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PubMed2003

Contributions of nitric oxide synthase isozymes to exhaled nitric oxide and hypoxic pulmonary vasoconstriction in rabbit lungs.

We investigated the source(s) for exhaled nitric oxide (NO) in isolated, perfused rabbits lungs by using isozyme-specific nitric oxide synthase (NOS) inhibitors and antibodies. Each inhibitor was studied under normoxia and hypoxia. Only nitro-L-arginine methyl ester (L-NAME, a nonselective NOS inhibitor) reduced exhaled NO and increased hypoxic pulmonary vasoconstriction (HPV), in contrast to 1400W, an inhibitor of inducible NOS (iNOS), and 7-nitroindazole, an inhibitor of neuronal NOS (nNOS). Acetylcholine-mediated stimulation of vascular endothelial NOS (eNOS) increased exhaled NO and could only be inhibited by L-NAME. Selective inhibition of airway and alveolar epithelial NO production by nebulized L-NAME decreased exhaled NO and increased hypoxic pulmonary artery pressure. Immunohistochemistry demonstrated extensive staining for eNOS in the epithelia, vasculature, and lymphatic tissue. There was no staining for iNOS but moderate staining for nNOS in the ciliated cells of the epithelia, lymphoid tissue, and cartilage cells. Our findings show virtually all exhaled NO in the rabbit lung is produced by eNOS, which is present throughout the airways, alveoli, and vessels. Both vascular and epithelial-derived NO modulate HPV.

Acetylcholine↗
PubMed1982

Regional diffusing capacity in normal lungs during a slow exhalation.

From an analysis of carbon monoxide uptake and xenon-133 distribution after two bolus inhalations of these gases, we calculated regional diffusing capacity in the upper and lower volume halves of the lungs during the middle 60% of an exhaled vital capacity in five seated normal subjects. We found that the regional diffusing capacity of the upper half of the lungs was 11.6 +/- 4.2 (mean +/- SD) ml.min-1.Torr-1 and that the regional diffusing capacity of the lower half of the lungs was 24.4 +/- 2.4 ml.min-1.Torr-1 after 25% of the vital capacity had been exhaled. These values remained relatively constant as lung volume decreased from 25 to 75% of the exhaled vital capacity. Diffusing capacity in the upper half of the lungs ranged from 9.4 to 12.4 ml.min-1.Torr-1 during exhalation, and in the lower half of the lungs from 21.0 to 28.6 ml.min-1.Torr-1 during exhalation. These results suggest that total lung diffusing capacity remains relatively constant over this midrange of lung volumes and that this occurs because the regional diffusing capacities in both the upper and lower halves of the lungs remain relatively constant.

Adult↗
PubMed1995

Exhaled nitric oxide in isolated pig lungs.

Endothelium-derived nitric oxide (NO) is an important regulator of vascular resistance. Low concentrations of NO have been recorded in the exhaled breath of spontaneously breathing animals and humans. To determine whether NO synthesis in the lung contributes to the NO measured in the breath, we measured the concentration of NO in the exhaled air of isolated perfused and ventilated porcine lungs by using a chemiluminescence method. With NO-free normoxic ventilation (21% O2-5% CO2-74% N2) of eight porcine lungs perfused with a Krebs-dextran and albumin perfusate, baseline exhaled NO was 5.8 +/- 1.8 parts per billion (ppb) and pulmonary vascular resistance (PVR) was 8.9 +/- 1.8 mmHg.l-1.min. Hypoxic ventilation (5% O2-5% CO2-90% N2) caused a fall in NO to 3.6 +/- 1.8 ppb and a rise in PVR to 13.6 +/- 3.6 mmHg.l-1.min. Vasoconstriction with the thromboxane analogue U-46619 (10(-9) M) raised PVR to 31.7 +/- 6.8 mmHg.l-1.min but did not decrease NO levels from baseline. Subsequent addition of acetylcholine (10(-6)M) lowered PVR to 22.1 +/- 4.5 mmHg.l-1.min and increased exhaled NO to 7.0 +/- 2.0 ppb. Addition of a NO synthase inhibitor, NG-nitro-L-arginine methyl ester (10(-5) M), to four lungs caused a rise in PVR to 43.0 +/- 7.0 mmHg.l-1.min and a decrease in NO to 1.5 +/- 1.0 ppb. Addition of autologous blood to the perfusate of four lungs caused no change in PVR from baseline but decreased exhaled NO to 2.7 +/- 0.5 ppb.(ABSTRACT TRUNCATED AT 250 WORDS)

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1997

Marked flow-dependence of exhaled nitric oxide using a new technique to exclude nasal nitric oxide.

Exhaled nitric oxide (NO) may aid in monitoring pulmonary disease. The single-breath NO profile (subjects with nose clip) was described as a NO peak followed by a plateau (NO(PLAT)). Published exhaled NO values vary greatly, possibly due to contamination with nasal NO and differing respiratory maneuvers. We developed a technique to measure pulmonary NO, without nasal NO, by having the subject maintain a positive expiratory pressure (ensuring vellum closure), and we examined the variation in NO(PLAT) over a range of expiratory flows (4.2 to 1,550 ml/s). NO(PLAT) values rose almost 35-fold (3.2 +/- 1.4 ppb to 110.5 +/- 54.8 ppb) with decreasing flow, described by NO(PLAT) = 208.6795 x (flow rate)(-0.5995). However, NO excretion showed an almost 11-fold rise as flow increased. In summary, we present a simple technique for measuring exhaled NO without contamination by nasal NO. There is a marked flow dependence of exhaled NO concentration and excretion. Exhaled pulmonary NO is best measured at very low flow rates to amplify the signal and must be related to the expiratory flow employed.

Administration, Inhalation↗
PubMed1998

Relationship between exhaled nitric oxide and childhood asthma.

The purpose of the study was to determine if exhaled nitric oxide levels in children varied according to their asthmatic and atopic status. Exhaled nitric oxide was measured in a sample of 93 children attending the North West Lung Centre, Manchester, United Kingdom, for the clinical evaluation of a respiratory questionnaire being developed as a screening tool in general practice. The clinical assessment included full lung function, skin prick testing, and exercise challenge. Children were said to be asthmatic either by consensus decision of three independent consultant pediatricians, who reviewed all the clinical results except the nitric oxide measurements, or by positive exercise test. Atopic asthmatic children had higher geometric mean exhaled nitric oxide levels (consensus decision, 12.5 ppb [parts per billion] 95% CI, 8.3 to 18. 8; positive exercise test, 12.2 ppb 95% CI, 7.6 to 19.7) than did nonatopic asthmatic children (3.2 ppb 95% CI, 2.3 to 4.6; 3.2 ppb 95% CI, 2.0 to 5.0), atopic nonasthmatic children (3.8 ppb 95% CI, 2. 7 to 5.5; 5.7 ppb 95% CI, 4.1 to 8.0), or nonatopic nonasthmatic children (3.4 ppb 95% CI, 2.8 to 4.1; 3.5 ppb 95% CI, 3.0 to 4.1). Thus, exhaled nitric oxide was raised in atopic asthmatics but not in nonatopic asthmatics, and these nonatopic asthmatics had levels of exhaled nitric oxide similar to those of the nonasthmatics whether atopic or not.

Adolescent↗
PubMed1998

Combined use of exhaled hydrogen peroxide and nitric oxide in monitoring asthma.

Oxidative stress contributes to airway inflammation and exhaled hydrogen peroxide (H2O2) and nitric oxide (NO) are elevated in asthmatic patients. We determined the concentrations of expired H2O2 and NO in 116 asthmatic (72 stable steroid-naive, 30 stable steroid-treated, and 14 severe steroid-treated unstable patients) and in 35 healthy subjects, and studied the relation between exhaled H2O2, NO, FEV1, airway responsiveness, and eosinophils in induced sputum. Both exhaled H2O2 and NO levels were elevated in steroid-naive asthmatic patients compared with normal subjects (0.72 +/- 0.06 versus 0.27 +/- 0.04 microM and 29 +/- 1.9 versus 6.5 +/- 0. 32 ppb, respectively; p < 0.001) and were reduced in stable steroid-treated patients (0.43 +/- 0.08 microM, p < 0.05, and 9.9 +/- 0.97 ppb, p < 0.001). In unstable steroid-treated asthmatics, however, H2O2 levels were increased, but exhaled NO levels were low (0.78 +/- 0.16 microM and 6.7 +/- 1.0 ppb, respectively). There was a correlation between expired H2O2, sputum eosinophils and airway hyperresponsiveness (methacholine PC20). Exhaled NO also correlated with sputum eosinophils, but not with airway hyperresponsiveness. Our findings indicate that measurement of expired H2O2 and NO in asthmatic patients provides complementary data for monitoring of disease activity.

Administration, Inhalation↗
PubMed1998

Influence of environmental concentrations of NO on the exhaled NO test.

Measurement of levels of exhaled nitric oxide (NO) has been proposed as a noninvasive method for evaluating the degree of airway inflammation in asthmatic patients. Some concern in the interpretation of results of such measurement may arise from possible interference by high environmental concentrations of NO inhaled by these patients. The aim of this study was to verify whether environmental concentrations of NO in the range from 0 to 150 ppb can influence levels of exhaled NO. We tested two groups of subjects. The first group, consisting of 16 subjects, was tested when environmental levels of NO were from 0 to 3 ppb and from 20 to 60 ppb, and exhaled NO mean ppb (+/- SEM) levels were 9.81 +/- 1.43 and 9.78 +/- 1.47 (p = ns) (mean +/- SEM), respectively. The second group, consisting of 30 subjects, was tested at ambient NO concentrations of 0 to 3 ppm, 80 to 100 ppm, and 120 to 150 ppb, and for 18 of these subjects who underwent testing under all three conditions investigated, the mean levels of exhaled NO were 9.23 +/- 1.51, 7.78 +/- 1.19, and 9.33 +/- 1.55 ppb (p = ns), respectively. The results of this study suggest that significantly different ambient levels of NO have no effect on levels of exhaled NO.

Adult↗
PubMed1998

Prostaglandins E2 and F2alpha reduce exhaled nitric oxide in normal and asthmatic subjects irrespective of airway caliber changes.

Cyclooxygenase products modulate the expression of nitric oxide synthase (NOS) in certain cell types. We determined the effect of prostaglandins (PG) E2 and F2alpha on exhaled nitric oxide (NO) concentrations measured by chemiluminescence. Inhaled PGE2 and PGF2alpha significantly reduced exhaled NO. After the highest dose of PGE2 (100 micrograms), NO concentrations fell from 6.9 +/- 0.5 ppb to 4.0 +/- 0.8 ppb (p < 0.001), and from 22.9 +/- 2.0 ppb to 12.3 +/- 1. 2 ppb (p < 0.001), whereas after PGF2alpha, it fell from 6.5 +/- 0.6 ppb to 3.0 +/- 0.5 ppb (p < 0.001), and from 26.0 +/- 3.4 ppb to 11. 5 +/- 1.4 ppb (p < 0.001) in normal (n = 7) and asthmatic (n = 8) subjects, respectively. Although the prostaglandins did not change FEV1 in normal subjects, PGE2 caused an increase in asthmatics (from 3.6 +/- 0.3 L to 3.8 +/- 0.4 L, p < 0.05) and PGF2alpha caused a transient reduction in FEV1 from 4.0 +/- 0.2 L to 3.5 +/- 0.2 L (p < 0.05). To further determine the relationship between bronchoconstriction and exhaled NO levels, we examined the effect of inhaled methacholine which did not change exhaled NO concentrations in normal and asthmatic subjects despite a greater than 20% fall in FEV1 in asthmatics. Therefore, PGE2 and PGF2alpha reduce exhaled NO, an effect not related to airway caliber changes but which may result from an inhibition of nitric oxide synthase (NOS), particularly inducible NOS (iNOS).

Administration, Inhalation↗
PubMed1999

Exhaled nitric oxide does not provide a marker of vascular endothelial function in healthy humans.

In the lung, nitric oxide synthase (NOS) has been found in both alveolar epithelial and vascular endothelial cells. Nitric oxide (NO) in the exhaled air stemming from the lower respiratory tract has been claimed to represent a marker of the vascular endothelial NO production. Experimental evidence for this concept, however, is lacking. We compared, in eight healthy volunteers, effects on exhaled NO of epithelial NOS inhibition by N (G)-monomethyl-L-arginine (L-NMMA) inhalation (6 mg/kg over 15 min) with those of endothelial NOS inhibition by L-NMMA infusion (25 microgram/kg/min for 30 min). We also measured blood pressure, heart rate, and L-NMMA plasma concentration. The major new findings were that L-NMMA inhalation which did not have any detectable effect on hemodynamics and L-NMMA plasma concentration, decreased the pulmonary exhaled NO by almost 40%. In contrast, L-NMMA infusion that inhibited endothelial NOS, as evidenced by an increase in blood pressure and a decrease in heart rate, had only a barely detectable effect on exhaled NO (-11 +/- 4% from baseline). Pulmonary exhaled NO is mostly of epithelial rather than endothelial origin, and does not provide a marker for vascular endothelial NO production and/or endothelial function in healthy humans.

Administration, Inhalation↗
PubMed2000

Exhaled nitric oxide in high-altitude pulmonary edema: role in the regulation of pulmonary vascular tone and evidence for a role against inflammation.

High-altitude pulmonary edema (HAPE) is a life-threatening condition occurring in predisposed subjects at altitudes above 2,500 m. It is not clear whether, in addition to hemodynamic factors and defective alveolar fluid clearance, inflammation plays a pathogenic role in HAPE. We therefore made serial measurements of exhaled pulmonary nitric oxide (NO), a marker of airway inflammation, in 28 HAPE-prone and 24 control subjects during high-altitude exposure (4,559 m). To examine the relationship between pulmonary NO synthesis and pulmonary vascular tone, we also measured systolic pulmonary artery pressure (Ppa). In the 13 subjects who developed HAPE, exhaled NO did not show any tendency to increase during the development of lung edema. Throughout the entire sojourn at high altitude, pulmonary exhaled NO was roughly 30% lower in HAPE-prone than in control subjects, and there existed an inverse relationship between Ppa and exhaled NO (r = -0.51, p < 0.001). These findings suggest that HAPE is not preceded by airway inflammation. Reduced exhaled NO may be related to altered pulmonary NO synthesis and/or transport and clearance, and the data in our study could be consistent with the novel concept that in HAPE-prone subjects, a defect in pulmonary epithelial NO synthesis may contribute to exaggerated hypoxic pulmonary vasoconstriction and in turn to pulmonary edema.

Adult↗
PubMed2001

Extended exhaled NO measurement differentiates between alveolar and bronchial inflammation.

Lower respiratory tract inflammation can be detected by measuring exhaled nitric oxide (NO) concentration at a single exhalation flow rate, but this does not differentiate between alveolar and bronchial NO production. We assessed alveolar NO concentration and bronchial NO flux with an extended method of measuring exhaled NO at several exhalation flow rates in 40 patients with asthma, 17 patients with alveolitis, and 57 healthy control subjects. Bronchial NO flux was higher in asthma (2.5 +/- 0.3 nl/s, p < 0.001) than in alveolitis (0.7 +/- 0.1 nl/s) and healthy control subjects (0.7 +/- 0.1 nl/s). Alveolar NO concentration was higher in alveolitis (4.1 +/- 0.3 ppb, p < 0.001) than in asthma (1.1 +/- 0.2 ppb) and healthy control subjects (1.1 +/- 0.1 ppb). In asthma, bronchial NO flux correlated with serum level of eosinophil protein X (EPX) (r = 0.60, p < 0.001) and bronchial hyperresponsiveness (r = 0.55, p < 0.001). In alveolitis, alveolar NO concentration correlated inversely with pulmonary diffusing capacity (r = -0.55, p = 0.022) and pulmonary restriction. Glucocorticoid treatment or allergen avoidance normalized bronchial NO flux in asthma and decreased alveolar NO concentration toward normal in alveolitis. In conclusion, extended exhaled NO measurement can be used to separately assess alveolar and bronchial inflammation and to assess disease activity/severity in asthma and alveolitis.

Adult↗
PubMed2001

Alterations in exhaled gas profile during allergen-induced asthmatic response.

The source of exhaled carbon monoxide (CO) and the relationship to airway inflammation are not clear. If CO is produced by the inflamed airway, we hypothesized that inflammation induced by allergen challenge would increase exhaled CO of atopic asthmatics. Eight atopic asthmatics underwent whole lung allergen challenge. CO, nitric oxide (NO), oxygen, and carbon dioxide (CO(2)) were measured simultaneously in exhaled breath which was collected into Mylar balloons before (baseline), immediately after, and at subsequent times after allergen. NO was higher in asthmatics than control subjects at baseline, increased further in seven of the eight asthmatics after allergen, and was inversely correlated to specific conductance. In contrast, exhaled CO of asthmatics was not higher than that of control individuals at baseline, decreased immediately after allergen, and returned to baseline levels during the late asthmatic response. Thus, allergen-induced airway inflammation did not lead to increased exhaled CO in asthma.

Adult↗
PubMed2002

Increased leukotrienes in exhaled breath condensate in childhood asthma.

Cysteinyl leukotrienes (cys-LTs; LTC4, LTD4, and LTE4) are generated predominantly by mast cells and eosinophils and induce airway smooth muscle contraction, microvascular leakage, and mucous hypersecretion whereas leukotriene B4 (LTB4) is a potent chemoattractant of neutrophils. We measured cys-LTs and LTB4 in exhaled breath condensate from children aged 7-14 years including healthy nonatopic children (n = 11) and children with mild intermittent asthma (steroid naive, n = 11), mild persistent asthma (low-dose inhaled steroid treatment, n = 13), or moderate to severe persistent asthma (high-dose inhaled steroid treatment, n = 13). Exhaled LTB4 levels were increased in patients with mild and moderate to severe persistent asthma compared with patients with mild intermittent asthma (126.0 +/- 8.8 and 131.9 +/- 7.1 versus 52.7 +/- 3.8 pg/ml, p < 0.001 and p < 0.0001) and normal subjects (126.0 +/- 8.8 and 131.9 +/- 7.1 versus 47.9 +/- 4.1 pg/ml, p < 0.0001). Elevated exhaled cys-LT levels were found in patients with mild and moderate to severe persistent asthma compared with normal subjects (27.9 +/- 2.8 and 31.5 +/- 4.5 versus 18.5 +/- 0.5 pg/ml, p < 0.01 and p < 0.05). There was an inverse correlation between exhaled cys-LTs and LTB4 in patients with mild persistent asthma. We conclude that exhaled cys-LTs and LTB4 may be noninvasive markers of airway inflammation in pediatric asthma.

Adolescent↗
PubMed2003

Effects of sex and of gene variants in constitutive nitric oxide synthases on exhaled nitric oxide.

Genetic factors may contribute to the variability of exhaled nitric oxide in healthy individuals. We studied exhaled nitric oxide and genetic variants in both neuronal and endothelial nitric oxide synthases in 105 healthy nonsmoking and smoking subjects. Genomic DNA was screened for a repeat polymorphism in intron 20 of the neuronal nitric oxide synthase gene and for the 894G/T mutation of the endothelial nitric oxide synthase gene. Exhaled nitric oxide was significantly higher in males than females among both nonsmokers (p < 0.0001) and smokers (p = 0.003). No association was found between exhaled nitric oxide and the endothelial nitric oxide synthase gene variant. However, healthy nonsmoking females with greater numbers of repeats (i.e., both alleles with 12 or more repeats) in neuronal nitric oxide synthase had significantly lower nitric oxide levels than did females with fewer numbers of repeats (i.e., at least one allele with fewer than 12 repeats) (13.6 +/- 1.6 versus 19.4 +/- 1.6 ppb, p = 0.02). No association was found between exhaled nitric oxide and neuronal nitric oxide synthase genotype in males. These data suggest that variants in the neuronal nitric oxide synthase gene contribute to the variability of airway nitric oxide concentrations in healthy females.

Adolescent↗
PubMed2003

Exhaled breath condensate detects markers of pulmonary inflammation after cardiothoracic surgery.

Cardiac surgery using cardiopulmonary by-pass and, to a greater extent, lung resection, causes acute lung injury that is usually subclinical. Analysis of mediators in exhaled breath condensate is a promising means of monitoring inflammation in a variety of airway diseases but the contribution of the airway lining fluid from the lower respiratory tract is uncertain. We compared the analysis of markers of lung injury in exhaled breath condensate and bronchoalveolar lavage in endotracheally intubated patients before and after coronary artery bypass graft surgery with cardiopulmonary bypass and lobectomy. The neutrophil count and leukotriene B4 concentration in bronchoalveolar lavage fluid rose after coronary artery bypass graft surgery (p < 0.05), but there was no significant change in leukotriene B4, hydrogen peroxide, or hydrogen ion concentrations in exhaled breath condensate. By contrast, after lobectomy, the concentration in exhaled breath condensate of leukotriene B4, hydrogen peroxide and hydrogen ions rose significantly (p < 0.05). Exhaled breath condensate is a safe, noninvasive method of sampling the milieu of the distal lung and is sufficiently sensitive to detect markers of inflammation and oxidative stress in patients after lobectomy, but not after the milder insult associated with cardiac surgery.

Aged↗
PubMed2006

Inhaled L-arginine improves exhaled nitric oxide and pulmonary function in patients with cystic fibrosis.

RATIONALE: Nitric oxide formation is deficient in airways of patients with cystic fibrosis (CF). Since nitric oxide has bronchodilatory effects, nitric oxide deficiency may contribute to airway obstruction in CF. OBJECTIVES: We reasoned that inhalation of l-arginine, the precursor of enzymatic nitric oxide formation, could improve airway nitric oxide formation and pulmonary function in patients with CF. MEASUREMENTS: Exhaled nitric oxide, pulmonary function, and peripheral oxygen saturation were measured before and after a single inhalation of nebulized l-arginine solution in patients with CF and in healthy subjects. A saline solution of similar osmolarity (1.7%) was used as control. RESULTS: Nebulized l-arginine not only significantly increased exhaled nitric oxide concentrations but also resulted in a sustained improvement of FEV(1) in patients with CF. Oxygen saturation also increased significantly after the inhalation of l-arginine. Nebulized saline resulted in a small but significant increase in exhaled nitric oxide but a decrease in FEV(1) in patients with CF. In control subjects inhalation of l-arginine increased exhaled nitric oxide concentrations, but FEV(1) decreased. No effect of saline on exhaled nitric oxide, pulmonary function, or oxygen saturation was observed in healthy subjects. CONCLUSIONS: These data suggest that a single inhalation of l-arginine acutely and transiently improves pulmonary function in CF through the formation of nitric oxide. Augmentation of airway nitric oxide formation by inhalation of l-arginine is a promising therapeutic approach in patients with CF.

Administration, Inhalation↗
PubMed2002

Response of ventilator-dependent patients to delayed opening of exhalation valve.

In conventional mechanical ventilation, the inflation cycle often extends into neural expiration (TEN), potentially exacerbating dynamic hyperinflation (DH). We wished to determine the extent to which patients defend against DH when this happens. Such defense may include prolongation of TEN (timing response) and/or expiratory muscle recruitment (neuromuscular response). Fifty patients were ventilated in the Proportional Assist mode, allowing us to infer these responses noninvasively. At random intervals, exhalation of single breaths was delayed by briefly delaying the opening of exhalation valve (occlusion) (T(occ) = 0.78 +/- 0.34 seconds). Timing response was assessed from the change in TEN. Neuromuscular response was assessed from the difference between volume exhaled after release of occlusion and volume exhaled in unoccluded breaths over a similar expiratory flow duration (DeltaV(iso-time)). There was no evidence of an acute neuromuscular response; DeltaV(iso-time) averaged 0.005 +/- 0.023 L (NS). Forty-five of 50 patients significantly lengthened TEN. However, the timing response offset only 36 +/- 20% of the delay in expiration. Because of absent neuromuscular responses and weak timing responses, DH increased in most patients in postocclusion breaths (DeltaDH = 0.10 +/- 0.08 L, p = 2E-10). We conclude that acute compensatory responses to delays in opening of exhalation value are weak in ventilator-dependent patients. As a result, such nonsynchrony tends to exacerbate DH.

Adult↗
PubMed2001

"Haemoxygenase-1 induction and exhaled markers of oxidative stress in lung diseases", summary of the ERS Research Seminar in Budapest, Hungary, September, 1999.

In recent years, there has been increasing interest in noninvasive monitoring of airway inflammation and oxidative stress. Several volatile and nonvolatile substances can be measured in exhaled breath and have been suggested as potential biomarkers of these events. Exhaled gases, including carbon monoxide (CO), alkanes (ethane, pentane), and substances measured in breath condensate, such as hydrogen peroxide (H2O2) and isoprostanes were all suggested as potential markers of oxidative stress in the lung. A European Respiratory Society (ERS) International Research Seminar entitled "Haemoxygenase-1 induction and exhaled markers of oxidative stress in lung diseases" was organized by the Airway Regulation and Provocation Group of the Clinical Allergy and Immunology Assembly in Budapest, Hungary in September, 1999 to integrate the latest knowledge on these issues and accelerate further improvement in this area. During this 2-day event several issues were raised about: the use and standardization of measurements in exhaled breath; problems of measuring expired H2O2 and other mediators in breath condensate; role and regulation of haemoxygenase (HO)-1 in the lung; and conditions and factors influencing exhaled CO. This report is a summary of the main presentations at the seminar, together with the current areas of research in this rapidly expanding field.

Antioxidants↗