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PubMed2000

Effects of short-term exposure to 0.2 ppm ozone on biomarkers of inflammation in sputum, exhaled nitric oxide, and lung function in subjects with mild atopic asthma.

To gain further insight into the kinetics of airway inflammatory response and explore the possibility of nitric oxide as a surrogate marker of the lower airway inflammatory response to ozone, nine subjects with mild atopic asthma were exposed to filtered air or 0.2 ppm ozone for 2 hours with intermittent exercise. Lung function was measured at baseline and immediately after exposures. Sputum induction was performed at 6 hours and at 24 hours after exposures, and exhaled nitric oxide levels were measured at baseline, immediately, 6, and 24 hours after both exposures. A significant decline in forced expiratory volume in one second and inspiratory capacity was detectable following exposure to ozone. In addition, a 2-fold increase was observed in the percentage of polymorphonuclear leukocytes 6 hours after exposure to ozone, with no changes in other biomarkers at this time point. By 24 hours after ozone exposure, the neutrophilia had subsided but there was an increase in albumin, total protein, myeloperoxidase, and eosinophil cationic protein. Exhaled nitric oxide levels, histamine, interleukin-8, and growth-related oncogene-alpha in sputum did not change significantly following ozone exposure. It was concluded that short-term ozone exposure induces an acute inflammatory response in asthmatic airways, characterized by early polymorphonuclear leukocyte influx followed by plasma extravasation and activation of eosinophils and neutrophils. Exhaled nitric oxide is not a useful marker for detecting inflammatory response to ozone in persons with mild asthma.

Administration, Inhalation↗
PubMed2004

Exhaled nitric oxide reflects asthma severity and asthma control.

INTRODUCTION: This study was undertaken to a) evaluate whether exhaled nitric oxide (fraction of exhaled nitric oxide [FENO]) levels are reflective of asthma severity in concordance with the National Asthma Education and Prevention Program categorization and b) determine the usefulness of FENO using the single-breath exhalation technique for monitoring asthma control and compliance with steroid treatment. METHODS: Thirty patients with asthma (7-17 yrs old; 14 males and 16 females) that was mild (n=8), moderate (n=17), or severe (n=5) were included in the study. Fifteen patients were seen on more than one occasion for a total of 53 visits. Information obtained at each visit included asthma symptoms, beta-agonists and corticosteroids use, compliance to steroids, and forced expiratory volume in 1 sec (FEV1) and FENO measurements. Asthma control was judged by a pulmonologist based on overall evaluation of symptoms, FEV1 measurements, and the frequency of beta-agonists use at each visit. RESULTS: The mean +/- SD FENO was significantly different in the mild, moderate, and severe asthma categories (30 +/- 12, 65 +/- 48, 104 +/- 68, respectively; F(2,52)=6.02 p=.005). FENO was significantly correlated with asthma severity (r=.44, p=.001), compliance (r=-.75, p=.001), and control (r=-.51, p=.001). There were no statistically significant differences between asthma severity and compliance or FEV1. DISCUSSION: Our data suggest that a) FENO may be a practical tool to evaluate asthma severity and asthma control over time and b) FENO may be used as a marker of compliance with steroids even when FEV1 has not decreased significantly.

Adolescent↗
PubMed2004

Increased macrophage-derived chemokine in exhaled breath condensate and plasma from children with asthma.

BACKGROUND: Type 2 helper T lymphocyte-specific chemokines including macrophage-derived chemokine (MDC), thymus and activation-regulated chemokine (TARC) and eotaxin are important mediators for allergic airway inflammation. OBJECTIVE: We investigated whether these chemokines can be detected in exhaled breath condensate (EBC) and their relation to childhood asthma. METHODS: Asthmatics recruited from paediatric clinics of a university teaching hospital were classified into intermittent asthma (IA) and persistent asthma (PA) according to Global Initiative for Asthma guidelines. EBC was collected by a disposable collection kit, whereas fractional exhaled nitric oxide (FENO) was measured by a chemiluminescence analyser. Concentrations of MDC, TARC and eotaxin in both EBC and plasma were measured using sandwich enzyme immunoassay. The intra-subject reproducibility of exhaled chemokine measurements was determined by co-efficients of variation (CV). RESULTS: Forty-eight patients with PA, 36 children with IA and 18 controls were recruited. MDC and eotaxin were present in EBC from nearly all subjects, whereas TARC could be measured in EBC from 33 (32%) subjects only. The median MDC concentration in EBC was higher in PA (117 pg/mL) as compared with IA (106 pg/mL) and controls (105 pg/mL; P=0.003 for both). The median plasma MDC concentration in PA (648 pg/mL) was also higher than that in IA (520 pg/mL; P=0.002) and controls (490 pg/mL; P=0.008). The median plasma TARC concentration was also increased in PA as compared with IA (72 pg/mL vs. 35 pg/mL; P=0.004). MDC concentrations in EBC were lower in patients with PA who received high-dose inhaled corticosteroid (P=0.005). FENO was significantly higher in asthmatics than controls (P<0.0001), but it was not associated with chemokines in EBC or plasma. The mean (range) CV for measuring MDC, TARC and eotaxin in EBC (n=6) were 5.5 (2.0-7.2%), 8.8 (3.6-14.4%) and 5.2 (2.8-7.9%), respectively. CONCLUSIONS: Our results suggest that MDC in EBC and MDC and TARC in plasma are increased in children with PA as compared with IA or control. MDC concentrations in EBC are suppressed in patients on high-dose inhaled corticosteroid treatment.

Adolescent↗
PubMed2006

Comparison of two methods for exhaled breath condensate collection.

BACKGROUND: Exhaled breath condensate (EBC) is a noninvasive method to obtain samples from fluids lining the respiratory surfaces. Even though various methods and devices are now available, the relative efficiency of these methods for recovering airway mediators and characterizing EBC has not been established. AIM: To compare the volume, pH, lipid mediator, and protein concentrations in EBCs collected by two commonly used commercially available devices, RTube and ECoScreen. METHODS: Exhaled breath condensates were obtained consecutively using the RTube and ECoScreen methods from 30 healthy, nonallergic adults. Samples were immediately placed on dry ice after collection. pH was measured after argon deaeration. Cysteinyl leukotrienes (cys-LTs) were measured as a representative lipid mediator and eotaxin as the protein mediator by using enzyme-linked immunosorbent assay. RESULTS: The mean volume of samples obtained with ECoScreen (1880 +/- 116 microl) was significantly higher than that obtained with RTube (1405 +/- 82 microl) (P < 0.001). Concentrations of both cys-LTs [205.4 pg/ml (65.5-472.3) with ECoScreen vs 21.6 (11.87-152.2) with RTube, P < 0.001] and eotaxin [17.0 pg/ml (11.4-22.4) with ECoScreen vs 11.7 (10.5-13.5) with RTube, P = 0.01] were significantly higher in samples collected with ECoScreen than with RTube. There was no significant difference between the pH measurements. CONCLUSION: Compared with RTube, collection of exhaled breath by ECoScreen allows larger volumes to be collected and detects protein and lipid mediators with greater sensitivity. These differences in mediator recovery may be due to the differences in the collection temperature.

Adult↗
PubMed2000

Exhaled 8-isoprostane as a new non-invasive biomarker of oxidative stress in cystic fibrosis.

BACKGROUND: Cystic fibrosis is characterised by oxidative stress in the airways. Isoprostanes are prostaglandin isomers formed by free radical catalysed peroxidation of arachidonic acid. 8-Isoprostane is increased in interstitial lung diseases, asthma, chronic obstructive pulmonary disease, and adult respiratory distress syndrome. Exhaled nitric oxide (NO) and carbon monoxide (CO) are biomarkers of inflammation and oxidative stress in the airways, respectively. METHODS: Concentrations of 8-isoprostane in the breath condensate of 10 normal subjects and 19 patients with stable cystic fibrosis were measured using an enzyme immunoassay (EIA). Breath condensate is a non-invasive method of collecting airway secretions. Exhaled nitric oxide (NO) and carbon monoxide (CO) levels were measured by a chemiluminescence analyser. RESULTS: Concentrations of 8-isoprostane in the breath condensate of patients with stable cystic fibrosis were increased about threefold compared with normal subjects (42.7 (4.5) pg/ml vs 15.2 (1.7) pg/ml; p<0.005, 95% CI 14.6 to 40.9). 8-Isoprostane concentrations were negatively correlated with forced expiratory volume in one second in patients with cystic fibrosis (r = -0.61; p<0.005). Exhaled CO was also increased in patients with cystic fibrosis compared with normal subjects (6.7 (1.2) ppm vs 2.9 (0.3) ppm; p<0.05, 95% CI 0.2 to 7.4). 8-Isoprostane concentrations were significantly correlated with CO levels (r = 0.66; p<0.002). CONCLUSIONS: The results of this study show that oxidative stress is increased in cystic fibrosis and may be quantified by measuring 8-isoprostane concentrations in breath condensate.

Adult↗
PubMed2001

Effects of nitrogen dioxide exposure and ascorbic acid supplementation on exhaled nitric oxide in healthy human subjects.

BACKGROUND: Nitric oxide (NO) is detectable in the exhaled breath, is involved in airway defence and inflammation, and probably modulates bronchial smooth muscle tone. Given the sensitivity of nitrogen oxides to local redox conditions, we postulated that exposure to oxidant or antioxidant compounds could alter concentrations of NO in the exhaled breath (eNO). We assessed the effect of nitrogen dioxide (NO(2)) and ascorbic acid exposure on eNO in healthy human subjects. METHODS: Ten healthy subjects were randomised to undergo a 20 minute single blind exposure to NO(2) (1.5 parts per million) or medical air in a crossover fashion. Exhaled NO and pulmonary function were measured before and for 3 hours after exposure. In a separate double blind crossover study 20 healthy subjects received ascorbic acid 500 mg twice daily or placebo for 2 weeks with a 6 week interim washout. Serum ascorbic acid levels and eNO were measured before and after each supplementation phase. RESULTS: NO(2) induced a decrease of 0.62 (95% CI 0.32 to 0.92) ppb in the mean post-exposure eNO (p<0.01) with no change in forced expiratory volume in 1 second (FEV(1)). Oral supplementation with ascorbic acid increased the mean serum ascorbic acid concentration by 7.4 (95% CI 5.1 to 9.7) microg/ml (63%) but did not alter eNO. CONCLUSIONS: NO(2) exposure causes a decrease in eNO, an effect which may be mediated through changes in epithelial lining fluid redox state or through a direct effect on epithelial cells. In contrast, ascorbic acid does not appear to play a significant role in the metabolism of NO in the epithelial lining fluid.

Adult↗
PubMed2001

Controlled low flow off line sampling of exhaled nitric oxide in children.

BACKGROUND: The aim of this study was to validate exhaled nitric oxide (eNO) values obtained with an alternative off line, single breath, low flow balloon sampling method against on line sampling according to ERS and ATS guidelines in children who could perform both methods. METHODS: One hundred and twenty seven white children of median age 14.1 years, all pupils of a secondary school, participated in the study. They performed the two different sampling techniques at three different flows of 50, 100, 150 ml/s. Additional measurements were done in random subgroups to determine the influence of the dead space air on eNO values obtained off line by excluding the first 220 ml of exhaled air. All children completed a questionnaire on respiratory and allergic disorders and underwent spirometric tests. RESULTS: The off line eNO values were significantly higher than the on line values at all flows. At 50 ml/s the geometric mean (SE) off line eNO was 18.7 (1.1) ppb and the on line eNO was 15.1 (1.1) ppb (p<0.0001). However, when dead space air was discarded, off line and on line values were similar: at 50 ml/s off line eNO was 17.7 (1.0) ppb and on line eNO 16.0 (1.2) ppb. There was a good agreement between off line eNO values without dead space air and on line eNO: for 50 ml/s the mean on/off line ratio was 0.95 (95% agreement limits 0.63 to 1.27). The off line eNO level at 50 ml/s in 80 children with negative questionnaires for asthma, rhinitis, and eczema was 13.6 (1.0) ppb compared with 33.3 (1.1) ppb in the remaining children with positive questionnaires on asthma and allergy and/or recent symptoms of cold (p<0.0001). CONCLUSIONS: In children, off line assessment of eNO using constant low flow sampling and excluding dead space air is feasible and produces similar results as on line assessment with the same exhalation flow rate. Both sampling methods are sufficiently sensitive to differentiate between groups of otherwise healthy school children with and without self-reported asthma, allergy, and/or colds. We propose that, for off line sampling, similar low flow rates should be used as are recommended for on line measurements.

Adolescent↗
PubMed2002

Exhaled nitric oxide levels in atopic children: relation to specific allergic sensitisation, AHR, and respiratory symptoms.

BACKGROUND: Exhaled nitric oxide (eNO), which has been proposed as a measure of airway inflammation, is increased in atopic subjects. This raises the question of whether eNO provides any additional information about airway inflammation in asthmatic subjects, other than as a marker for atopy. A study was undertaken to determine whether eNO levels in a population of atopic children are associated with sensitisation or natural exposure to specific allergens, and to examine the relationship between eNO, airway responsiveness, and current respiratory symptoms. METHODS: Exhaled NO and airway responsiveness to histamine were measured in winter and in summer in 235 children aged 8-14 years who had been classified as atopic by skin prick testing. Current respiratory symptoms, defined as wheeze or cough during the month preceding the test, were measured by a parent completed questionnaire. Airway hyperresponsiveness (AHR) was defined as a dose response ratio (DRR) of >8.1 (% fall in forced expiratory volume in 1 second (FEV(1))/micromol + 3). RESULTS: Sensitisation to house dust mite was associated with raised eNO levels in winter while sensitisation to Cladosporium was associated with raised eNO levels in both winter and summer. Grass pollen sensitisation was not associated with raised eNO levels in either season. Exhaled NO correlated significantly with DRR histamine (r=0.43, p<0.001) independently of whether the children had current symptoms or not. In children with current wheeze, those with AHR had eNO levels 1.53 (95% CI 1.41 to 1.66) times higher than those without AHR (p=0.006). Neither DRR (p=1.0) nor eNO levels (p=0.92) differed significantly between children with or without persistent dry cough in the absence of wheeze. CONCLUSIONS: In atopic children, raised eNO levels are associated with sensitisation to perennial allergens, but not to seasonal allergens such as grass pollen. In this population, an increase in eNO is associated with AHR and current wheezing, suggesting that eNO is more than just a marker for atopy.

Adolescent↗
PubMed2003

Exhaled leukotrienes and prostaglandins in COPD.

BACKGROUND: The role of eicosanoids, including leukotrienes (LTs) and prostaglandins (PGs), in chronic obstructive pulmonary disease (COPD) is uncertain. The aim of this study was to investigate whether eicosanoids are measurable in exhaled breath condensate (EBC), a non-invasive method of collecting airway secretions, in patients with stable mild to moderate COPD, and to show possible differences in their concentrations compared with control subjects. METHODS: LTB(4), LTE(4), PGE(2), PGD(2)-methoxime, PGF(2alpha), and thromboxane B(2) (TxB(2)) were measured in EBC in 15 healthy ex-smokers, 20 steroid naïve patients with COPD who were ex-smokers, and in 25 patients with COPD who were ex-smokers and who were treated with inhaled corticosteroids. The study was of cross sectional design and all subjects were matched for age and smoking habit. RESULTS: LTB(4) and PGE(2) concentrations were increased in steroid naïve (LTB(4): median 100.6 (range 73.5-145.0) pg/ml, p<0.001; PGE(2): 98.0 (range 57.0-128.4) pg/ml, p<0.001) and steroid treated patients with COPD (LTB(4): 99.0 (range 57.9-170.5) pg/ml, p<0.001; PGE(2): 93.6 (range 52.8-157.0) pg/ml, p<0.001) compared with control subjects (LTB(4): 38.1 (range 31.2-53.6) pg/ml; PGE(2): 44.3 (range 30.2-52.1) pg/ml). Both groups of patients had similar concentrations of exhaled LTB(4) (p=0.43) and PGE(2) (p=0.59). When measurable, LTE(4) and PGD(2)-methoxime concentrations were similar in COPD patients and controls, whereas PGF(2alpha) concentrations were increased in the former. TxB(2)-LI was undetectable in any of the subjects. CONCLUSIONS: There is a selective increase in exhaled LTB(4) and PGE(2) in patients with COPD which may be relatively resistant to inhaled corticosteroid therapy.

Administration, Inhalation↗
PubMed1998

Effect of inhaled L-arginine on exhaled nitric oxide in normal and asthmatic subjects.

BACKGROUND: Nitric oxide (NO) plays an important part in the regulation of many physiological functions and may also be involved in several pulmonary diseases. Endogenous NO is synthesised by different isoforms of NO synthase (NOS) from L-arginine. METHODS: The effect of inhaled L-arginine 0.75 g (six normal and six asthmatic subjects), 1.5 g (six normal and six asthmatic subjects), and 3 g (seven normal and six asthmatic subjects) has been studied in a double blind placebo controlled, randomised, parallel group design study. In addition, the effect of a single dose (3 g) of inhaled L-alanine has been assessed in five normal and five asthmatic subjects. RESULTS: L-arginine increased exhaled NO in a dose-dependent fashion with a maximum at 60 minutes. The cumulative effect of L-arginine (3 g) on NO in asthmatic subjects, expressed as the area under the curve in arbitrary units (au) and compared with the effect of placebo (0.9% NaCl), was significantly higher (mean 0.11 au; 95% confidence interval (CI) 0.03 to 0.19) than in normal subjects (0.012 au; 95% CI 0.002 to 0.022). There was a negative correlation (r = -0.72) between the increase in exhaled NO and the fall in forced expiratory volume in one second (FEV1) (0.034 au, 95% CI 0.030 to 0.038) after 3 g L-arginine in asthmatic subjects. Inhalation of 3 g of L-alanine produced a similar reduction in FEV1 (0.033 au, 95% CI 0.007 to 0.059) but no significantly different changes in exhaled NO (0.017 au, 95% CI 0.001 to 0.039) compared with placebo (0.020 au, 95% CI 0.001 to 0.042). CONCLUSIONS: An increase in the amount of substrate for NOS increases the formation of endogenous NO. L-arginine may have therapeutic potential in diseases in which there is defective production of NO, but in asthma it may amplify the inflammatory response in the airways.

Administration, Inhalation↗
PubMed1987

Contribution of continuing gas exchange to phase III exhaled PCO2 and PO2 profiles.

Changes in PCO2 and PO2 during expiration have been ascribed to simultaneous gas exchange, but other factors such as ventilation-perfusion inhomogeneity in combination with sequential emptying may also contribute. An experimental and model approach was used to study the relationship between gas exchange and changes in expired PCO2 and PO2 in anesthetized dogs during prolonged high tidal volume expirations. Changes in PCO2 and PO2 were quantified by taking the area bounded by the sloping exhalation curve and a line drawn horizontally from a point where the Fowler dead space plus 250 ml had been expired. This procedure is similar to using the slope of the exhalation curve but it circumvents problems caused by nonlinearity of the PCO2 and PO2 curves. The gas exchange components of the CO2 and O2 areas were calculated using a single-alveolus lung model whose input parameters were measured in connection with each prolonged expiration. The relationship between changes in experimental CO2 areas caused by sudden reductions in mixed venous PCO2 (produced by right atrial infusions of NaOH) and those calculated by the model was also studied. In seven dogs, calculated CO2 and O2 areas were 13% higher and 25% lower than the respective experimental areas, but interindividual variations were large. Changes in experimental CO2 areas caused by step changes in mixed venous PCO2 were almost identical to changes in the calculated areas. We conclude that the changes in PCO2 and PO2 during expiration cannot be explained solely by gas exchange. However, the single-alveolus lung model accurately predicts changes in the CO2 exhalation curve caused by alterations in the alveolar CO2 flow.

Animals↗
PubMed1989

Flow distribution through human and canine airways during inhalation and exhalation.

Airflow distribution through the tracheobronchial tree is influenced by many factors. In a hollow cast of the central airways, the only factors involved are resistance and inertia of the airflow. Distribution of steady flow during both inhalation and exhalation was measured at different total flow rates in human and canine tracheobronchial casts. The resulting airflow rates in peripheral segments were measured with a sensitive apparatus, which did not disturb the distribution of flow. Inertia of the airflow was found to be small but significant in airways of the human cast and substantially greater in the canine airway cast than in the human cast during inhalation. The influence of airflow inertia during inhalation was largely responsible for the different distributions of flow during inhalation and exhalation through the airway casts. Airflow resistance was found to be considerably greater during exhalation and may have contributed to the redistribution of flow. The forces involved are small but should be considered when modeling the in vivo distribution of airflow.

Airway Resistance↗
PubMed1997

Nitric oxide response in exhaled air during an incremental exhaustive exercise.

This study examines the response of the exhaled nitric oxide (NO) concentration (CNO) and the exhaled NO output (VNO) during incremental exercise and during recovery in six sedentary women, seven sedentary men, and eight trained men. The protocol consisted of increasing the exercise intensity by 30 W every 3 min until exhaustion, followed by 5 min of recovery. Minute ventilation (VE), oxygen consumption (VO2), carbon dioxide production, heart rate, CNO, and VNO were measured continuously. The CNO in exhaled air decreased significantly provided that the exercise intensity exceeded 65% of the peak VO2. It reached similar values, at exhaustion, in all three groups. The VNO increased proportionally with exercise intensity up to exhaustion and decreased rapidly during recovery. At exhaustion, the mean values were significantly higher for trained men than for sedentary men and sedentary women. During exercise, VNO correlates well with VO2, carbon dioxide production, VE, and heart rate. For the same submaximal intensity, and thus a given VO2 and probably a similar cardiac output, VNO appeared to be similar in all three groups, even if the VE was different. These results suggest that, during exercise, VNO is mainly related to the magnitude of aerobic metabolism and that this relationship is not affected by gender differences or by noticeable differences in the level of physical training.

Adult↗
PubMed1998

Low nitric oxide concentrations in exhaled gas and nasal airways of mammals without paranasal sinuses.

To investigate whether relevant levels of nasal nitric oxide (NO) are produced in the absence of paranasal sinuses, we studied 17 healthy baboons, mammals without any paranasal sinuses. The animals were anesthetized with ketamine hydrochloride and breathed spontaneously. While the baboons breathed through a face mask (mouths closed) connected to a respirator, NO concentrations in exhaled gas were sampled from the expiratory limb and analyzed by chemiluminescence. While the animals were breathing ambient air, nasal gas was sampled via a thin plastic tube and analyzed for NO concentrations by chemiluminescence. Mean NO concentration in the exhaled gas was 1.00 +/- 0.59 parts/billion, and NO release was 4.28 +/- 2.72 nl/min. A NO concentration of 4.79 +/- 2.08 parts/billion was found in the nasal gas (NO release: 7.18 +/- 3.13 nl/min). An age-dependent increase in nasal NO levels was not observed. Exhaled and nasal NO concentrations in baboons were markedly lower than in mammals with paranasal sinuses, suggesting that paranasal sinuses might be an anatomic requirement for production of relevant nasal NO levels.

Animals↗
PubMed2003

Assessment of exhaled nitric oxide kinetics in healthy infants.

Exhaled nitric oxide (Fe(NO)) measurements provide a noninvasive approach to the evaluation of airway inflammation. Flow-independent NO exchange parameters [airway NO transfer factor (D(NO)) and airway wall NO concentration (Cw(NO))] can be estimated from Fe(NO) measurements at low flows and may elucidate mechanisms of disturbances in NO exchange. We measured Fe(NO) in sedated infants by using an adaptation of a raised lung volume rapid thoracic compression technique that creates forced expiration through a mass-flow controller that lasts 5-10 s, at a constant preset flow. We measured Fe(NO) at expired flows of 50, 25, and 15 ml/s in five healthy infants (7-31 mo). Median Fe(NO) increased [24, 40, and 60 parts per billion (ppb)] with decreasing expiratory flows (50, 25, and 15 ml/s). Group median (range) for D(NO) and Cw(NO) were 12.7 (3.2-37) x 10(-3) nl. s(-1). ppb(-1) and 108.9 (49-385) ppb, respectively, similar to values reported in healthy adults. Exhaled NO is flow dependent; flow-independent parameters of exhaled NO kinetics can be assessed in infants and are similar to values described in adults.

Breath Tests↗
PubMed2002

Variability of exhaled hydrogen peroxide in stable COPD patients and matched healthy controls.

BACKGROUND: Because inflammation induces oxidative stress, exhaled hydrogen peroxide (H(2)O(2)), which is a marker of oxidative stress, may be used as a non-invasive marker of airway inflammation in chronic obstructive pulmonary disease (COPD). There are no data on the circadian variability of exhaled H(2)O(2) in COPD patients. OBJECTIVE: The aim of this study was to investigate the variability of the H(2)O(2) concentration in breath condensate of stable COPD patients and of matched healthy control subjects. METHODS: We included 20 patients with stable mild COPD (forced expiratory volume in 1 s approximately 70% of predicted) and 20 healthy subjects, matched for age, sex and pack-years, all smokers or ex-smokers. Breath condensate was collected and its H(2)O(2) concentration determined fluorometrically three times on day 0 (9 and 12 a.m., and 3 p.m.) and once on days 1, 2, 3, 8 and 21. RESULTS: The mean H(2)O(2) concentration increased significantly during the day in both the patient and control groups (p = 0.02 and p < 0.01, respectively). Over a longer period up to 21 days, the mean concentration did not change in both groups. There was no significant difference between patients and controls. The mean coefficient of variation over 21 days was 45% in the patient group and 43% in the control group (p = 0.8). CONCLUSIONS: The exhaled H(2)O(2) concentration increased significantly during the day in both stable COPD patients and controls. Over a period of 3 weeks, the mean H(2)O(2) concentration did not change and the variability within the subjects was similar in both groups.

Aged↗
PubMedDate not supplied

Effects of inhaled corticosteroids with different lung deposition on exhaled hydrogen peroxide in stable COPD patients.

BACKGROUND: The effects of inhaled corticosteroids (ICS) on markers of oxidative stress in patients with stable COPD are unclear. OBJECTIVES: The aim was to investigate the effect of ICS on exhaled H(2)O(2) in stable COPD patients and to compare ICS with different lung deposition. METHODS: Forty-one stable patients with moderate COPD (FEV(1) approximately 60% predicted) were randomized to sequence 1; first HFA-134a beclomethasone dipropionate (HFA-BDP, an ICS with more peripheral deposition) 400 microg b.i.d., then fluticasone propionate (FP, an ICS with more central deposition) 375 microg b.i.d. (n = 20) or sequence 2; first FP, then HFA-BDP (n = 21). Both 4-week treatment periods were preceded by a 4-week washout period. After each period, the concentration of H(2)O(2) in exhaled breath condensate was measured. RESULTS: The H(2)O(2) concentration decreased significantly after the first treatment period in both sequence 1 and 2 (p < 0.05, p = 0.01, respectively). In neither sequence was there a return to baseline values after the second washout, indicating a carry-over effect. The concentrations remained low in both sequences during the second treatment period. CONCLUSIONS: Both ICS appeared to reduce exhaled H(2)O(2) in stable COPD patients. However, this study showed no difference between ICS with different deposition patterns, which in part may be due to the carry-over effect.

Aerosol Propellants↗
PubMed2000

Effect of enalapril on exhaled nitric oxide in normotensive and hypertensive subjects.

We investigated whether an angiotensin-converting enzyme (ACE) inhibitor increases the production of nitric oxide (NO) in exhaled air in normotensive and hypertensive subjects. In study 1, 8 normotensive male subjects received a single oral dose of enalapril (5 mg) or nitrendipine (10 mg) in a crossover manner. Exhaled air was collected at baseline, and at 2, 4, and 8 hours after administration of the drug. In study 2, 10 normotensive subjects (6 men and 4 women) and 10 hypertensive subjects (6 men and 4 women) received a single oral dose of enalapril (5 mg). Exhaled air was collected at baseline and at 2 and 4 hours after administration of the drug. In study 1, enalapril significantly increased the NO release rate from the lung in normotensive subjects (36.9+/-5.1 pmol/s at baseline versus 58.3+/-7.3 pmol/s at 4 hours, P<0.01). Nitrendipine did not change the NO release rate. In study 2, enalapril significantly increased the release of NO from the lung in normotensive subjects (40.4+/-6.0 pmol/s at baseline versus 70. 3+/-11.4 pmol/s at 4 hours, P<0.01) but not in hypertensive subjects. ACE inhibition increased NO production from the lung in normotensive subjects but not in hypertensive patients. The reduction of angiotensin II production and/or the accumulation of bradykinin in the pulmonary tissue may be responsible for increased NO production in components of the lung, such as the pulmonary vascular endothelium, bronchial epithelial cells, macrophages, nasopharyngeal cells, and neurons. However, the effects of ACE inhibition on NO production from the lung differ between hypertensive subjects and normotensive subjects.

Adult↗