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PubMed2005

Liquid chromatography/mass spectrometry analysis of exhaled leukotriene B4 in asthmatic children.

BACKGROUND: The role of leukotriene (LT) B4, a potent inflammatory mediator, in atopic asthmatic and atopic nonasthmatic children is largely unknown. The lack of a gold standard technique for measuring LTB4 in exhaled breath condensate (EBC) has hampered its quantitative assessment in this biological fluid. We sought to measure LTB4 in EBC in atopic asthmatic children and atopic nonasthmatic children. Exhaled nitric oxide (NO) was measured as an independent marker of airway inflammation. METHODS: Fifteen healthy children, 20 atopic nonasthmatic children, 25 steroid-naïve atopic asthmatic children, and 22 atopic asthmatic children receiving inhaled corticosteroids were studied. The study design was of cross-sectional type. Exhaled LTB4 concentrations were measured using liquid chromatography/mass spectrometry-mass spectrometry (LC/MS/MS) with a triple quadrupole mass spectrometer. Exhaled NO was measured by chemiluminescence with a single breath on-line method. LTB4 values were expressed as the total amount (in pg) of eicosanoid expired in the 15-minute breath test. Kruskal-Wallis test was used to compare groups. RESULTS: Compared with healthy children [87.5 (82.5-102.5) pg, median and interquartile range], exhaled LTB4 was increased in steroid-naïve atopic asthmatic [255.1 (175.0-314.7) pg, p < 0.001], but not in atopic nonasthmatic children [96.5 (87.3-102.5) pg, p = 0.59)]. Asthmatic children who were receiving inhaled corticosteroids had lower concentrations of exhaled LTB4 than steroid-naïve asthmatics [125.0 (25.0-245.0) pg vs 255.1 (175.0-314.7) pg, p < 0.01, respectively]. Exhaled NO was higher in atopic nonasthmatic children [16.2 (13.5-22.4) ppb, p < 0.05] and, to a greater extent, in atopic steroid-naïve asthmatic children [37.0 (31.7-57.6) ppb, p < 0.001] than in healthy children [8.3 (6.1-9.9) ppb]. Compared with steroid-naïve asthmatic children, exhaled NO levels were reduced in asthmatic children who were receiving inhaled corticosteroids [15.9 (11.5-31.7) ppb, p < 0.01]. CONCLUSION: In contrast to exhaled NO concentrations, exhaled LTB4 values are selectively elevated in steroid-naïve atopic asthmatic children, but not in atopic nonasthmatic children. Although placebo control studies are warranted, inhaled corticosteroids seem to reduce exhaled LTB4 in asthmatic children. LC/MS/MS analysis of exhaled LTB4 might provide a non-invasive, sensitive, and quantitative method for airway inflammation assessment in asthmatic children.

Asthma↗
PubMed1997

Corticosteroids decrease exhaled nitric oxide in children with acute asthma.

OBJECTIVES: Nitric oxide (NO) produced in human airways seems to have both homeostatic and proinflammatory actions in the respiratory system. NO production has been shown to be higher in the exhaled air of asthmatic adults than in normal subjects. The aim of this study was to evaluate exhaled NO production during asthma exacerbation in children and the effect of a rescue course of oral steroid therapy. STUDY DESIGN: We measured NO in the exhaled air of 16 children (8 girls and 8 boys, aged 6 to 13 years) with an acute asthmatic episode before and after 5 days of therapy with prednisone, and in 16 healthy children. To measure NO, children inhaled NO-free air and, breathing at tidal volume, exhaled in a circuit from which a chemiluminescence analyzer sampled continuously. To assess the effect of acute changes in bronchial caliber on exhaled NO levels, we measured NO before and after a positive bronchodilation test result with albuterol in seven children with asthma whose disease was stable. RESULTS: In the group with acute asthma (forced expiratory volume in 1 second 62% +/- 4.4% predicted, mean +/- SEM), NO levels were significantly higher (31.3 +/- 4.2 parts per billion [ppb]) than in healthy children (5.4 +/- 0.4 ppb, p < 0.001). Administration of prednisone (1 mg/kg per day orally) for 5 days resulted in a mean decrease of 46% +/- 4% in exhaled NO concentrations (16.5 +/- 2.3 ppb, p < 0.001) compared with baseline, accompanied by a significant improvement in lung function (forced expiratory volume in 1 second 90.7% +/- 4.3% predicted). However, in patients with asthma exhaled NO levels remained significantly higher than in control children (p < 0.001) after steroid treatment. When exhaled NO was measured before and after a positive result after bronchodilator reversibility testing, we found no difference in exhaled NO levels (24 +/- 3.8 ppb vs 23.8 +/- 3 ppb; difference not significant). This demonstrates that inhaled albuterol and acute changes in bronchial caliber do not affect exhaled NO measurement. CONCLUSIONS: These data show that children with asthma exacerbation have high levels of exhaled NO that rapidly decrease with oral steroid therapy. We suggest that measurement of exhaled NO may represent a noninvasive method of monitoring airway inflammation in children with asthma.

Acute Disease↗
PubMed2000

Characterization of exhaled nitric oxide: introducing a new reproducible method for nasal nitric oxide measurements.

Nitric oxide (NO) is present in the human nasal airways and has been suggested to originate primarily from the paranasal sinuses. The aim of this study was to establish a new and reproducible method for measurement of nasal NO. Through repeated single-breath measurements the intra- and inter-individual variations of NO levels in nasally (into a tightly fitting mask covering the nose) and orally exhaled air were determined in healthy humans. Variations due to the methods used were investigated. The contribution of oral NO to the nasal exhalations by introducing a mouthwash procedure was also studied. This study shows distinct individual values of NO in nasally and orally exhaled air of healthy humans. Some diurnal variability was also found with a rise in NO in nasally and orally exhaled air over the day, but no, or little, day-to-day variability when comparing the results from separate mornings. There was no correlation between NO levels in nasally and orally exhaled air, whereas there was a strong correlation between NO levels in air exhaled through the left and right nostril. The levels of NO in air exhaled at 0.17 L x s(-1) through either nostril separately were higher than in air exhaled at the same flow rate through both nostrils simultaneously. After the introduction of a mouthwash procedure the level of NO in orally, but not nasally exhaled air was reduced. To conclude the method using nasal exhalation into a nose mask is highly reproducible. It is also suggested that subtracting the level of NO in orally exhaled air, after mouthwash, from that in nasally exhaled air, would adequately reflect nasal NO levels.

Adult↗
PubMed1999

Increased carbon monoxide in exhaled air of patients with seasonal allergic rhinitis.

BACKGROUND: Carbon monoxide (CO) can be detected in exhaled air and is increased in asthmatic patients. However, it is uncertain whether exhaled CO is increased in patients with allergic rhinitis. OBJECTIVE AND METHODS: To study whether exhaled CO is increased in patients with allergic rhinitis, exhaled CO concentrations were measured on a CO monitor by vital capacity manoeuvre in 86 patients with seasonal allergic rhinitis during and out of the cedar pollen season. RESULTS: During the season, exhaled CO concentrations were 3. 6 +/- 0.3 p.p.m. and decreased to 1.2 +/- 0.1 p.p.m. out of the season. The values of exhaled CO out of the season were similar to those in age-matched non-smoking healthy control subjects (1.2 +/- 0. 1 p.p.m.). Exhaled CO concentrations were significantly higher in patients with symptoms than in those without symptoms (P < 0.01). Exhaled CO concentrations in patients did not differ significantly among oral and nasal exhalation, and oral exhalation with an expiratory resistance (P > 0.20). CONCLUSION: These findings suggest that allergic rhinitis increases the concentration of CO in exhaled air and increases in exhaled CO may be derived from lower airways.

Adult↗
PubMed2000

A small dose of ethanol increases the exhalation of mercury in low-level-exposed humans.

Inorganic mercury is mainly eliminated by urinary and fecal excretion, but it is also eliminated by exhalation and sweat. There are only a few reports on exhalation of mercury in humans. In volunteers with short-term mercury exposure, an increased exhalation of mercury was found after alcohol intake. The aim of this study was to determine mercury in end-exhaled air and the influence of ethanol on mercury exhalation in subjects with long-term mercury exposure from diet, amalgam fillings, or the work environment. Fourteen subjects, with different grades of mercury exposure, were given 0.2 g ethanol/kg body weight. Measurements of mercury in end-exhaled air were performed before and after alcohol intake. Mercury in end-exhaled air could be detected in all subjects. In 10 individuals without amalgam fillings the mercury concentration was 3 to 12 pg/L. A marked increase, in general about fivefold, in mercury concentrations in end-exhaled air was seen in all subjects 30 min after intake of alcohol, regardless of the level of mercury exposure. Higher ethanol doses resulted in higher mercury levels in end-exhaled air and longer time periods before a return to background levels. An increase was seen even after an ethanol dose of only 0.1 g ethanol/kg body weight (about 0.08 L wine). The decrease in exhaled mercury at higher alcohol doses followed approximately zero-order kinetics and probably reflects the elimination of ethanol in tissues. In conclusion, low levels of mercury can be detected in end-exhaled air also in individuals without amalgam fillings. About a fivefold increase was seen 30 min after alcohol intake, and the relative increase seemed to be independent of the body burden of mercury. Exhalation of mercury represents only a small percentage of the total elimination of mercury.

Adult↗
PubMed2003

Basal and nitroglycerin-induced exhaled nitric oxide before and after cardiac surgery with cardiopulmonary bypass.

BACKGROUND: Exhaled nitric oxide (NO) may reflect NO production and consumption but the pulmonary origin of NO in exhaled gas is not clear. There are also conflicting data on exhaled NO after cardiopulmonary bypass (CPB). Because intravenous nitrovasodilators increase exhaled NO by conversion to NO in the lung, we measured basal and nitroglycerin (GTN)-induced exhaled NO in patients having low-risk coronary artery bypass graft (CABG) operations using routine CPB. We reasoned that GTN-induced exhaled NO would be a primarily vascular mechanism, which would contrast with the airway epithelial origin of basal exhaled NO, and that they might be differentially influenced by CPB. METHODS: Breath-to-breath concentrations of gas phase NO were measured in 12 CABG patients before and 1, 3 and 6 h after CPB. After the baseline measurements, three increasing doses of 1, 2 and 3 micro g kg(-1) intravenous GTN were given by a central venous catheter and exhaled NO and haemodynamic responses were recorded. RESULTS: Intravenous administration of 1, 2 and 3 micro g kg(-1) doses of GTN produced a dose-dependent increase in exhaled NO and a reduction in systemic blood pressure. Baseline exhaled NO remained unchanged. Exhaled NO but not blood pressure responses were reduced 1 and 3 h after CPB. CONCLUSIONS: The capacity of the lungs to increase exhaled NO in response to intravenous GTN is reduced after CPB, suggesting microvascular injury and/or atelectasis after routine open-heart surgery.

Aged↗
PubMed2000

Exhaled nitric oxide production by nitric oxide synthase-deficient mice.

Nitric oxide (NO) is produced in the nasal cavities, airways, and lungs and is exhaled by normal animals and humans. Although increased exhaled NO concentrations in airway inflammation have been associated with increased airway expression of nitric oxide synthase 2 (NOS 2), it is uncertain which NOS isoform is responsible for baseline levels of exhaled NO. We therefore studied wild-type mice and mice with a congenital deficiency of NOS 1, NOS 2, or NOS 3. By studying a closed chamber in which the exhaled gas of a group of mice was collected, gaseous NO production rates were measured. Wild-type mice exhaled 362 +/- 35 x 10(-15) mol g(-1) min(-1) NO (mean +/- SE, n = 16 groups of five mice), NOS 1-deficient mice exhaled 592 +/- 74 x 10(-15) mol g(-1) min(-1) NO (n = 15 groups, p < 0.05 versus wild-type and NOS 2-deficient mice), NOS 2-deficient mice 330 +/- 74 x 10(-15) mol g(-1) min(-1) NO (n = 14 groups) and NOS 3-deficient mice 766 +/- 101 x 10(-15) mol g(-1) min(-1) NO (n = 16 groups, p < 0.001 versus wild-type and NOS 2-deficient mice). Pharmacological NOS inhibition with L-NAME decreased (p < 0.05) the exhaled NO production rate of wild-type and NOS 3-deficient but not of NOS 2-deficient mice. L-Arginine administration increased exhaled NO production rate in all but NOS 2-deficient mice. Absence of NOS 1 or 3 is associated with increased murine exhaled NO production rates. Since NOS 2-deficient mice were the only genotype to lack substrate- and inhibitor-regulated changes of NO exhalation, we suggest that NOS 2 is an important isoform contributing to exhaled NO exhalation in healthy mice.

Animals↗
PubMed1997

Effect of short- and long-acting inhaled beta2-agonists on exhaled nitric oxide in asthmatic patients.

Increased concentrations of exhaled nitric oxide (NO) occur in patients with asthma, and exhaled NO may be useful for assessing the effect of drug therapy on airway inflammation. Beta2-agonists have been proposed to have both proinflammatory and anti-inflammatory effects. We therefore assessed exhaled NO after beta2-agonists in asthmatic patients. Two randomized, double-blind, placebo-controlled studies were conducted. Firstly, exhaled NO was measured in 18 asthmatics (9 taking inhaled glucocorticosteroids (GCS)) before and after nebulized salbutamol (5 mg), or identical placebo (0.9% saline). Exhaled NO and forced expiratory volume in one second (FEV1) were measured at 15 min intervals for 1 h (Study 1). Secondly, the effect of 1 week of treatment with the long-acting beta2-agonist, salmeterol (50 microg b.i.d.), added to either budesonide (800 microg b.i.d.) or placebo, was studied in eight mild asthmatic subjects (Study 2). Exhaled NO was measured by a chemiluminescence analyser, adapted for on-line recording. In Study 1, exhaled NO showed no significant change at any time-point in patients not taking inhaled GCS. In asthmatics on inhaled GCS, exhaled NO increased compared to placebo at 15 and 30 min, but this did not reach statistical significance. In Study 2, treatment with salmeterol increased FEV1, but exhaled NO levels were not significantly changed, either after budesonide treatment (143+/-35 to 179+/-67 ppb), or after placebo (201+/-68 to 211+/-65 ppb). Our results confirm that single high dose salbutamol does not increase exhaled nitric oxide in asthmatics not taking inhaled glucocorticosteroids. Salbutamol may increase exhaled nitric oxide in asthmatics taking inhaled glucocorticosteroids. However, regular use of salmeterol resulted in no change in exhaled nitric oxide, either used alone or in combination with inhaled glucocorticosteroids.

Administration, Inhalation↗
PubMed2000

Increased exhaled nitric oxide in chronic bronchitis: comparison with asthma and COPD.

STUDY OBJECTIVES: To test the hypothesis that exhaled nitric oxide (NO) is increased in patients with chronic bronchitis, and to compare the results with exhaled NO in patients with asthma and COPD. STUDY DESIGN: Cross-sectional survey. SETTING AND PATIENTS: Veterans Administration pulmonary function laboratory. Patients (n = 179) were recruited from 234 consecutive patients. Two nonsmoking control groups of similar age, with normal spirometry measurements and no lung disease, were used (18 patient control subjects and 20 volunteers). MEASUREMENTS: Participants completed questionnaires and spirometry testing. Exhaled NO was measured by chemiluminescence using a single-breath exhalation technique. RESULTS: Current smoking status was associated with reduced levels of exhaled NO (smokers, 9. 2 +/- 0.9 parts per billion [ppb]; never and ex-smokers, 14.3 +/- 0. 6 ppb; p < 0.0001). Current smokers (n = 57) were excluded from further analysis. Among nonsmokers, the levels of exhaled NO were significantly higher in patients with chronic bronchitis (17.0 +/- 1. 1 ppb; p = 0.035) and asthma (16.4 +/- 1.3 ppb; p = 0.05) but not in those with COPD (14.7 +/- 1.0 ppb; p = 0.17) when compared with either control group (patient control subjects, 11.1 +/- 1.6 ppb; outside control subjects, 11.5 +/- 1.5 ppb). The highest mean exhaled NO concentration occurred in patients with both chronic bronchitis and asthma (20.2 +/- 1.6 ppb; p = 0.005 vs control subjects). CONCLUSIONS: Exhaled NO is increased in patients with chronic bronchitis. The increase of exhaled NO in patients with chronic bronchitis was similar to that seen in patients with asthma. The highest mean exhaled NO occurred in patients with both chronic bronchitis and asthma. Exhaled NO was not increased in patients with COPD. Although chronic bronchitis and asthma have distinct histopathologic features, increased exhaled NO in patients with both diseases suggests common features of inflammation.

Asthma↗
PubMed2004

Childhood asthma: exhaled markers of airway inflammation, asthma control score, and lung function tests.

Exhaled markers of airway inflammation become increasingly important in the management of childhood asthma. The aims of the present study are: 1) to compare exhaled markers of inflammation (nitric oxide, carbon monoxide, and acidity of breath condensate) with conventional asthma measures (lung function tests and asthma control score) in childhood asthma; and 2) to investigate the detectability of albumin, CRP, IL-6, IL-8, TNF-alpha, sICAM-1, and sTNF-R75 in the exhaled breath condensate (EBC) of asthmatic children. Thirty-two children with mild to moderate persistent asthma and healthy controls aged 6-12 years were studied. We measured exhaled NO and CO, and subsequently EBC was collected. Inflammatory mediators in EBC were measured using an enzyme-linked immunosorbent assay. Respiratory symptoms and asthma control were assessed using the asthma control questionnaire (ACQ) of Juniper et al. (Eur Respir J 1999;14:902-907). Exhaled NO showed a significant correlation with exhaled CO (r = 0.59, P < 0.05) and FEV1 (r = -0.59, P < 0.05), but not with ACQ score (r = 0.48, P = 0.06). Exhaled CO was correlated with prebronchodilator FEV1 (r = -0.45, P < 0.05), but not with asthma control (r = 0.18, P = 0.35). Acidity of EBC was significantly lower in asthmatic children than in healthy controls (P < 0.05), but did not correlate with any of the conventional asthma measures. We were not able to demonstrate the presence of CRP, IL-6, IL-8, TNF-alpha, sICAM-1, and sTNF-R75 in EBC. Albumin was found in two EBC samples of asthmatic children. We conclude that exhaled NO had a better correlation with lung function parameters and asthma control than exhaled CO and acidity of EBC, in mild to moderate persistent childhood asthma. However, exhaled NO, CO, and deaerated pH of EBC did not differ between asthmatic children and controls, possibly because of a too homogeneous and well-controlled study population. To further evaluate the clinical utility of exhaled markers in monitoring childhood asthma, more studies are required on a wider range of asthma severity, and preferably with repeated measurements of markers and of asthma control.

Adolescent↗
PubMed2006

Exhaled carbon monoxide levels in school-age children with episodic asthma.

Carbon monoxide (CO) can be detected in exhaled air and is increased in adult and childhood persistent asthmatic patients. However, little is known about the exhaled CO concentration in episodic childhood asthma. This study aimed to clarify whether measurement of exhaled CO is useful in monitoring disease activity in children with episodic asthma. We measured exhaled CO concentration by modified Micro-Smokerlyzer in 217 elementary school children (132 boys; mean age, 10 +/- 1 (SE) years; range, 9-12 years), in whom 29 had infrequent episodic asthma without current exacerbations. We also measured exhaled CO concentrations in 22 children with episodic asthma (13 boys; mean age, 10 +/- 3 years; range, 8-12 years), who had acute mild asthmatic attacks during examination. In these patients with mild asthmatic attacks, exhaled CO was measured both before and after combination therapy with salbutamol and sodium cromoglycate (SCG) by powered nebulizer. Among 217 schoolchildren, exhaled CO levels in infrequent episodic asthmatic children (1.1 +/- 0.1 parts per million (ppm), n = 29) were not significantly different from those in healthy schoolchildren (1.0 +/- 0.1 ppm, n = 188, P > 0.68). The exhaled CO concentrations during asthma attacks in children with episodic asthma were significantly higher (5.1 +/- 0.4 ppm, n = 22) compared with those in healthy children (P < 0.001) or those in asymptomatic asthmatic children (P < 0.001). The elevated exhaled CO levels were significantly decreased after inhalation therapy of a combination of salbutamol and SCG (3.2 +/- 0.5 ppm, n = 22, P < 0.02). In conclusion, exhaled CO levels were significantly elevated during acute asthma exacerbations, and partially recovered after treatment with beta(2)-agonist and SCG in children with mild episodic asthma. These findings indicate that measurement of exhaled CO might provide another noninvasive measurement of asthma exacerbations that would be suitable for use in children with acute mild episodic asthma.

Acute Disease↗
PubMed1996

Exhaled nitric oxide in childhood asthma.

UNLABELLED: Endogenous synthesis of nitric oxide (NO) and its presence in exhaled air was observed in various species including humans. Particularly high levels were found in adults with bronchial asthma, possibly because of the underlying pulmonary inflammatory activity. We studied oral and nasal exhaled NO by chemiluminescence in 47 children aged between 6 and 10 years. Thirty children had bronchial asthma, 17 were healthy controls. In asthmatic children oral exhaled NO was 13.4 +/- 1.4 parts per billion (ppb) (mean +/- SEM), nasal exhaled NO was 21.7 +/- 1.5 ppb. In healthy controls oral exhaled NO was 7.2 +/0 1.0 ppb, nasal exhaled NO was 18.2 +/- 22 ppb. Oral exhaled NO was significantly higher in asthmatic children compared to healthy controls (P = 0.0017). Nasal exhaled NO did not differ significantly in the two groups. There was a significant negative correlation between oral exhaled NO and forced expiratory volume in 1 s (FeV1). No significant correlation between oral or nasal exhaled NO and other markers of obstructive lung function impairment, oral minute ventilation, the body mass index and the presence of upper respiratory tract infection could be found. CONCLUSION: Children with bronchial asthma have significantly higher levels of orally exhaled nitric oxide than healthy controls.

Asthma↗
PubMed1996

Increased levels of exhaled nitric oxide during nasal and oral breathing in subjects with seasonal rhinitis.

BACKGROUND: Allergic rhinitis is associated with nasal mucosal inflammation. Exhaled nitric oxide may be a useful marker of inflammation and has recently been shown to be increased in patients with asthma. OBJECTIVE: The purpose of this study was to determine whether exhaled levels of nitric oxide are increased with nasal breathing in patients with seasonal allergic rhinitis compared with nonatopic individuals and whether there is an increase with oral breathing consistent with lower respiratory inflammation in the absence of clinical asthma. METHODS: Nitric oxide levels in exhaled air were measured by chemiluminescence in 18 nonatopic volunteers and 32 patients with seasonal rhinitis. Measurements were made with both nasal and oral exhalation and orally after 10 seconds and 60 seconds of breath-holding. The detection limit was 1 part per billion (ppb). RESULTS: In control subjects nasal levels of nitric oxide in exhaled air (mean +/- SD, 24.7 +/- 9.2 ppb) were higher than those after oral exhalation (11.1 +/- 2.5 ppb, p less than 0.0001). Breath-holding significantly increased levels of nitric oxide in exhaled air in a time-dependent manner. Levels of exhaled nitric oxide were significantly higher for all measurements in patients with seasonal rhinitis, with levels without breath-holding of 35.4 +/- 11.3 ppb (p less than 0.001) in nasally exhaled air and 16.3 +/- 5.9 ppb (p less than 0.001) in orally exhaled air. Nasal levels were significantly higher than oral levels in subjects with rhinitis (p less than 0.0001). CONCLUSIONS: The results indicate that exhaled nitric oxide may be a useful marker for nasal inflammation in patients with seasonal rhinitis and suggest that generalized airway inflammation may be present, even without clinical asthma, in such patients.

Adult↗
PubMed2001

Relation between exhaled carbon monoxide levels and clinical severity of asthma.

Carbon monoxide (CO) can be detected in exhaled air and is increased in asthmatic patients not treated with corticosteroids. However, it is uncertain whether exhaled CO is related to severity of asthma. To study whether exhaled CO is related to severity of asthma in clinical courses, exhaled CO concentrations were measured on a CO monitor by vital capacity manoeuvre in 20 mild asthmatics treated with inhaled beta2-agonists alone, 20 moderate asthmatics treated with inhaled corticosteroids, and 15 stable asthmatics treated with high dose inhaled corticosteroids and oral corticosteroids once a month over 1 years. Exhaled CO concentrations were also measured in 16 unstable severe asthmatics who visited the hospital every 7 or 14 days for treatment with high dose inhaled corticosteroids and oral corticosteroids. The mean values of exhaled CO in severe asthma over 1 year were 6.7 +/- 9.5 p.p.m. (n = 31, mean +/- SD) and significantly higher than those of non-smoking control subjects (1.2 +/- 0.9 p.p.m., n = 20, P < 0.01). Exhaled CO concentrations in unstable severe asthmatics were significantly higher than those in stable severe asthmatics. However, exhaled CO concentrations in mild and moderate asthmatics did not differ significantly from those in non-smoking control subjects (P > 0.20). There was a significant relationship between the exhaled CO concentrations and forced expiratory volume in one second in all asthmatic patients. These findings suggest that exhaled CO concentrations may relate to the severity of asthma and measurements of exhaled CO concentrations may be a useful means of monitoring airway inflammation in asthma.

Adult↗
PubMed1995

Positive end-expiratory pressure ventilation elicits increases in endogenously formed nitric oxide as detected in air exhaled by rabbits.

BACKGROUND: Nitric oxide (NO) formed from L-arginine is exhaled by mammals and regulates pulmonary vascular tone. Little is known about how its formation is stimulated. METHODS: The concentration of NO in exhaled air was monitored by chemiluminescence in pentobarbital-anesthetized rabbits receiving mechanical ventilation by tracheostomy with graded positive end-expiratory pressure (PEEP). RESULTS: Introduction of PEEP (2.5-15 cmH2O) elicited dose-dependent and reproducible increments in exhaled NO and in arterial oxygen tension (PaO2). The increase in exhaled NO exhibited a biphasic pattern, with an initial peak followed by a partial reversal during the 4-min period at each level of PEEP. Thus, at a PEEP of 10 cmH2O, exhaled NO initially increased from 19 +/- 4 to 30 +/- 5 parts per billion (ppb) (P < 0.001, n = 9) and then decreased to 27 +/- 5 ppb (P < 0.005) at the end of the 4-min observation period. Simultaneously, PaO2 increased from 75 +/- 12 mmHg in the control situation to 105 +/- 11 mmHg (P < 0.05) at a PEEP of 10 cmH2O. After bilateral vagotomy, including bilateral transection of the depressor nerves, the increase in exhaled NO in response to PEEP was significantly reduced (P < 0.01). Thus, after vagotomy, a PEEP of 10 cmH2O elicited an increase in the concentration of exhaled NO from 13 +/- 3 to 17 +/- 3 ppb (n = 7). Vagotomy did not affect the baseline concentration of NO in exhaled air. The PEEP-induced increments in PaO2 were not affected by the NO synthase inhibitor L-N omega-arginine-methylester (30 mg.kg-1 intravenously). In open-chest experiments, PEEP (10 cmH2O) induced a reduction in cardiac output from 317 +/- 36 to 235 +/- 30 ml.min-1 and an increase in exhaled NO from 23 +/- 6 to 30 +/- 7 ppb (P < 0.05, n = 5). Reduction in cardiac output from 300 +/- 67 to 223 +/- 52 ml.min-1 by partial obstruction of the pulmonary artery did not significantly increase exhaled NO (from 23 +/- 7 to 25 +/- 6, difference not significant; n = 3). CONCLUSIONS: PEEP elicited increments in exhaled NO, perhaps by a stretch-dependent effect on the respiratory system. This finding may be attributed in part to a vagally influenced mechanism.

Animals↗
PubMed1998

Exhaled nitric oxide (NO) is reduced shortly after bronchoconstriction to direct and indirect stimuli in asthma.

Exhaled NO is increased in patients with asthma and may reflect disease severity. We examined whether the level of exhaled NO is related to the degree of airway obstruction induced by direct and indirect stimuli in asthma. Therefore, we measured exhaled NO levels before and during recovery from histamine and hypertonic saline (HS) challenge (Protocol 1) or histamine, adenosine 5'-monophosphate (AMP), and isotonic saline (IS) challenge (Protocol 2) in 11 and in nine patients with mild to moderate asthma, respectively. The challenges were randomized with a 2-d interval. Exhaled NO and FEV1 were measured before and at 4, 10, 20, and 30 min after each challenge. NO was measured during a slow VC maneuver with a constant expiratory flow of (0.05 x FVC)/s against a resistance of 1 to 2 cm H2O. Baseline exhaled NO levels were not significantly different between study days in Protocol 1 (mean +/- SD: 4.8 +/- 1.8 ppb [histamine] versus 5.4 +/- 2.1 ppb [HS], p = 0.4) or in Protocol 2 (7.9 +/- 4.7 ppb [histamine], 8.3 +/- 5.2 ppb [AMP], and 7.2 +/- 3.7 ppb [IS], p = 0.7). A significant reduction in exhaled NO was observed directly after HS (mean +/- SEM: 39.2 +/- 3.9 %fall) and AMP challenge (32.3 +/- 7.3 %fall) (MANOVA, p < 0.001), respectively, whereas exhaled NO levels tended to decrease after histamine challenge. Isotonic saline challenge did not induce changes in exhaled NO (p = 0.7). There was a positive correlation between %fall in FEV1 and the %fall in exhaled NO after histamine, HS, and AMP challenge as indicated by the mean slope of the within-subject regression lines (p <= 0.04). We conclude that acute bronchoconstriction, as induced by direct and indirect stimuli, is associated with a reduction in exhaled NO levels in asthmatic subjects. This suggests that airway caliber should be taken into account when monitoring exhaled NO in asthma.

Adult↗
PubMed2001

Off-line sampling of exhaled air for nitric oxide measurement in children: methodological aspects.

Measurement of nitric oxide in exhaled air is a noninvasive method to assess airway inflammation in asthma. This study was undertaken to establish the reference range of exhaled NO in healthy school-aged children and to determine the influence of ambient NO, noseclip and breath-holding on exhaled NO, using an off-line balloon sampling method. All children attending a primary school (age range 8-13 yrs) underwent NO measurements on two occasions with high and low ambient NO. Each time, the children performed four expiratory manoeuvres into NO-impermeable balloons, with and without 10 s of breath-holding and with and without wearing a noseclip. Exhalation flow and pressure were not controlled. NO was measured within 4 h after collection, by means of chemiluminescence. All children completed a questionnaire on respiratory and allergic disorders, and performed flow/volume spirometry. With low ambient NO, the mean exhaled NO value of 72 healthy children with negative questionnaires and normal lung function was 5.1 +/- 0.2 parts per billion (ppb) versus a mean of 6.8 +/- 0.3 ppb in the remaining 49 children with positive questionnaires for asthma and allergy, and/or recent symptoms of cold (p=0.001). Exhaled and ambient NO were significantly related, especially with ambient NO > 10 ppb (r = 0.86, p=0.0001 versus r=0.34, p=0.004 for ambient values <10 ppb). The use of a noseclip, with low ambient NO and without breath-holding, caused a small decrease in exhaled NO values (p=0.001). The effect of breath-holding on exhaled NO depended on ambient NO. With ambient NO > 10 ppb, exhaled NO decreased, whereas with ambient NO < 10 ppb, exhaled NO increased after 10 s breath-hold. It is concluded that off-line sampling in balloons is a simple and, hence, attractive method for exhaled nitric oxide measurements in children which differentiates between groups with and without self-reported asthma, allergy and colds, when ambient nitric oxide is < 10 parts per billion. Wearing a noseclip and breath-holding affected measured values and should, therefore be standardized or, preferably, avoided.

Adolescent↗
PubMedDate not supplied

Exhaled biomarkers in COPD: their potential role in diagnosis, treatment and prognosis.

Several diagnostic tools have been developed for diagnosing, monitoring and evaluating Chronic Obstructive Pulmonary Disease (COPD). There is an increasing interest in the use of non or less invasive biological markers (biomarkers) which reflect the character and intensity of the pathological processes in the lungs of COPD patients. The main goal of this review was to discuss the origin and current role of exhaled biomarkers in the diagnosis, evaluation of treatment and prognosis of COPD. Data of cross-sectional, cohort and intervention studies on exhaled biomarkers were studied. These studies were identified by a Medline search on papers in the English language published from 1990 to November 2001. The following markers were discussed: exhaled nitric oxide (NO), exhaled carbon monoxide (CO), exhaled alkanes, exhaled hydrogen peroxide (H2O2), exhaled isoprostanes, exhaled NO metabolites and exhaled thiobarbituric acid-reactive substances (TBARs). Data on these markers were summarized. The origin of each marker, the technique of analysis, the values in healthy controls and COPD patients, the effect of treatment and the correlation with other parameters were presented. Most studies, however, were cross-sectional studies with small populations. It was also difficult to compare studies because of differences in technique and study population. This review shows that exhaled biomarkers need to be studied further before using them in clinical practice. There is a need for standardization of the measurements, for comparison of COPD patients with healthy persons matched for age and smoking-status, for data on reproducibility and variability of all markers, for correlation of exhaled markers with other parameters and for intervention studies.

Biomarkers↗