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PubMed2000

The concentration of hydrogen peroxide in exhaled air depends on expiratory flow rate.

Hydrogen peroxide (H2O2) is known to be detectable in exhaled air. The present study aimed to determine whether the concentration of exhaled H2O2 depends on expiratory flow rate in order to make inferences on the site of its production within the lung. Breath condensate was collected in cooled Teflon tubes, at three different expiratorv flow rates, in 15 healthy or mild asthmatic subjects. Tests were repeated 2-5 times to assess reproducibility. Mean+/-SEM concentrations of H2O2 at flow rates of 140, 69 and 48 mL.s(-1) were 0.12+/-0.02, 0.19+/-0.02 and 0.32+/-0.03 microM, respectively. These values differed significantly from each other (p<0.001). For comparison, average coefficients of variability within repeated measurements at each of the three flow rates were 68, 62 and 82%, respectively. These data demonstrate that the concentration of exhaled hydrogen peroxide depends on expiratory flow rate. Since flow dependence is an indicator of production within the airways, this result suggests that, to a large extent, the exhaled hydrogen peroxide originates within the airways. However, even under strictly controlled conditions, a high degree of variability persists, which may limit the usefulness of exhaled hydrogen peroxide as a marker of airway inflammation.

Adult↗
PubMed1996

The effect of the menstrual cycle on exhaled nitric oxide and urinary nitrate concentration.

Exhaled nitric oxide (NO), early morning urinary nitrites/nitrates and urinary female sex steroid conjugates were measured daily to investigate whether there was a variation in NO generation during the menstrual cycle. Exhaled NO concentrations and early morning urine samples were taken for 30 consecutive days in five healthy normotensive women with proven ovulation. The urine samples were analysed for nitrite-nitrate creatinine ratios, oestrone-3-glucuronide (EG) and pregnanediol-3-alpha glucuronide (PG). The mean (95% CI) exhaled NO concentration was 52 ng g-1 in the 150 readings and the mean molar urinary nitrate-creatinine ratio was 0.18. There was no temporal relationship between the measurement of NO production and urinary sex steroid conjugates within the menstrual cycle. These findings suggest that oestrogens do not modulate exhaled NO concentration and appear not to increase the production of the early morning urinary nitrates in healthy premenopausal women. There was also no sex difference in exhaled NO generation.

Adolescent↗
PubMed2001

A noninvasive method to collect nasally exhaled air condensate in humans of all ages.

BACKGROUND: The analysis of exhaled breath condensate may provide valuable insights into inflammatory and other metabolic processes of the lungs. However, its collection by active exhalation with conventional methods is cumbersome, demands a substantial level of co-operation with high motivation and is very difficult or impossible in children younger than about 4-6 years or in the elderly. A comfortable, noninvasive and efficient method is desirable. DESIGN AND PATIENTS: For collection a high-performance pump connected to a cold trap and nasal prongs were used. The volume of the condensate collected was assessed in 141 children of all ages and five adults. As an example for a low molecular component, H2O2 a marker of oxidative stress, was determined fluorometrically. RESULTS: On average, in healthy children from 4 weeks to 18 years of age, 84.0 (79.4, 87.3) microL min(-1) of nasally exhaled air condensate were collected. The volume obtained was about 45% less in 1-6-year-old children, increased linearly with collection time, and averaged about 20-30% of the exhaled water vapour. The concentration of H2O2 in the healthy children was 0.49 (0.48, 0.61) microM and did not depend on age, the time of the day, family, or personal history of atopy and sex. CONCLUSIONS: The method described is generally applicable, comfortable, noninvasive, safe and efficient and allows the collection of nasally exhaled air condensate for the evaluation of metabolic processes of the lungs.

Adolescent↗
PubMed2001

Role of exhaled nitric oxide in asthma.

Nitric oxide (NO), an evanescent atmospheric gas, has recently been discovered to be an important biological mediator in animals and humans. Nitric oxide plays a key role within the lung in the modulation of a wide variety of functions including pulmonary vascular tone, nonadrenergic non-cholinergic (NANC) transmission and modification of the inflammatory response. Asthma is characterized by chronic airway inflammation and increased synthesis of NO and other highly reactive and toxic substances (reactive oxygen species). Pro- inflammatory cytokines such as TNFalpha and IL-1beta are secreted in asthma and result in inflammatory cell recruitment, but also induce calcium- and calmodulin-independent nitric oxide synthases (iNOS) and perpetuate the inflammatory response within the airways. Nitric oxide is released by several pulmonary cells including epithelial cells, eosinophils and macrophages, and NO has been shown to be increased in conditions associated with airway inflammation, such as asthma and viral infections. Nitric oxide can be measured in the expired air of several species, and exhaled NO can now be rapidly and easily measured by the use of chemiluminescence analysers in humans. Exhaled NO is increased in steroid-naive asthmatic subjects and during an asthma exacerbation, although it returns to baseline levels with appropriate anti-inflammatory treatment, and such measurements have been proposed as a simple non-invasive method of measuring airway inflammation in asthma. Here the chemical and biological properties of NO are briefly discussed, followed by a summary of the methodological considerations relevant to the measurement of exhaled NO and its role in lung diseases including asthma. The origin of exhaled NO is considered, and brief mention made of other potential markers of airway inflammation or oxidant stress in exhaled breath.

Animals↗
PubMed1999

Measurement of exhaled nitric oxide concentration using nasal continuous negative pressure.

Contamination of nasal nitric oxide (NO) is a major obstacle when one needs to sample exhaled NO originating only from the lungs. To eliminate nasal NO, we used the nasal continuous negative pressure (nasal CNP) technique which, we verified, caused closure of the vellum. Exhaled gas was sampled from six healthy volunteers into fraction 1 (initially exhaled 200 mL) and fraction 2 (remainder of the gas) under three conditions; while subjects were wearing a noseclip, using nasal CNP at -5, -10 and -20 cm H2O, and under endotracheal intubation. Exhaled NO concentration ([NO]) obtained with nasal CNP was significantly lower, regardless of the pressure applied, than that measured with a noseclip, and was similar to and closely correlated to that obtained under intubation (F1, r = 0.90; F2, r = 0.88; P < 0.05). Real-time recorded [NO] obtained with nasal CNP of -5 cm H2O was again lower than that measured with a noseclip at any expiratory flow rate examined, indicating nasal NO contamination was eliminated irrespective of the flow rate. In conclusion, because a nasal CNP of -5 cm H2O was easily tolerated without any discomfort, this technique is a simple, easy and effective technique to eliminate nasal NO which should be widely applicable for the measurement of exhaled [NO].

Adult↗
PubMed1997

Exhaled nitric oxide and oxygenation abnormalities in hepatic cirrhosis.

Impaired arterial oxygenation, ranging from increased alveolar-arterial oxygen gradient (AaDo2) to hypoxemia, is commonly present in patients with cirrhosis. Nitric oxide (NO), through pulmonary vasodilatation, may play a major role in the oxygen abnormalities of cirrhosis. Our aim was to study the relationship between NO production and O2 abnormalities in 45 nonsmoking patients with cirrhosis and without major cardiovascular and respiratory diseases. Intrapulmonary shunting was detected by contrast-enhanced (CE) echocardiography. Lung volumes and diffusion, arterial blood gas analysis, serum NO2-/NO3-, NO output in the exhaled air, and cardiac index by the echocardiographic method were determined in all patients. Twenty-seven (60%) patients had an abnormally increased (> 15 mm Hg) AaDo2. The mean values of exhaled NO output and serum NO2-/NO3- were significantly higher in cirrhotic patients than in controls (252 +/- 117 vs. 75.2 +/- 19 nL/min/m2, P < .0001; and 47.5 +/- 29.4 vs. 32.9 +/- 10.1 micromol/L, P < .02, respectively). In all patients, there was a significant correlation between exhaled NO and AaDo2 (r = .78, P < .0001). Twelve patients (26.6%) were found to have CE-echocardiographic evidence of intrapulmonary shunting (positive CE-echo). Nine patients were considered to have hepatopulmonary syndrome (HPS) on the basis of an AaDo2 > 15 mm Hg and positive CE-echo. These 9 patients had a mean value of exhaled NO significantly higher than patients without HPS (331 +/- 73.2 vs. 223 +/- 118.4 nL/min/m2, P < .05). In all patients, cardiac index was positively correlated with exhaled NO (r = .47, P < .001) and with serum NO2-/NO3- (r = .43, P < .01). The results suggest an important role of NO in the oxygenation and circulatory abnormalities of patients with cirrhosis.

Adult↗
PubMed2001

Long-term administration of N-acetylcysteine decreases hydrogen peroxide exhalation in subjects with chronic obstructive pulmonary disease.

Patients with chronic obstructive pulmonary disease (COPD) exhale more hydrogen peroxide (H2O2) and lipid peroxidation products than healthy subjects. This may reflect oxidative stress in the airways that plays important role in the development and progression of COPD. N-acetylcysteine (NAC), a mucolytic drug, possesses antioxidant properties as it is a precursor of reduced glutathione that together with glutathione peroxidase may decompose H2O2 and lipid peroxides. We aimed to determine the effect of NAC, 600 mg effervescent tablets (Fluimucil), once a day for 12 months, and placebo on the concentration of H2O2 and thiobarbituric acid reactive substances (TBARs) in expired breath condensate and serum levels of two lipid peroxidation products (TBARs, lipid peroxides) in patients with COPD. The study was performed as a double-blind, double-dummy comparison between active drug and placebo in two parallel groups. Forty-four outpatients with stable COPD (22 in the NAC group and 22 in the placebo group) completed the study. Specimens of expired breath condensate and serum were collected at the randomization visit and then every 3 months over 1 year. The concentration of TBARs and H2O2 in expired breath condensate was measured spectrofluorimetrically by the thiobarbituric acid and homovanillic acid methods, respectively. Serum levels of lipid peroxides were determined spectrophotometrically after extraction with butanol and pyridine. Initially, H2O2 exhalation did not differ between the placebo and NAC groups up to 6 months of treatment. After this the significant differences were observed. After 9 and 12 months of treatment NAC group exhaled 2.3-fold (0.17+/-0.33 microM vs. 041+/-0.26 microM, P<0.04) [median 0.01 microM, quartile range (qr)=0.22 vs. median 0.15 microM, qr =0.43] and 2.6-fold (0.15+/-0.23 microM vs. 0.40+/-0.25 microN, P<0.05) median = 0.00 microM, qr = 0.23 vs. median = 0.36 microM, qr = 0.51] less H2O2 than placebo receivers, respectively. No significant effect of NAC administration on TBARs exhalation and serum levels of TBARs and lipid peroxides were noted over the whole treatment period. Also no significant associations between exhaled H2O2 and concentrations of lipid peroxidation products were noted in both treatment groups at any time-point. These results indicate that long-term oral administration of NAC attenuates H2O2 formation in the airways of COPD subjects and prove anti-oxidant action of drug. However, further studies are necessary to estimate the clinical significance of this finding.

Acetylcysteine↗
PubMedDate not supplied

Exhaled nitric oxide: a novel biomarker of adverse respiratory health effects in epidemiological studies.

The sampling of exhaled breath is a noninvasive procedure that can be performed easily in adults, children, and patients with respiratory disease. Several studies have demonstrated increased exhaled nitric oxide in patients with pulmonary disease, including asthma. In addition, exhaled nitric oxide may be an elegant tool for monitoring of environmental health effects of air pollution and the prevalence of atopy in epidemiological surveys. Recent literature about exhaled nitric oxide is presented in this article. Technical, physiological, and behavioral confounding factors of exhaled nitric oxide measurement are outlined.

Biomarkers↗
PubMed2003

Position of exhalation port and mask design affect CO2 rebreathing during noninvasive positive pressure ventilation.

OBJECTIVE: Noninvasive positive pressure ventilation may be considered a first line intervention to treat patients with hypercapnic respiratory failure. However, CO2 rebreathing from the ventilator circuit or mask may impair CO2 elimination and load the ventilatory muscles. This study was conducted to evaluate the effect of exhalation port location and mask design on CO2 rebreathing during noninvasive positive pressure ventilation. DESIGN: Lung model evaluation. SETTING: Experimental laboratory of a large university-affiliated hospital. SUBJECTS: A dual-chamber test lung was used to simulate the ventilatory mechanics of a patient with obstructive lung disease. INTERVENTION: Hypercapnic respiratory failure (end-tidal CO2 of 75 mm Hg) and obstructive lung disease were simulated in a double-chamber lung model. A facial mask (inner volume of 165 mL) with exhalation port within the mask (Facial-MEP) or the same mask with exhalation port in the ventilator circuit (Facial-WS) and a total face mask with exhalation port within the mask (inner volume 875 mL, Total Face) were tested during continuous positive airway pressure and pressure support ventilation provided by a single-limb circuit ventilator at the same frequency and tidal volume. MEASUREMENTS AND MAIN RESULTS: A capnometer and a flow transducer were placed in the lung model upper airway to measure the volume of CO2 rebreathed and tidal volume (Vt). The inspiratory load was estimated from the pressure variation in the lung model driving chamber (PDR). Volume of CO2 rebreathed was smaller during Facial-MEP compared with the other masks in all tested conditions (p <.001). The Vt and PDR necessary to decrease end-tidal CO2 20% (from 75 to 60 mm Hg) was different among the tested masks (Facial-MEP, Vt 701 +/- 9 mL, PDR 8.1 +/- 0.1 cm H2O/sec; Facial-WS, Vt 745 +/- 9 mL, PDR 10.2 +/- 0.1 cm H2O/sec; Total Face, Vt 790 +/- 12 mL, PDR 11.4 +/- 0.2 cm H2O/sec, p <.001). CONCLUSION: Facial-MEP with its exhalation port within the mask and the smallest mask volume demonstrated less rebreathed CO2 and a lower PDR than either the Facial-WS or Total Face masks. Additional studies are necessary to confirm if mask design can clinically affect patient's inspiratory effort during noninvasive positive pressure ventilation.

Carbon Dioxide↗
PubMed1993

Allergen-induced airway obstruction in guinea-pigs is associated with changes in nitric oxide levels in exhaled air.

Endogenously produced nitric oxide (NO) was monitored in exhaled air from ovalbumin-sensitized and pentobarbital anaesthetized guinea-pigs. Stable levels of nitric oxide were detected in exhaled air over a 30-min control period in each experiment (9.2 +/- 1.4 parts per billion, [ppb]). Insufflation pressure and NO in exhaled air immediately increased, in a dose dependent manner, in response to challenge with nebulized allergen (Ovalbumin, 0.1-10 mg). Indomethacin (5 mg kg-1) augmented the allergen-induced increases in insufflation pressure and NO. Fifteen min after the challenge the insufflation pressure remained elevated while NO in exhaled air had dropped below control levels. The increase in insufflation pressure induced by inhalation of PGF2 alpha (5 micrograms) was accompanied by an increase in nitric oxide in exhaled air, which however was significantly less than the increase in NO induced by allergen challenge. The results suggest a role for NO mechanisms in asthma.

Animals↗
PubMed2001

Impact of volume-dependent alveolar diffusing capacity on exhaled nitric oxide concentration.

Exhaled endogenous nitric oxide (NO) holds promise as a potential biomarker of pulmonary inflammation. Previous experimental and theoretical work has concluded that the alveolar concentration approaches a constant steady state value at end exhalation due to both a constant maximum flux or release of NO (J(max,alv)) and a constant diffusing capacity (D(NO,alv)) in the alveolar region. We have recently demonstrated that D(NO,alv) is not constant, but increases with alveolar volume (VA) given by the following average relationship: D(NO,alv) =48*VA(2/3) ml/min/mmHg (where VA is expressed in liters, STPD). We investigated the potential impact of a variable D(NO,alv) on exhaled concentration by incorporating the volume dependence into the currently accepted two-compartment model for NO exchange dynamics. Our results suggest that the mechanism underlying the plateau in exhaled concentration is a constant ratio J(max,alv)/D(NO,alv) This constant ratio requires a volume dependence of J(max,alv) similar to D(NO,alv), and is likely due to a decreasing alveolar surface area during exhalation.

Biomedical Engineering↗
PubMed2000

Increase in exhaled carbon monoxide during exacerbations of cystic fibrosis.

BACKGROUND: Non-invasive assessment of inflammation is likely to be useful in the management of cystic fibrosis (CF). Exhaled carbon monoxide (CO) concentrations are increased in patients with clinically stable CF. A study was undertaken to determine whether this marker of oxidative damage is further increased during exacerbations of the disease. METHODS: Exhaled CO concentrations were measured in 12 healthy non-smoking control subjects (six men) of mean (SE) age 37 (2) years with forced expiratory volume in one second (FEV(1)) 95 (1)% predicted and in 44 patients with CF (20 men) of mean (SE) age 29 (1) years with FEV(1) 56 (3)% predicted using an on-line CO analyser. RESULTS: Twenty nine patients were in a stable condition while 15 had clinically defined respiratory exacerbations (increased cough and production of sputum, change in the quality of the sputum, shortness of breath, sensation of chest congestion, and deterioration of FEV(1)) and represented the unstable group. Exhaled CO concentrations were 2.0 (0.15) ppm in the control group, were increased in the stable CF group to 2.7 (0.13) ppm (differences between means -0.67 (0.22), 95% confidence interval (CI) 0.22 to 1.12, p<0.01) and further increased in the unstable group to 4.8 (0.3) ppm (differences between means -2.15 (0.32), 95% CI 1.50 to 2.79, p<0.001). A significant correlation was found between the deterioration in FEV(1) and exhaled CO concentrations. CONCLUSIONS: This study shows that the measurement of exhaled CO is of potential value as an indicator of exacerbations in patients with CF and could be used as a simple method to monitor the course of the disease.

Adrenal Cortex Hormones↗
PubMed2002

Reduction in exhaled nitric oxide immediately after methacholine challenge in asthmatic children.

BACKGROUND: The measurement of exhaled nitric oxide (NO) has recently been proposed as a useful technique for the evaluation of airway inflammation in asthma. The purpose of this study was to determine the effect of methacholine bronchial provocation on the levels of exhaled NO in asthmatic children. METHOD: Exhaled NO was measurement immediately before and after methacholine provocation in 51 children with mild to moderate asthma. RESULTS: A significant decrease occurred in the level of exhaled NO (p<0.0001) after methacholine bronchial provocation which was not correlated with the percentage fall in forced expiratory volume in 1 second (FEV(1)). CONCLUSIONS: The methacholine test should not be used immediately before measurement of exhaled NO in children with asthma.

Adolescent↗
PubMed1998

Increase in exhaled nitric oxide levels in patients with difficult asthma and correlation with symptoms and disease severity despite treatment with oral and inhaled corticosteroids. Asthma and Allergy Group.

BACKGROUND: Patients with difficult asthma suffer chronic moderate to severe persistent asthma symptoms despite high doses of inhaled and oral corticosteroid therapy. These patients suffer a high level of treatment and disease related morbidity but little is known about the degree of airway inflammation in these patients. METHODS: Fifty two patients were examined to assess levels of exhaled nitric oxide (NO) as a surrogate marker of inflammatory activity in this condition. From this group, 26 patients were defined with severe symptoms and current physiological evidence of reversible airway obstruction requiring high dose inhaled (> or = 2000 micrograms beclomethasone dipropionate (BDP) equivalent) or oral steroid therapy to maintain disease control. RESULTS: Exhaled NO levels were higher in subjects with difficult asthma (mean 13.9 ppb, 95% CI 9.3 to 18.5) than in normal controls (7.4 ppb, 95% CI 6.9 to 7.8; p < 0.002), but lower than levels in steroid naive mild asthmatics (36.9 ppb, 95% CI 34.6 to 39.3; p < 0.001). Prednisolone treated patients had higher exhaled NO levels than patients only requiring inhaled corticosteroids (17.5 ppb, 95% CI 11.1 to 24.0 versus 7.2 ppb, 95% CI 4.6 to 9.8; p = 0.016), suggesting greater disease severity in this group. Non-compliance with prednisolone treatment was observed in 20% of patients but this did not explain the difference between the treatment groups. Exhaled NO levels were closely correlated with symptom frequency (p = 0.03) and with rescue beta agonist use (p < 0.002), but they did not correlate with lung function. CONCLUSIONS: Exhaled NO may serve as a useful complement to lung function and symptomatology in the assessment of patients with chronic severe asthma, and in the control and rationalisation of steroid therapy in these patients.

Administration, Inhalation↗
PubMed1999

Increased carbon monoxide in exhaled air of patients with cystic fibrosis.

BACKGROUND: Inflammation, oxidative stress, and recurrent pulmonary infections are major aggravating factors in cystic fibrosis. Nitric oxide (NO), a marker of inflammation, is not increased, however, probably because it is metabolised to peroxynitrite. Exhaled carbon monoxide (CO), a product of heme degradation by heme oxygenase 1 (HO-1) which is induced by inflammatory cytokines and oxidants, was therefore tested as a non-invasive marker of airway inflammation and oxidative stress. METHODS: Exhaled CO and NO concentrations were measured in 29 patients (15 men) with cystic fibrosis of mean (SD) age 25 (1) years, forced expiratory volume in one second (FEV(1)) 43 (6)%, 14 of whom were receiving steroid treatment. RESULTS: The concentration of exhaled CO was higher in patients with cystic fibrosis (6.7 (0.6) ppm) than in 15 healthy subjects (eight men) aged 31 (3) years (2.4 (0.4) ppm, mean difference 4.3 (95% CI 2.3 to 6.1), p<0.001). Patients not receiving steroid treatment had higher CO levels (8.4 (1.0) ppm) than treated patients (5.1 (0.5) ppm, mean difference 3.3 (95% CI -5.7 to -0.9), p<0.01). Normal subjects had higher NO levels (6.8 (0.4) ppb) than patients with cystic fibrosis (3.2 (0.2) ppb, mean difference 3.8 (95% CI 2.6 to 4.9), p<0.05) and were not influenced by steroid treatment (3.8 (0.4) ppb and 2.7 (0. 3) ppb for treated and untreated patients, respectively, mean difference 0.8 (95% CI -0.6 to 2.3), p>0.05). Patients homozygous for the DeltaF508 CFTR mutation had higher CO and NO concentrations than heterozygous patients (CO: 7.7 (1.8) ppm and 4.0 (0.6) ppm, respectively, mean difference 3.7 (95% CI -7.1 to -0.3), p<0.05; NO: 4.1 (0.5) ppb and 1.9 (0.7) ppb, respectively, mean difference 2.2 (95% CI -3.7 to -0.6), p<0.05). CONCLUSIONS: High exhaled CO concentrations in patients with cystic fibrosis may reflect induction of HO-1. Measurement of exhaled CO concentrations may be clinically useful in the management and monitoring of oxidation and inflammatory mediated lung injury.

Adrenal Cortex Hormones↗
PubMed1999

Effect of inhaled ozone on exhaled nitric oxide, pulmonary function, and induced sputum in normal and asthmatic subjects.

BACKGROUND: Nitric oxide (NO) may have a role in the pathophysiology of tissue injury in response to inhaled ozone in animals. METHODS: A double blind, randomised, placebo controlled, crossover study was undertaken to investigate the effects of inhaled ozone in 10 normal and 10 atopic asthmatic volunteers. Subjects were exposed to 200 ppb ozone or clean air for four hours with intermittent exercise, followed by hourly measurement of spirometric parameters and exhaled NO for four hours. Nasal NO and methacholine reactivity were measured and exhaled breath condensate and induced sputum samples were collected four and 24 hours after exposure. RESULTS: Exposure to ozone caused a fall in forced expiratory volume in one second (FEV(1)) of 7% in normal subjects (p<0.05) and 9% in asthmatic subjects (p<0.005). There was a 39% increase in sputum neutrophils at four hours in normal subjects (p<0.05) and a 35% increase at four hours in asthmatic subjects, remaining high at 24 hours (p<0.005 and p<0.05, respectively). There were no differences between normal and asthmatic subjects. There were no changes in methacholine reactivity, exhaled or nasal NO, nitrite levels in exhaled breath condensate, or sputum supernatant concentrations of interleukin 8, tumour necrosis factor alpha, or granulocyte-macrophage colony stimulating factor in either group. CONCLUSIONS: Exposure to 200 ppb ozone leads to a neutrophil inflammatory response in normal and asthmatic subjects but no changes in exhaled NO or nitrite levels.

Adult↗
PubMed1999

Markers of nitric oxide metabolism in sputum and exhaled air are not increased in chronic obstructive pulmonary disease.

BACKGROUND: Nitric oxide (NO) is involved in inflammation and host defence of the lung. It has been found in increased concentrations in the airways in asthmatic subjects but its levels in patients with chronic obstructive pulmonary disease (COPD) have not been investigated. A study was undertaken to determine whether markers of NO metabolism (NO in exhaled air, iNOS expression in sputum cells, and nitrite + nitrate (NO2-/NO3-) in sputum supernatant) are increased in subjects with COPD, and whether they correlate with inflammatory indices in induced sputum. The associations of these markers with smoking were also assessed. METHODS: Sixteen subjects with COPD (median age 66 years, median forced expiratory volume in one second (FEV1) 63% predicted, eight current smokers) and 16 healthy subjects (median age 63 years, median FEV1 113% predicted, eight current smokers) participated in the study. NO was measured during tidal breathing and sputum was induced by inhalation of hypertonic saline. RESULTS: No differences were observed between subjects with COPD and healthy controls in exhaled NO excretion rate (median 5.15 and 6.25 nmol/min), sputum macrophage iNOS expression (14% and 12%), and sputum supernatant NO2-/NO3- (46 and 73 microM). NO in exhaled air correlated with the percentage of sputum eosinophils in patients with COPD (rho = 0.65, p = 0.009) but not in healthy individuals. Exhaled NO and supernatant NO2-/NO3- levels were lower in healthy smokers than in healthy non/ex-smokers. CONCLUSIONS: Our findings indicate that NO metabolism is not increased in patients with stable COPD. The close association between exhaled NO levels and sputum eosinophils suggests a role for NO in airway inflammation in COPD. Studies performed during exacerbations may clarify this role.

Aged↗
PubMed2005

Effects of changes to the stable environment on the exhalation of ethane, carbon monoxide and hydrogen peroxide by horses with respiratory inflammation.

The aim of this study was to assess the effects of changes to the stable environment on exhaled markers of respiratory inflammation in six horses with clinical histories of recurrent airway obstruction. The horses were maintained for two weeks under conventional stable management (straw bedding and hay) and for two weeks on a reduced-dust regimen (paper bedding and ensiled grass), in a crossover study design. Exhaled ethane and carbon monoxide (CO) and exhaled breath condensate hydrogen peroxide (H(2)O(2)) were measured every three days under each regimen. The presence of clinical signs of airway inflammation (nasal discharge and cough) was monitored daily. The reduced-dust regimen was associated with fewer clinical signs of airway inflammation than the conventional regimen. Exhaled ethane and CO were significantly lower on the reduced-dust regimen and these markers were correlated with clinical signs of respiratory inflammation, but exhaled H(2)O(2) was not affected by the management regimen.

Airway Obstruction↗