric Oxide and Biological Mediators in Pediatric Chronic Rhinosinusitis and Asthma

2019 ◽  
Vol 8 (11) ◽  
pp. 1783 ◽  
Author(s):  
Valentina Agnese Ferraro ◽  
Stefania Zanconato ◽  
Eugenio Baraldi ◽  
Silvia Carraro
Keyword(s):  
Nitric Oxide ◽  
Chronic Rhinosinusitis ◽  
Exhaled Breath Condensate ◽  
Main Body ◽  
Exhaled Breath ◽  
Non Invasive ◽  
Volatile Organic ◽  
Exhaled Air ◽  
Breath Condensate

Background: In the context of the so-called unified airway theory, chronic rhinosinusitis (CRS) and asthma may coexist. The inflammation underlying these conditions can be studied through the aid of biomarkers. Main body: We described the main biological mediators that have been studied in pediatric CRS and asthma, and, according to the available literature, we reported their potential role in the diagnosis and management of these conditions. As for CRS, we discussed the studies that investigated nasal nitric oxide (nNO), pendrin, and periostin. As for asthma, we discussed the role of fractional exhaled nitric oxide (feNO), the role of periostin, and that of biological mediators measured in exhaled breath condensate (EBC) and exhaled air (volatile organic compounds, VOCs). Conclusion: Among non-invasive biomarkers, nNO seems the most informative in CRS and feNO in asthma. Other biological mediators seem promising, but further studies are needed before they can be applied in clinical practice.

Role of airway nitric oxide on the regulation of pulmonary circulation by carbon dioxide

2001 ◽  
Vol 91 (3) ◽  
pp. 1121-1130 ◽  
Author(s):  
Yasushi Yamamoto ◽  
Hitoshi Nakano ◽  
Hiroshi Ide ◽  
Toshiyuki Ogasa ◽  
Toru Takahashi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Arterial Pressure ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
No Synthase ◽  
No Production ◽  
Pulmonary Vasoconstriction ◽  
Exhaled No ◽  
Progressive Hypoxia ◽  
Pulmonary Arterial

The effects of hypercapnia (CO2) confined to either the alveolar space or the intravascular perfusate on exhaled nitric oxide (NO), perfusate NO metabolites (NOx), and pulmonary arterial pressure (Ppa) were examined during normoxia and progressive 20-min hypoxia in isolated blood- and buffer-perfused rabbit lungs. In blood-perfused lungs, when alveolar CO2concentration was increased from 0 to 12%, exhaled NO decreased, whereas Ppa increased. Increments of intravascular CO2levels increased Ppa without changes in exhaled NO. In buffer-perfused lungs, alveolar CO2 increased Ppa with reductions in both exhaled NO from 93.8 to 61.7 (SE) nl/min ( P < 0.01) and perfusate NOx from 4.8 to 1.8 nmol/min ( P < 0.01). In contrast, intravascular CO2 did not affect either exhaled NO or Ppa despite a tendency for perfusate NOx to decline. Progressive hypoxia elevated Ppa by 28% from baseline with a reduction in exhaled NO during normocapnia. Alveolar hypercapnia enhanced hypoxic Ppa response up to 50% with a further decline in exhaled NO. Hypercapnia did not alter the apparent K m for O2, whereas it significantly decreased the V max from 66.7 to 55.6 nl/min. These results suggest that alveolar CO2 inhibits epithelial NO synthase activity noncompetitively and that the suppressed NO production by hypercapnia augments hypoxic pulmonary vasoconstriction, resulting in improved ventilation-perfusion matching.

scholarly journals Role of interleukin-8 and nitric oxide in airway inflammation.

1996 ◽  
Vol 71 ◽  
pp. 27
Author(s):  
H. Aizawa ◽  
H. Inoue ◽  
K. Matsumoto ◽  
M. Shigyo ◽  
S. Takata ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Airway Inflammation ◽  
Interleukin 8

Prognostic Role of Exhaled Breath Condensate pH and Fraction Exhaled Nitric Oxide in Systemic Sclerosis Related Interstitial Lung Disease

2017 ◽  
Vol 53 (3) ◽  
pp. 120-127
Author(s):  
Alfredo Guillen-del Castillo ◽  
Sara Sánchez-Vidaurre ◽  
Carmen P. Simeón-Aznar ◽  
María J. Cruz ◽  
Vicente Fonollosa-Pla ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Systemic Sclerosis ◽  
Interstitial Lung Disease ◽  
Lung Disease ◽  
Exhaled Breath Condensate ◽  
Exhaled Breath ◽  
Prognostic Role ◽  
Breath Condensate ◽  
Fraction Exhaled Nitric Oxide

scholarly journals The Clinical Significance of Exhaled Nitric Oxide in Asthma

2008 ◽  
Vol 15 (2) ◽  
pp. 99-106 ◽  
Author(s):  
Sachin Pendharkar ◽  
Sanjay Mehta
Keyword(s):  
Nitric Oxide ◽  
Airway Inflammation ◽  
Asthma Control ◽  
Asthma Severity ◽  
Exhaled Breath ◽  
Asthma Therapy ◽  
Clinical Markers ◽  
Noninvasive Technique ◽  
Promising Tool ◽  
Frequency Of Use

Asthma is an inflammatory disease of the airways, for which many therapeutic options are available. Guidelines for the management of asthma suggest a stepwise approach to pharmacotherapy based on assessment of asthma severity and control. However, the assessment of asthma control presently relies on surrogate measures, such as the frequency of symptoms or the frequency of use of short-acting beta2-adrenergic agonists. There is no simple, noninvasive technique for the assessment of severity of actual airway inflammation in asthma. The collection and analysis of nitric oxide (NO) levels in exhaled breath has recently become feasible in humans. Based on increased exhaled NO (eNO) levels in patients with asthma, eNO analysis has been proposed as a novel, noninvasive approach to the assessment and monitoring of airway inflammation, and as a basis for adjustments in asthma therapy. In the present paper, the relationship of elevated eNO levels in asthma with inflammatory, physiological and clinical markers of asthma in adults was reviewed. Use of eNO is a promising tool for diagnosing asthma, for monitoring asthma control and for guiding optimal anti-inflammatory asthma therapy. However, because of many unresolved questions, eNO cannot be recommended at present for routine clinical management of adults with asthma.

scholarly journals Increased nitric oxide metabolites in exhaled breath condensate after exposure to tobacco smoke

Thorax ◽  
2001 ◽  
Vol 56 (6) ◽  
pp. 456-461
Author(s):  
B Balint ◽  
L E Donnelly ◽  
T Hanazawa ◽  
S A Kharitonov ◽  
P J Barnes
Keyword(s):  
Nitric Oxide ◽  
Exhaled Breath Condensate ◽  
Exhaled Breath ◽  
Baseline Visit ◽  
Exhaled No ◽  
The Mean ◽  
Nitric Oxide Metabolites ◽  
Nitrite Nitrate ◽  
Breath Condensate ◽  
Reactive Molecule

BACKGROUNDCigarette smoking reduces the level of exhaled nitric oxide (NO) in healthy subjects, although the mechanism is unclear. NO is a highly reactive molecule which can be oxidised or complexed with other biomolecules, depending on the microenvironment. The stable oxidation end products of NO metabolism are nitrite and nitrate. This study investigated the effect of smoking on NO metabolites in exhaled breath condensate.METHODSFifteen healthy current smokers were recruited together with 14 healthy non-smokers. Measurement of exhaled NO, lung function, and collection of exhaled breath condensate were performed. Nitrite, nitrite + nitrate, S-nitrosothiols, and nitrotyrosine levels were measured. The effect of inhaling two cigarettes in smokers was also evaluated. The mean level of exhaled NO in smokers was significantly lower than in non-smokers (4.3 (0.3) ppb v 5.5 (0.5) ppb, p<0.05).RESULTSThere was no difference in the levels of nitrite, nitrite + nitrate, S-nitrosothiols, and nitrotyrosine in the exhaled breath condensate at the baseline visit between smokers and non-smokers. After smoking, nitrite + nitrate levels were significantly but transiently increased (from 20.2 (2.8) μM to 29.8 (3.4) μM, p<0.05). There was no significant change in the levels of exhaled NO, nitrite, S-nitrosothiols, or nitrotyrosine 30 and 90 minutes after smoking.CONCLUSIONSThese findings suggest that acute smoking can increase the level of nitrate, but not nitrite, S-nitrosothiols, or nitrotyrosine in breath condensate. The deleterious effect of oxidant radicals induced by smoking may contribute to the epithelial damage of airways seen in smokers.

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