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PubMed2001

Noninvasive measurement of exhaled nitric oxide in a spontaneously breathing mouse.

Nitric oxide (NO) has been detected in the exhaled gas of animals and humans. In previous work, investigators have used anesthetized, mechanically ventilated animals to obtain exhaled NO (E(NO)) measurements, which has unclear effects on the levels of E(NO) and does not allow for repeated analysis of E(NO). We sought to measure E(NO) from a single, spontaneously breathing mouse. The mouse was placed in a small Plexiglas chamber and allowed to acclimatize before exhaled gas was collected for E(NO) analysis. Under optimal operating conditions of flow and pressure, the mean concentration of exhaled NO (FE(NO)) of 25 mice was 10.1 +/- 1.0 ppb. The maximal variation of FE(NO) when repeatedly measured daily in individual animals was 2.1 ppb. Administration of L-NAME, a nonselective NOS inhibitor, reduced FE(NO) by 51 +/- 6% (p < 0.01). Intraperitoneally administered lipopolysaccharide induced acute lung injury and increased FE(NO) by 30 +/- 7% (p < 0.05). We have demonstrated that it is possible to noninvasively measure E(NO) from a single, spontaneously breathing mouse. This novel technique provides a stable, reproducible, and responsive measure of E(NO) in mice. This technique will be of use in determining cellular and isoform sources of E(NO), as well as the role of endogenous NO in lung disease.

Analysis of Variance↗
PubMed2001

Low-dose theophylline reduces eosinophilic inflammation but not exhaled nitric oxide in mild asthma.

Theophylline is well-established in the management of asthma, and there is some evidence of an antiinflammatory effect in asthma. It is not known whether theophylline affects inflammatory markers such as sputum eosinophils and exhaled nitric oxide (NO) in patients with mild asthma not receiving inhaled steroid therapy. In a double-blind, placebo-controlled, cross-over study of 15 patients with mild asthma, we assessed the effect of low-dose theophylline therapy (250 mg twice per day) on eosinophils in induced sputum, bronchoalveolar lavage (BAL) and airway biopsies at the end of both the treatment and placebo periods. Measurements of exhaled nitric oxide (NO) were made at the end of the active and placebo treatment periods of 5 wk each. Low-dose theophylline (mean serum level, 6.1 mg/L) led to a significant reduction in mean (95% confidence interval [CI]) sputum eosinophils from 11.3% (7.80-14.76%) to 8.0% (5.46-10.44%), BAL eosinophils from 3.4% (2.4-4.4%) to 1.7% (1.1-2.3%) and biopsy eosinophils from 1.83% (0.76-2.89%) to 1.20% (0.27-2.13%) compared with placebo (all p < 0.05). There was no significant change in levels of exhaled NO or improvement in lung function and bronchial responsiveness. Low-dose theophylline induced antiinflammatory effects in asthma, reflected by a fall in airway eosinophils with no change in exhaled NO or changes in lung function.

Adult↗
PubMed1987

Passive exhalation technique correlates with esophageal balloon measurements of respiratory mechanics in beagle pups.

We correlated respiratory system mechanics measured by passive exhalation technique with pulmonary mechanics assessed by esophageal balloon technique to determine the ability of each to detect histamine-aerosol-induced changes in conductance and compliance. Eight beagle pups were anesthetized with chloralose and mechanically ventilated 6 times over a 2-wk period of an acute canine parainfluenza II infection. Measurements of respiratory mechanics were obtained by both methods after aerosol challenge with 5 breaths of saline and after each of 9 increasing doses of histamine. Pulmonary conductance and static compliance of the lung were measured by the esophageal balloon method. The rate constant of the respiratory system was calculated by computer-assisted analysis of passive exhalation. Static compliance of the respiratory system was measured after 2 s of apnea, and conductance of the respiratory system was calculated as compliance multiplied by rate constant. Paired data were obtained on 349 measurements. As expected, both conductance and compliance decreased significantly (p less than 0.05) after histamine aerosol challenge by both techniques. Rate constant did not change significantly by either method. The 2 techniques were highly correlated (p less than 0.001) for conductance (r = 0.76), compliance (r = 0.94), and rate constant (r = 0.66). We conclude that analysis of respiratory mechanics using the passive exhalation method correlates well with esophageal balloon data. Furthermore, passive exhalation techniques are technically simple and can detect changes in respiratory mechanics associated with histamine challenges.

Animals↗
PubMed2002

Increased exhaled cysteinyl-leukotrienes and 8-isoprostane in aspirin-induced asthma.

The pathogenesis of aspirin-induced asthma (AIA) has not yet been clearly elucidated, although eicosanoid metabolites appear to play an important role. We hypothesized that levels of eicosanoids in exhaled air condensate are abnormal in patients with AIA and that they change in patients receiving steroid therapy. We measured cysteinyl-leukotrienes (cys-LTs), prostaglandin E(2) (PGE(2)), and leukotriene B(4) (LTB(4)), and also 8-isoprostane as a marker of oxidative stress, by enzyme immunoassay in exhaled breath condensate from patients with AIA (17 steroid naive; mean age, 41 +/- 23 years; FEV(1), 63%pred), 26 patients with aspirin-tolerant asthma (ATA) (11 steroid naive; mean age, 47 +/- 18 years; FEV(1), 69%pred), and 16 healthy subjects (mean age, 45 +/- 17 years; FEV(1), 93%pred). Cys-LTs were significantly higher in steroid-naive patients with AIA compared with steroid-naive patients with ATA and healthy subjects (152.3 +/- 30.4 and 36.6 +/- 7.1 versus 19.4 +/- 2.8 pg/ml; p < 0.05 and p < 0.05, respectively). Steroid-naive patients with AIA also had higher levels of 8-isoprostane than normal subjects (131.8 +/- 31.0 versus 21.9 +/- 4.5 pg/ml; p < 0.05). There were significantly lower levels of both cys-LTs and 8-isoprostanes in steroid-treated patients with AIA. There was no difference in either the PGE(2) or LTB(4) level between the patient groups. This is the first study to show that cys-LTs and 8-isoprostanes are elevated in expired breath condensate of steroid-naive patients with AIA, and that cys-LTs are decreased in steroid-treated patients. Exhaled PGE(2) levels are not reduced, so that it is unlikely that a deficiency of PGE(2) is an important mechanism, whereas exhaled LTB(4) levels are unchanged, indicating an abnormality beyond 5-lipoxygenase.

Adult↗
PubMed2001

High levels of exhaled nitric oxide (NO) and NO synthase III expression in lesional smooth muscle in lymphangioleiomyomatosis.

Smooth-muscle proliferation is the hallmark of lymphangioleiomyomatosis (LAM). Although little is known about the pathogenesis of LAM, nitric oxide (NO) is a key regulator of smooth-muscle proliferation. NO is linked to the pathogenesis of other lung diseases such as asthma, in part by the finding of higher-than-normal levels of exhaled NO. If NO were involved in the abnormal smooth-muscle proliferation in LAM, we reasoned that exhaled NO from individuals with LAM would also differ from that of healthy control subjects. To evaluate this hypothesis, we studied exhaled NO in individuals with LAM in comparison with healthy and asthmatic women using a chemiluminescent NO analyzer. Women with LAM had higher exhaled NO than did healthy women but lower than asthmatic women (NO [parts per billion] median (25 to 75%): LAM 8 [7 to 15] [n = 28], control 6 [5 to 8] [n = 21], asthma 14 [8 to 25] [n = 22]; Kruskal-Wallis P < 0.001). Immunohistochemical studies on formalin-fixed, paraffin-embedded sections of surgical and autopsy material from lungs of individuals with LAM showed diffuse NO synthase III (NOSIII) expression in the lesional smooth muscle of LAM similar to that in the vascular endothelium. NOSIII expression was limited to the vascular endothelium and bronchial smooth muscle in healthy control lungs. The increased NO and the presence of NOSIII expression in lesional smooth muscle warrants further study into the potential role for NO in the pathogenesis of LAM.

Adult↗
PubMed2001

Glucocorticoid treatment reduces exhaled nitric oxide in cystic fibrosis patients.

In cystic fibrosis (CF), low concentrations of exhaled nitric oxide (NO) and reduced expression of inducible nitric oxide synthase (iNOS) in airway epithelium have been reported. However, abundant iNOS expression has been found in the subepithelial tissues and elevated concentrations of NO metabolites in breath condensate and sputum. These conflicting results may be explained by increased scavenging of NO by superoxide radicals, resulting in rapid conversion to peroxynitrite, so that only a small proportion of the NO produced in the lung tissue reaches the airway lumen. If iNOS were active in the CF lung, exhaled NO would be further reduced by glucocorticoid treatment. CF patients (n = 13) were recruited to a double-blind, placebo-controlled study with crossover. Treatment comprised prednisolone or placebo for 5 days with a 9 day washout. After each treatment, exhaled NO was measured, spirometry performed and blood collected for measurement of serum nitrogen dioxide/nitrous oxide (NO2/NO3). Ten patients (8 male) completed the study. Following prednisolone treatment (mean +/- SD) exhaled NO concentration (3.1 +/- 1.6 parts per billion (ppb)) was significantly reduced versus placebo treatment (4.9 +/- 4.2 ppb; p<0.05, Wilcoxon signed-rank test). Spirometric indices and serum NO2/NO3 concentration were unchanged. These findings support the hypothesis that glucocorticoids suppress nitric oxide production in cystic fibrosis airways by reducing inducible nitric oxide synthase expression or by inhibiting recruitment of neutrophils, cells which express inducible nitric oxide synthase.

Adult↗
PubMed2002

Measurement of exhaled nitric oxide in children, 2001.

Measurement of fractional exhaled nitric oxide in exhaled air is an exciting innovative technique that gives new insights in to the pathophysiology of lung disease and asthma in particular, with many potential clinical applications. Careful standardisation of measurement techniques will facilitate the use of this new measurement in paediatric respiratory medicine: this Task Force was set up for this purpose. Methodologies, for use in all age groups, are already available and there are abundant questions relating to interpretation and application of fractional exhaled nitric oxide waiting to be addressed. Noninvasiveness and instantaneous results potentially make it a suitable monitoring instrument for use in children. Exhaled nitric oxide measurement has definitely found its way into clinical research in paediatric respiratory medicine. Evidence for clinically-useful applications is accumulating, and the merits of this new technique must now be demonstrated in larger studies, using standardised methodology in an appropriate setting.

Adolescent↗
PubMed2004

Prevalence of asthma and exhaled nitric oxide are increased in bleachery workers exposed to ozone.

The aims of the present study were to determine whether exposure to high peaks of ozone resulted in an increased prevalence of asthma or respiratory symptoms among bleachery workers and whether nitric oxide (NO) was elevated in the exhaled air of these workers. Bleachery workers (n=228) from three Swedish pulp mills who had been exposed to ozone, together with 63 unexposed control subjects, were investigated by means of spirometry, Phadiatop, exhaled and nasal NO and answers to a questionnaire concerning respiratory symptoms and exposure. Exposure to an ozone peak that gave rise to respiratory symptoms was defined as a "gassing". Bleachery workers reporting four or more gassings involving ozone had an increased prevalence of adult-onset asthma, wheeze, and current asthma symptoms. They also had a higher median concentration of exhaled NO in comparison with those who reported no such gassings (19.2 versus 15.7 parts per billion). No such associations were found in respect of nasal NO. The results from this study show that bleachery workers who have been repeatedly exposed to ozone gassings have an increased prevalence of adult-onset asthma. The results also indicate exhaled nitric oxide may be a marker of airway inflammation in bleachery workers who have been exposed to high peaks of ozone.

Adult↗
PubMed2003

Slower rise of exhaled breath temperature in chronic obstructive pulmonary disease.

In chronic obstructive pulmonary disease (COPD) there is decreased vascularity of the bronchi and inflammation of the airways that may have opposite effects on the regulation of heat loss. Exhaled air temperature increase (delta(e) T) was measured in 23 patients with moderate COPD (18 male, mean age +/- SEM 70 +/- 1 yrs; forced expiratory volume in one second (FEV1) 45 +/- 3%, FEV1/forced vital capacity 54 +/- 4%) and 16 normal volunteers (64 +/- 4 yr) and compared to exhaled nitric oxide (eNO) and inflammatory cells in induced sputum as a marker of airway inflammation. Delta(e) T was measured during a flow- and pressure-controlled single exhalation with a fast-response thermometer. delta(e) T was reduced in patients with COPD (1.86 +/- 0.15 delta C x s(-1)) compared to normal subjects (4.00 +/- 0.26 delta C x s(-1)). There was no difference in delta(e) T between patients treated with inhaled steroids and those who were steroid naïve. Delta(e) T was correlated with eNO (r=0.60) but not with sputum neutrophilia. In COPD patients, delta(e) T was increased (2.26 +/- 0.16 delta C x s(-1)) after the inhalation of 200 microg of albuterol, which is a known vasodilator, indicating that delta(e) T and bronchial blood flow may be correlated. Exhaled temperature increase is reduced in chronic obstructive pulmonary disease patients and is increased by the inhalation of vasodilators and therefore may be related to changes of bronchial blood flow and tissue remodelling.

Aged↗
PubMed2006

Effect of smoking on exhaled nitric oxide and flow-independent nitric oxide exchange parameters.

It is a well-known fact that smoking is associated with a reduction in exhaled nitric oxide (NO) levels. There is, however, limited knowledge relating to the smoking-induced changes in production or exchange of NO in different compartments of the airways. This study comprised 221 adult subjects from the European Community Respiratory Health Survey II, who were investigated in terms of their exhaled NO, lung function, immunoglobulin E sensitisation and smoking habits. The following parameters were determined using extended NO analysis: airway tissue nitric oxide concentration (Caw,NO), airway transfer factor (or diffusing capacity) for nitric oxide (Daw,NO), alveolar nitric oxide concentration (CA,NO) and fractional exhaled nitric oxide concentration at a flow rate of 50 mL x s(-1) (FeNO,0.05). Maximum total airway nitric oxide flux (J'aw,NO) was calculated from Daw,NO(Caw,NO-CA,NO). Current smokers (n = 35) exhibited lower (geometric mean) FeNO,0.05 (14.0 versus 22.8 ppb), Caw,NO (79.0 ;versus 126 ppb) and J'aw,NO (688 versus 1,153 pL x s(-1)) than never-smokers (n = 111). Ex-smokers (n = 75) were characterised by lower FeNO,0.05 (17.7 versus 22.8 ppb) and Jaw,NO (858 versus 1,153 pL x s(-1)) than never-smokers. These relationships were maintained after adjusting for potential confounders (sex, age, height, immunoglobulin E sensitisation and forced expiratory volume in one second), and, in this analysis, a negative association was found between current smoking and CA,NO. Snus (oral moist snuff) consumption (n = 21) in ex-smokers was associated with an increase in Daw,NO and a reduction in Caw,NO, after adjusting for potential confounders. Passive smoking was associated with a higher CA,NO. Using extended nitric oxide analysis, it was possible to attribute the reduction in exhaled nitric oxide levels seen in ex- and current smokers to a lower total airway nitric oxide flux in ex-smokers and reduced airway and alveolar nitric oxide concentrations in current smokers. The association between snus (oral tobacco) use and reduced nitric oxide concentrations in the airways and increased nitric oxide transfer from the airways warrants further studies.

Adult↗
PubMed1995

Elevated exhaled nitric oxide in patients with hepatopulmonary syndrome.

The hypoxaemia of hepatopulmonary syndrome, seen in severe chronic liver dysfunction, occurs as a result of precapillary pulmonary arterial dilatation and arteriovenous communications. These abnormalities contribute to the mismatch between ventilation and perfusion, and the right to left blood flow shunting. Nitric oxide (NO) is a powerful vasodilator concerned with the regulation of pulmonary vascular tone in man. Using a chemiluminescence analyser, we have measured endogenously produced NO in the exhaled air of three patients with the hepatopulmonary syndrome, six normoxaemic cirrhotic patients and six healthy volunteers. The subjects breathed NO-free air throughout the measurements. The molar rate of production of exhaled NO was raised almost threefold in the patients with hepatopulmonary syndrome compared with normal volunteers and with normoxaemic cirrhotic patients. Hypoxia per se, achieved in the normal volunteers by breathing a hypoxic gas mixture, reduced rather than increased the exhaled NO. One hepatopulmonary syndrome patient received an orthotopic liver transplant and achieved normoxaemia after 3 months. The exhaled NO also returned to normal. Increased pulmonary production of NO could contribute to the development of the hepatopulmonary syndrome.

Blood Gas Analysis↗
PubMed1996

The effect of alcohol ingestion on exhaled nitric oxide.

The concentration of nitric oxide (NO) is increased in the exhaled air of patients with inflammatory lung diseases, including asthma, possibly reflecting cytokine-mediated chronic airway inflammation. Endogenous NO is generated from L-arginine by the action of several types of NO synthase (NOS). NOS have structural similarities with cytochrome P450 reductases. Alcohol decreases exhaled NO in animals, but this has not previously been investigated in man. We studied the effect of alcohol ingestion in nine asthmatic and 12 normal subjects, measuring the peak concentration of exhaled NO using a modified chemiluminescence analyser. A significant decrement in NO occurred in asthmatic patients (mean +/- SEM before ethanol 204 +/- 58 to 158 +/- 59 parts per billion (ppb) after ethanol; p < 0.02), without significant change in the normal subjects (122 +/- 14 to 114 +/- 15 ppb). Thus, in our study, alcohol decreased exhaled nitric oxide in asthmatic subjects but not in normal individuals. This may reflect preferential action on inducible nitric oxide synthase which is expressed in asthmatic airways. An inhibitory effect of ethanol on inducible nitric oxide synthase may contribute towards the effect of alcohol in asthma.

Adult↗
PubMed1998

Exhaled single-breath nitric oxide measurements are reproducible, repeatable and reflect levels of nitric oxide found in the lower airways.

Measurement of exhaled nitric oxide (NO) may allow noninvasive assessment of inflammatory disease in the lung. We determined immediate and day-to-day reproducibility of single-breath NO measurements at different points on the exhaled test, and whether levels recorded reflect levels of NO in the lower airways. Using a rapid chemiluminescence analyser, 55 healthy control subjects performed three sequential tests on each of two days. NO levels were compared at the level corresponding with: 1) the time the mouth pressure fell below 4 cmH2O (MP); 2) the plateau of end-exhaled CO2 (CO2); and 3) the NO plateau (NOp). NO levels were measured directly from the lower airways of 15 lung transplant recipients and compared with NO levels from a single-breath test performed in the same cohort. For measurements performed at MP, CO2 and NOp, the mean +/- SD differences between the two closest levels performed on the same day were 0.11+/-0.18, 0.095+/-0.16 and 0.094+/-0.13 parts per billion (ppb), respectively, and between days were 0.18+/-0.76, 0.19+/-0.78 and 0.17+/-0.8 ppb, respectively. End-expiratory levels recorded at the mouth from a single-breath test and in the lower airways were highly correlated (mouth versus trachea r2=0.95, p<0.0001, mouth versus bronchus r2=0.92, p<0.0001). Single-breath exhaled nitric oxide levels are a simple, reproducible and valid measure of nitric oxide production from the lower respiratory tract.

Breath Tests↗
PubMed1999

Exhaled nitric oxide is increased in active fibrosing alveolitis.

STUDY OBJECTIVES: Interstitial inflammation is a major aggravating factor in fibrosing lung disease associated with scleroderma (FASSc) and cryptogenic fibrosing alveolitis (CFA). Exhaled nitric oxide (NO) production is increased in asthma and bronchiectasis and reflects the degree of inflammation. We investigated whether measuring levels of exhaled NO is valuable in assessing disease activity in patients with CFA and patients with FASSc. MEASUREMENTS AND RESULTS: NO levels were measured in 11 patients with CFA (mean age +/- SEM, 58 +/- 12 years old; 5 were male) and 17 patients with FASSc (mean age, 48 +/- 9 years old; 5 were male), and they were compared to BAL cell counts and lung function. Patients with CFA and FASSe had elevated NO levels (11.2 +/-1.0 parts per billion [ppb] and 9.8 +/- 1.0 ppb, respectively; p > 0.05), whereas in a group of 13 nonsmoking normal subjects, the NO levels were not elevated (6.9 +/- 0.5 ppb; p < 0.05). Patients with FASSc (n = 8) who had active BAL (defined as either lymphocytes > 14%, neutrophils > 4%, or eosinophils > 3%) had significantly higher NO levels (13.2 +/- 1.8 ppb), and neutrophil (16.5 +/- 4.0%) and lymphocyte (26.8 +/- 3.4%) BAL cell counts than did patients with FASSc who had inactive BAL (6.7 +/- 1.2 ppb; 1.3 +/- 1.0% and 7.5 +/- 1.3%, respectively; p < 0.05). There was a significant correlation between exhaled NO and lymphocyte cell count in patients with FASSc (r = 0.58; p < 0.05). All patients with CFA had active BAL; however, those treated with corticosteroids (12.9 +/- 1.0% ppb, p < 0.05) had lower NO levels (9.0 +/- 1 ppb) and higher BAL lymphocyte cell couits (16.6 +/- 2.0%) than did those not treated with corticosteroids (7.2 +/- 1.7%; p < 0.05). CONCLUSIONS: We conclude that exhaled NO may be a useful addition to BAL cell counts in disease monitoring.

Breath Tests↗
PubMed1999

A method for the standardized offline collection of exhaled nitric oxide.

STUDY OBJECTIVES: Exhaled nitric oxide (ENO) is a noninvasive marker of airway inflammation. The purpose of this study was to compare a standardized offline ENO measurement apparatus with a validated on-line method. DESIGN: Asthmatic volunteers (n = 21) had ENO measured by the two following methods: (1) inhalation to total lung capacity (TLC) followed by exhalation at a constant flow (45 mL/s) against a high resistance, while monitoring nitric oxide (NO) and pressure on-line; and (2) inhalation to TLC and exhalation into mylar balloons via an apparatus that included the same resistance and flow rate as used in the on-line method. We also examined NO stability in mylar balloons over 48 h. MEASUREMENTS AND RESULTS: ENO values (given as geometric mean in parts per billion [ppb]; 95% confidence intervals) differed between the on-line method (69.6; 42.6 to 113.8) and the offline method (49.5; 30.9 to 79.3), indicating that the offline method gave lower ENO measures than the on-line method (p < 0.001). Furthermore, this difference between measures increased with increasing mean values. The intraclass correlation coefficient (0.931), however, showed excellent correlation between the on-line and offline methods. Within-subject repeatability, as assessed by the coefficient of repeatability (CR), was good for both the on-line and offline methods (CR, 1.09 and 1.17, respectively). Geometric mean NO concentrations (95% confidence limits) in mylar balloons containing exhalate increased from a baseline of 55.8 ppb (36.9, 84.4) to 64.5 ppb (45.6, 91.1) and 69.5 ppb (51.4, 94.0) at 24 h and 48 h, respectively. CONCLUSIONS: The offline method gave reproducible ENO values that were consistently smaller than, but showed good correlation with, values obtained with on-line ENO collection. This method is suitable for offline collection, but the measured values are not interchangeable with those obtained by on-line measurement.

Airway Resistance↗
PubMed2001

Elevated concentrations of exhaled hydrogen peroxide in asthmatic patients.

BACKGROUND: Airway inflammation is important in the development and progression of asthma. Activation of inflammatory cells induces a respiratory burst resulting in the production of reactive oxygen species, such as H(2)O(2). The aim of this study was to measure the concentration of H(2)O(2) in exhaled breath condensate and its correlation with airway obstruction, airway hyperresponsiveness, and concentration of eosinophil cationic protein (ECP) in serum in 70 steroid-naive, atopic patients with unstable asthma (20 men; age range, 18 to 62 years) and 17 normal subjects (7 men; age range, 19 to 34 years). METHODS: Exhaled H(2)O(2) was measured using a colorimetric assay, and the concentration of ECP in serum was measured using radioimmunoassay. Airway hyperresponsiveness was expressed as the provocative concentration of inhaled histamine causing a 20% fall in FEV(1) (PC(20)). RESULTS: In patients with asthma, the mean H(2)O(2) concentration was significantly elevated compared to values in normal subjects: 0.127 +/- 0.083 mol/L vs 0.024 +/- 0.016 mol/L (p < 0.001). There was a significant correlation among H(2)O(2) concentration, FEV(1), PC(20), and ECP in serum. CONCLUSION: We conclude that exhaled H(2)O(2) is significantly elevated in asthmatic patients. This is correlated with disease severity and indirect markers of airway inflammation. Measurement of exhaled H(2)O(2) may be useful to assess airway inflammation and oxidative stress in asthmatic patients.

Adolescent↗
PubMed2001

A new method for the remote collection of nasal and exhaled nitric oxide.

STUDY OBJECTIVES: The present study introduces a method that has been developed to improve the remote collection and transportation of gas samples from the nose and lungs. DESIGN: Assessment of agreement between two methods of clinical measurements. SETTING: Noninvasive exhaled gas measurement at a respiratory research laboratory. PARTICIPANTS: Ten nonsmoking adult volunteers (median age, 44 years; age range, 33 to 53 years; men, 6; women, 4) were recruited. MEASUREMENTS AND RESULTS: Exhaled nitric oxide (ENO) and nasal nitric oxide (NNO) outputs were measured directly (on-line) and remotely (off-line). With the velum closed, lung air was exhaled at fixed flows (ie, 6, 8, and 10 L/min) (ENO) or room-air was aspirated through the nose in series at one fixed flow (ie, 5 to 8 L/min) (NNO). The off-line nitric oxide (NO) measurements were achieved by a gas collection tube system, which consisted of a flow control unit, a tube reservoir with one-way valves at both ends, and an interrupter valve allowing the trapping of gas inside the tube and eliminating the inclusion of "dead space." After clamping, the reservoir may store and transport the gas samples for delayed analysis. The coefficient of variation of three consecutive NO measurements was < 3% for both on-line and off-line ENO and NNO. The correlations between on-line and off-line measurements in both ENO and NNO outputs were high (r = 0.99; R(2) = 0.99), and, unlike previous studies using bag-collection, the ENO outputs for on-line and off-line measurements were in good agreement (Bland-Altman test) at all flows tested. CONCLUSIONS: The tube gas collection system eliminates the dead space and contamination during the gas sampling and permits the cost-effective and reliable off-line collection of both nasal and exhaled gas samples.

Adult↗
PubMed2002

Exhaled H(2)O(2) in steady-state bronchiectasis: relationship with cellular composition in induced sputum, spirometry, and extent and severity of disease.

STUDY OBJECTIVES: To determine the concentration of exhaled H(2)O(2) in patients with bronchiectasis, and to study the relationship between levels of exhaled H(2)O(2), extent of disease, symptoms score, spirometry, and cellular composition obtained from induced sputum; furthermore, to account for possible confounding effects of inhaled corticosteroids (ICS) usage, long-term oral antibiotic treatment, and chronic colonization with Pseudomonas aeruginosa. DESIGN: Cross-sectional study. PATIENTS: Thirty patients with steady-state bronchiectasis. RESULTS: Mean (95% confidence interval [CI]) exhaled H(2)O(2) levels were significantly elevated in patients with bronchiectasis compared to normal subjects: 1.1 (0.87 to 1.29) microM vs 0.3 (0.19 to 0.36) microM, respectively (p < 0.0001). Patients treated with ICS had similar values as steroid-naïve patients. The group of patients with P aeruginosa colonization showed a significantly increased concentration of H(2)O(2) compared to the group without P aeruginosa colonization. Patients receiving long-term oral antibiotic treatment had significantly higher values of H(2)O(2) compared to those not receiving antibiotics. There was a significant positive correlation between H(2)O(2) and either the percentage of neutrophils in induced sputum or the extent of the disease as defined by high-resolution CT. A significant negative correlation was found between H(2)O(2) and FEV(1) percent predicted. Finally, there was a significant positive correlation between H(2)O(2) and the symptoms score. CONCLUSIONS: Patients with bronchiectasis in stable condition showed increased levels of exhaled H(2)O(2). The above-mentioned levels were not decreased either by ICS or long-term oral antibiotic treatment, but were significantly affected by chronic colonization with P aeruginosa. H(2)O(2) levels could be an indirect index of neutrophilic inflammation, impairment of lung function, and extension and severity of the disease.

Administration, Inhalation↗