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PubMedDate not supplied

Application of the can technique and radon gas analyzer for radon exhalation measurements.

A passive "can technique" and an active radon gas analyzer with an emanation container were applied for radon exhalation rate measurements from different construction materials, viz. five marble seven ceramic and 100 granite tiles used in Saudi Arabia. The marble and ceramic tiles did not show detectable radon exhalation using the active radon gas analyzer system. However the granite tiles showed relatively high radon exhalations, indicating a relatively high uranium content. A comparison of the radon exhalation rates measured by the two techniques showed a linear correlation coefficient of 0.57. The radon exhalation rates from the granites varied from 0.02 to 6.58 Bqm(-2)h(-1) with an average of 1.35+/-1.40 Bqm(-2)h(-1). The geometric mean and the geometric standard deviation of the frequency distribution were found to be 0.80 and 3.1, respectively. The track density found on the nuclear track detectors in the can technique exposed to the granites, having high exhalation rates, varied linearly with exposure time with a linear correlation coefficient of 0.99. This experimental finding agrees with the theoretical prediction. The can technique showed sensitivity to low radon exhalation rates from ceramic, marble and some granite over a period of 2 months, which were not detectable by the active radon gas analyzer system. The reproducibility of data with both measuring techniques was found to be within a 7% deviation.

Ceramics↗
PubMed1999

Exhaled and nasal NO levels in allergic rhinitis: relation to sensitization, pollen season and bronchial hyperresponsiveness.

Exhaled nitric oxide is a potential marker of lower airway inflammation. Allergic rhinitis is associated with asthma and bronchial hyperresponsiveness. To determine whether or not nasal and exhaled NO concentrations are increased in allergic rhinitis and to assess the relation between hyperresponsiveness and exhaled NO, 46 rhinitic and 12 control subjects, all nonasthmatic nonsmokers without upper respiratory tract infection, were randomly selected from a large-scale epidemiological survey in Central Norway. All were investigated with flow-volume spirometry, methacholine provocation test, allergy testing and measurement of nasal and exhaled NO concentration in the nonpollen season. Eighteen rhinitic subjects completed an identical follow-up investigation during the following pollen season. Exhaled NO was significantly elevated in allergic rhinitis in the nonpollen season, especially in perennially sensitized subjects, as compared with controls (p=0.01), and increased further in the pollen season (p=0.04), mainly due to a two-fold increase in those with seasonal sensitization. Nasal NO was not significantly different from controls in the nonpollen season and did not increase significantly in the pollen season. Exhaled NO was increased in hyperresponsive subjects, and decreased significantly after methacholine-induced bronchoconstriction, suggesting that NO production occurs in the peripheral airways. In allergic rhinitis, an increase in exhaled nitric oxide on allergen exposure, particularly in hyperresponsive subjects, may be suggestive of airway inflammation and an increased risk for developing asthma.

Adolescent↗
PubMed1999

Flow-dependency of exhaled nitric oxide in children with asthma and cystic fibrosis.

The concentration of nitric oxide in exhaled air, a marker of airway inflammation, depends critically on the flow of exhalation. Therefore, the aim of this study was to determine the effect of varying the flow on end-expiratory NO concentration and NO output in children with asthma or cystic fibrosis (CF) and in healthy children. Nineteen children with stable asthma, 10 with CF, and 20 healthy children exhaled from TLC while controlling expiratory flow by means of a biofeedback signal at approximately 2, 5, 10 and 20% of their vital capacity per second. NO was measured in exhaled air with a chemiluminescence analyser. Comparisons between the three groups were made by analysing the NO concentration at the endexpiratory plateau and by calculating NO output at different flows. Exhaled NO decreased with increasing flow in all children. Children with asthma had significantly higher NO concentrations than healthy children, but only at the lowest flows. Asthmatics using inhaled steroids (n=13) tended to have lower median exhaled NO than those without steroids. The slope of linearized (log-log transformed) NO/flow plots was significantly steeper in asthmatics than in healthy controls. CF patients had a significantly lower NO concentration and output over the entire flow range studied, compared to asthmatic and control subjects, with a similar NO/flow slope as control subjects. In conclusion, the nitric oxide concentration in exhaled air is highly flow-dependent, and the nitric oxide-flow relationship differs between asthmatics versus cystic fibrosis patients and control subjects. Assessment of the nitric oxide/flow relationship may help in separating asthmatics from normal children.

Asthma↗
PubMed2000

Hydrogen peroxide and nitric oxide in exhaled air of children with cystic fibrosis during antibiotic treatment.

Cystic fibrosis (CF) patients characteristically have severe chronic airway inflammation associated with bacterial infection. A noninvasive marker of airway inflammation could be a useful guide to treatment of CF lung disease. The aim of this study was to assess whether measurement of hydrogen peroxide (H2O2) and nitric oxide (NO) in exhaled air can serve to monitor the effect of treatment with antibiotics in CF-children with acute infective pulmonary exacerbations. Sixteen CF-patients (mean age 12.3 yrs) with exacerbation of their lung infection were treated with intravenous antibiotics in an uncontrolled study. During treatment, H2O2 in exhaled air condensate was measured twice a week. In addition, serial NO measurements were performed in nine patients. During antibiotic treatment the median H2O2 concentration in exhaled air condensate decreased significantly from 0.28 microM (range 0.07-1.20 microM) to 0.16 microM (range 0.05-0.24 microM, p=0.002) and the mean forced expiratory volume in one second significantly increased from 55% predicted to 75% pred (p=0.001). In individual subjects, changes of H2O2 and FEV1 between pairs of serial measurements correlated weakly (p=0.08). Data on exhaled NO were inconclusive; exhaled NO did not change systematically during treatment. It is concluded that cystic fibrosis patients with an acute pulmonary exacerbation have abnormally high concentrations of hydrogen peroxide, but not of nitric oxide, in exhaled air, which decrease during intravenous antibiotic treatment. Further controlled studies should establish if exhaled hydrogen peroxide, may serve as a noninvasive parameter of airway inflammation to guide antibiotic treatment in cystic fibrosis lung disease.

Acute Disease↗
PubMed2001

Nerve growth factor increases airway responses and decreases levels of exhaled nitric oxide during histamine challenge in an in vivo guinea-pig model.

There is a growing body of evidence supporting the idea that nerve growth factor (NGF) may be involved in the development of asthma-associated symptoms, such as airway hyper-responsiveness. Increased levels of NGF have recently been described in serum and in the airways of asthmatics. We have examined whether exhaled nitric oxide (NO) levels might be altered during the increased airway responses upon NGF treatment in guinea-pigs in vivo. Intravenous (i.v.) administration of histamine normally elicits a rapid peak in insufflation pressure (IP) and in exhaled NO, followed by a period of decreased concentrations of exhaled NO. Anaesthetized guinea-pigs were pre-treated intravenously with either saline, 4 or 80 ng x kg(-1) NGF 30 min before i.v. challenge with 16 microg x kg(-1) histamine. At 80 ng x kg(-1) NGF significantly enhanced the airway obstruction caused by histamine, whereas the peak acute increase in exhaled NO was not enhanced. Following the increase, came a rapid drop, an effect enforced in the NGF treated animals. Subsequently, the time to return to 90% of resting exhaled NO was increased, from 12 min in saline-treated animals to 48 min in NGF-treated animals. Our data confirm that NGF can enhance airway responses to histamine. Moreover, our study shows a decrease in exhaled NO following a histamine challenge, an effect enhanced by NGF. A reduced ability to release exhaled NO may be a mechanism for increased airway responses during elevated NGF levels. The interaction between NGF and airway NO formation, and its relation to airway responses, merit further investigation.

Animals↗
PubMed2000

Exhaled nitric oxide levels correlate with measures of disease control in asthma.

BACKGROUND: Asthma guidelines emphasize maintaining disease control. However, objective measures of asthma disease control are lacking. OBJECTIVE: We sought to examine the relationship between exhaled nitric oxide (NO) levels and measures of asthma disease control versus asthma disease severity. METHODS: We performed a cross-sectional study of 100 patients (age range, 7-80 years) with asthma. We administered a questionnaire to identify characteristics of asthma, performed spirometric testing before and after administration of a bronchodilator, and measured exhaled NO levels in all participants. RESULTS: Exhaled NO was significantly correlated with the following markers of asthma disease control: asthma symptoms within the past 2 weeks (P =.02), dyspnea score (P =. 02), daily use of rescue medications (P =.01), and reversibility of airflow obstruction (P =.02). Exhaled NO levels were not correlated with the following markers of asthma disease severity: history of respiratory failure (P =.20), health care use (P =.08), fixed airflow obstruction (P =.91), or a validated asthma severity score (P =.19). Markers with relevance to both disease control and severity showed either a weak correlation (FEV(1) and FEV(1) percent predicted) or no correlation (controller drug use) with exhaled NO. CONCLUSION: We conclude that exhaled NO levels are correlated predominantly with markers of asthma control rather than asthma severity. Monitoring of exhaled NO may be useful in outpatient asthma management.

Adult↗
PubMed1987

Particle concentration in exhaled breath.

Measurements were made of the number concentrations of particles in exhaled breath under various conditions of exercise. A laser light scattering particle spectrometer was used to count particles exhaled by test subjects wearing respirators in a challenge environment of clean, dry air. Precautions were taken to ensure that particles were not generated by the the respirators and that no extraneous water or other particles were produced in the humid exhaled air. The number of particles detected in exhaled air varied over a range from less than 0.1 to about 4 particles per cm3 depending upon the test subject and his activity. Subjects at rest exhaled the lowest concentration of particles, whereas exercises producing a faster respiration rate caused increased exhalation of particles. Exhaled particle concentrations can limit the usefulness of nondiscriminating, ambient challenge aerosols for the fit testing of highly protective respirators.

Aerosols↗
PubMed1990

Aerosol penetration through respirator exhalation valves.

Exhalation valves are a critical component of industrial respirators. They are designed to permit minimal inward leakage of air contaminants during inhalation and provide low resistance during exhalation. Under normal conditions, penetration of aerosol through exhalation valves is minimal. The exhalation valve is, however, a vulnerable component of a respirator and under actual working conditions may become dirty or damaged to the point of causing significant leakage. Aerosol penetration was measured for normal exhalation valves and valves compromised by paint or fine copper wires on the valve seat. Penetration increased with increasing wire diameter. A wire 250 microns in diameter allowed greater than 1% penetration into the mask cavity. Dirt or paint accumulated on the exhalation valve allowed a similar level of penetration. Work rate had little effect on observed penetration. Penetration decreased significantly with increasing aerosol particle size. The amount of material on the valve or valve seat necessary for significant (greater than 0.5%) inward leakage in a half-mask respirator could be readily observed by careful inspection of the exhalation valve and its seat in good lighting conditions.

Aerosols↗
PubMed2002

Exhaled nitric oxide as a marker of lung injury in coronary artery bypass surgery.

BACKGROUND: Exhaled nitric oxide (NO) concentrations have been suggested as a marker of disease onset and severity in a number of inflammatory conditions such as acute asthma. Known markers of the onset of acute lung injury require invasive tests and laboratory based analysis and have limited clinical applicability. We performed a study of the use of exhaled NO as a marker of developing acute lung injury during and after coronary artery bypass grafting in patients requiring cardiopulmonary bypass. METHODS: Mixed expired air samples were taken from the patient breathing system and analysed for exhaled NO using chemiluminescence analysis. RESULTS: Exhaled nitric oxide concentrations in expired gas correlated with the PaO2/FlO2 ratio (r = 0.23, P < 0.01). There was a non-significant trend towards a reduction in exhaled NO levels from after induction of anaesthesia to post-bypass time points, with the lowest exhaled NO concentrations occurring at this time (P = 0.07). There was no correlation between mean arterial pressure (r = -0.1, P = 0.54) or mean pulmonary artery pressure (r = -0.1. P = 0.67) and expired NO levels. CONCLUSIONS: Further work is required to test whether exhaled NO concentration may be useful in diagnosing the onset of acute lung injury in patients undergoing coronary artery bypass grafting.

Biomarkers↗
PubMed1998

Inhibition of exhaled nitric oxide production during sepsis does not prevent lung inflammation.

OBJECTIVES: Increases in exhaled nitric oxide have been demonstrated to originate from the lungs of rats after septic lung injury. The aim of this study was to investigate whether treatment with the nitric oxide synthase inhibitor N-nitro-L-arginine methyl ester (L-NAME) would prevent lipopolysaccharide (LPS)-induced increases in exhaled nitric oxide and whether this would have an effect on septic lung inflammation. DESIGN: Prospective, randomized, placebo-controlled animal laboratory investigation. SETTING: University laboratory. SUBJECTS: Male, anesthetized, paralyzed, and mechanically ventilated Sprague-Dawley rats (n = 27). INTERVENTIONS: Rats were mechanically ventilated with air filtered to remove nitric oxide (expiratory rate 40 breaths/min, tidal volume 3 mL, positive end-expiratory pressure 0, FIO2 0.21). They were then randomized to receive intravenous injections of either L-NAME (25 mg/kg/hr x 4 hrs) (n = 11) or saline (n = 10). Both groups were again randomized to receive either LPS (Salmonella typhosa: 20 mg/kg i.v. x 1 dose) or an equal volume of saline 5 mins later. Thereafter, exhaled gas was collected in polyethylene bags for measurements of nitric oxide concentration. After 4 hrs, the rats were killed and the lungs were preserved and examined histologically. To examine the effect of L-NAME and LPS on mean arterial blood pressure, six additional rats underwent the same ventilation protocol with cannulation of the right internal carotid artery so that systemic arterial pressures could be measured. MEASUREMENTS AND MAIN RESULTS: Exhaled gas was collected and measurements of NO concentrations were made using chemiluminescence every 20 mins for 240 mins during ventilation. A total lung injury score was calculated by determining the extent of cellular infiltrate, exudate and hemorrhage. Mean arterial pressure was recorded every 5 mins for 20 mins and then at 20-min periods for 120 mins. Exhaled nitric oxide concentrations increased in all the LPS-treated rats that did not receive L-NAME by 120 mins; a plateau was reached by 190 mins that was approximately 4 times greater than control rats not treated with LPS (p < .001). In contrast, rats treated with L-NAME and LPS did not show an increase in exhaled NO. Administration of L-NAME induced a 10-min nonsustained increase in mean arterial pressure in two rats treated with L-NAME followed by LPS. This increase in mean arterial pressure was not seen in two placebo and two LPS-treated rats that did not receive L-NAME. Lung inflammation was significantly worse in the two groups of rats which received LPS compared with the two that did not. L-NAME did not cause lung inflammation in rats that did not receive LPS; however, LPS-treated rats that received L-NAME had more inflammatory interstitial infiltrate (p < .05) and a trend toward worse lung injury than did LPS-treated rats that did not receive L-NAME. CONCLUSION: We conclude that L-NAME can inhibit the increase in exhaled NO from the lungs of septic rats, but that this inhibition does not reduce lung inflammation, and may worsen it.

Analysis of Variance↗
PubMed1993

Increased ethane exhalation, an in vivo index of lipid peroxidation, in alcohol-abusers.

Ethane exhalation was measured in 42 control subjects, 52 patients with various non-alcoholic liver diseases, and 89 alcohol abusers who had been admitted to hospital for alcohol withdrawal and assessment of liver disease (six with normal liver tests, 10 with steatosis with or without fibrosis, six with alcoholic hepatitis, 29 with cirrhosis, 34 with both cirrhosis and alcoholic hepatitis, and four with both cirrhosis and a hepatocellular carcinoma). Ethane exhalation was similar in control subjects and in patients with non-alcoholic liver diseases, but was five times higher in alcohol abusers. Ethane exhalation in alcohol abusers was significantly, but very weakly, correlated with the daily ethanol intake before hospital admission, and the histological score for steatosis, but not with the inflammation or alcoholic hepatitis scores. Ethane exhalation was inversely correlated with the duration of abstinence before the test. In nine alcoholic patients, the exhalation of ethane was measured repeatedly, and showed slow improvement during abstinence. Ethane exhalation was significantly but weakly correlated with the Pugh's score in patients with alcoholic cirrhosis. It is concluded that the mean ethane exhalation is increased in alcohol abusers. One of the possible mechanisms may be the presence of oxidizable fat in the liver. The weak correlation with the Pugh's score is consistent with the contribution of many other factors in the progression to severe liver disease.

Adult↗
PubMed2001

Increased nitric oxide metabolites in exhaled breath condensate after exposure to tobacco smoke.

BACKGROUND: Cigarette smoking reduces the level of exhaled nitric oxide (NO) in healthy subjects, although the mechanism is unclear. NO is a highly reactive molecule which can be oxidised or complexed with other biomolecules, depending on the microenvironment. The stable oxidation end products of NO metabolism are nitrite and nitrate. This study investigated the effect of smoking on NO metabolites in exhaled breath condensate. METHODS: Fifteen healthy current smokers were recruited together with 14 healthy non-smokers. Measurement of exhaled NO, lung function, and collection of exhaled breath condensate were performed. Nitrite, nitrite + nitrate, S-nitrosothiols, and nitrotyrosine levels were measured. The effect of inhaling two cigarettes in smokers was also evaluated. The mean level of exhaled NO in smokers was significantly lower than in non-smokers (4.3 (0.3) ppb v 5.5 (0.5) ppb, p<0.05). RESULTS: There was no difference in the levels of nitrite, nitrite + nitrate, S-nitrosothiols, and nitrotyrosine in the exhaled breath condensate at the baseline visit between smokers and non-smokers. After smoking, nitrite + nitrate levels were significantly but transiently increased (from 20.2 (2.8) microM to 29.8 (3.4) microM, p<0.05). There was no significant change in the levels of exhaled NO, nitrite, S-nitrosothiols, or nitrotyrosine 30 and 90 minutes after smoking. CONCLUSIONS: These findings suggest that acute smoking can increase the level of nitrate, but not nitrite, S-nitrosothiols, or nitrotyrosine in breath condensate. The deleterious effect of oxidant radicals induced by smoking may contribute to the epithelial damage of airways seen in smokers.

Adult↗
PubMed2002

Exhaled nitric oxide correlates with airway eosinophils in childhood asthma.

BACKGROUND: Exhaled nitric oxide has been proposed as a marker for airway inflammation in asthma. The aim of this study was to compare exhaled nitric oxide levels with inflammatory cells and mediators in bronchoalveolar lavage fluid from asthmatic and normal children. METHODS: Children were recruited from elective surgical lists and a non-bronchoscopic bronchoalveolar lavage (BAL) was performed after induction of anaesthesia. Exhaled nitric oxide (parts per billion) was measured by two techniques: tidal breathing and restricted breath. RESULTS: Median (interquartile range) exhaled nitric oxide measured by restricted breath was increased in asthmatics compared with normal children (24.3 (10.5-66.5) v 9.7 (6.5-16.5), difference between medians 14.6 (95% CI 5.1 to 29.9), p=0.001). In asthmatic children exhaled nitric oxide correlated significantly with percentage eosinophils (r=0.78, p<0.001 (tidal breathing) and r=0.78, p<0.001 (restricted breath)) and with eosinophilic cationic protein (r=0.53, p<0.01 (restricted breath)), but not with other inflammatory cells in the BAL fluid. The area under the receiver operator characteristic curves for the prediction of the presence of eosinophilic airways inflammation by exhaled nitric oxide (tidal and restricted) was 0.80 and 0.87, respectively. CONCLUSIONS: Exhaled nitric oxide correlates closely with percentage eosinophils in BAL fluid in asthmatic children and is therefore likely to be a useful non-invasive marker of airway inflammation.

Asthma↗
PubMed2005

Effects of cyclo-oxygenase inhibition on exhaled eicosanoids in patients with COPD.

BACKGROUND: Leukotriene (LT) B4 concentrations are increased and prostaglandin (PG) E2 concentrations are decreased in exhaled breath condensate (EBC) in patients with chronic obstructive pulmonary disease (COPD). A study was undertaken to investigate the short term effects of cyclo-oxygenase (COX) inhibition on exhaled LTB4 and PGE2 concentrations in patients with COPD and to identify the COX isoform responsible for exhaled PGE2 production. METHODS: Two studies were performed. A double blind, crossover, randomised, placebo controlled study with ibuprofen (400 mg qid for 2 days), a non-selective COX inhibitor, was undertaken in 14 patients with stable COPD, and an open label study with oral rofecoxib (25 mg once a day for 5 days), a selective COX-2 inhibitor, was undertaken in a different group of 16 COPD patients. EBC was collected before and after drug treatment. Exhaled LTB4 and PGE2 concentrations were measured with specific immunoassays. RESULTS: All patients complied with treatment as indicated by a reduction in ex vivo serum thromboxane B2 concentrations (ibuprofen) and a reduction in lipopolysaccharide induced increase in ex vivo plasma PGE2 values (rofecoxib) of more than 80%. Exhaled LTB4 was increased after ibuprofen (median 175.5 (interquartile range 128.8-231.5) pg/ml v 84.0 (70.0-98.5) pg/ml, p < 0.001) and exhaled PGE2 was reduced (93.5 (84.0-105-5) pg/ml v 22.0 (15.0-25.5) pg/ml, p < 0.0001). Rofecoxib had no effect on exhaled LTB4 (p = 0.53) or PGE2 (p = 0.23). CONCLUSIONS: Non-selective COX inhibition decreases PGE2 and increases LTB4 in EBC, whereas selective COX-2 inhibition has no effect on these eicosanoids. PGE2 in EBC is primarily derived from COX-1 activity, and COX inhibition may redirect arachidonic acid metabolism towards the 5-lipoxygenase pathway.

Blood Gas Analysis↗
PubMed1998

Increased levels of exhaled carbon monoxide in bronchiectasis: a new marker of oxidative stress.

BACKGROUND: Bronchiectasis is a chronic inflammatory lung disease associated with increased production of oxidants due mostly to neutrophilic inflammation. Induction of heme oxygenase (HO-1) by reactive oxygen species is a general cytoprotective mechanism against oxidative stress. HO-1 catabolises heme to bilirubin, free iron and carbon monoxide (CO). Exhaled CO measurements may therefore reflect an oxidative stress and be clinically useful in the detection and management of inflammatory lung disorders. METHODS: The levels of exhaled CO of 42 non-smoking patients with bronchiectasis treated or not treated with inhaled corticosteroids were compared with CO levels in 37 normal non-smoking subjects. RESULTS: Levels of exhaled CO were raised in patients with bronchiectasis, both those treated with inhaled corticosteroids (n = 27, median 5.5 ppm, 95% CI 5.16 to 7.76) and those not treated with inhaled corticosteroids (n = 15, median 6.0 ppm. 95% CI 4.74 to 11.8), compared with normal subjects (n = 37, median 3.0 ppm, 95% CI 2.79 to 3.81, p = 0.0024). There was no correlation between exhaled CO and HbCO levels (r = 0.42, p = 0.12) in normal subjects (n = 7), nor between the urine cotinine concentration and exhaled CO levels (r = 0.2, p = 0.12). CONCLUSIONS: Increased levels of exhaled CO may reflect induction of HO-1 and oxidative stress in bronchiectasis. Measurement of exhaled CO may be useful in the management of bronchiectasis and possibly other chronic inflammatory lung disorders.

Androstadienes↗
PubMed1999

Increased exhaled nitric oxide in patients with stable chronic obstructive pulmonary disease.

BACKGROUND: Nitric oxide (NO) plays an important role as an inflammatory mediator in the airways. Since chronic obstructive pulmonary disease (COPD) is characterised by airway inflammation, a study was undertaken to determine NO levels in the exhaled air of patients with COPD. METHODS: Two groups of patients with clinically stable COPD were studied, 10 current smokers and 10 ex-smokers. Two control groups of healthy subjects consisting of 10 current smokers and 20 non-smokers were also studied. Exhaled NO levels were measured by the collection bag technique and NO chemiluminescence analyser. RESULTS: Mean (SE) levels of exhaled NO in ex-smokers and current smokers with COPD (25.7 (3.0) ppb and 10.2 (1.4) ppb, respectively) were significantly higher than in non-smoker and current smoker control subjects (9.4 (0.8) ppb and 4.6 (0.4) ppb, respectively). In current smokers with COPD exhaled levels of NO were significantly lower than in ex-smokers. In this latter group of patients there was a significant negative correlation between smoking history (pack years) and levels of exhaled NO (r = -0.8, p = 0.002). A positive correlation was seen between forced expiratory volume in one second (FEV1) and levels of exhaled NO (r = 0.65, p = 0.001) in patients with COPD. CONCLUSIONS: These data show that exhaled NO is increased in patients with stable COPD, both current and ex-smokers, compared with healthy control subjects.

Adult↗
PubMed2001

Bronchial hyperresponsiveness and exhaled nitric oxide in patients with cardiac disease.

BACKGROUND: Increased concentrations of exhaled nitric oxide (NO) correlate with increased airway inflammation and measurement of exhaled NO is a noninvasive method for the management of bronchial asthma. In various cardiac diseases, bronchial hyperresponsiveness is observed, as is bronchial asthma. However, there have been few studies on the relationship between exhaled NO and bronchial responsiveness in cardiac diseases. OBJECTIVE: The aim of this study was to clarify the association between exhaled NO and bronchial hyperresponsiveness in patients with cardiac disease. METHODS: We measured expired NO and bronchial responsiveness to inhaled methacholine in 19 patients with cardiac diseases and 17 with bronchial asthma. We divided the cardiac disease patients into two groups according to their bronchial responsiveness to inhaled methacholine: BHR(+) group consisted of 12 patients with bronchial hyperresponsiveness and BHR(-) group consisted of 7 patients without bronchial hyperresponsiveness. RESULTS: The concentration of exhaled NO in the asthmatic patients was significantly higher than that in the BHR(+) and BHR(-) groups (142.0 +/- 17.0, 33.6 +/- 6.4 and 42.3 +/- 10.3 ppb, respectively, p < 0.01). There was no significant difference in exhaled NO between BHR(+) and BHR(-) groups. There were also no significant differences in the parameters of bronchial hyperresponsiveness between the cardiac BHR(+) and bronchial asthma groups. These results indicate that bronchial hyperresponsiveness in patients with cardiac diseases is not a consequence of eosinophilic inflammation or of exhaled NO. CONCLUSION: We conclude that bronchial hyperresponsiveness in patients with cardiac diseases can occur independently of NO production.

Adult↗
PubMed2000

Exhaled nitric oxide--is it really a good marker of airway inflammation in bronchial asthma?

BACKGROUND: The concentration of exhaled nitric oxide ([NO]) has been reported to reflect the inflammatory process of airways in patients with bronchial asthma, particularly when they are steroid naive. However, it is not fully understood whether it equally reflects the degree of airway inflammation in patients receiving inhaled corticosteroids, but whose symptoms are not necessarily well controlled. OBJECTIVE: To examine whether the exhaled [NO] really reflects airway inflammation in patients with bronchial asthma, regardless of treatment with inhaled steroids. METHODS: Exhaled [NO] was measured in patients with bronchial asthma (43 steroid treated and 32 steroid naive), chronic obstructive pulmonary disease (COPD) (n = 36), bronchiectasis (n = 10) and in control subjects (n = 26). We examined in each asthmatic group whether the exhaled [NO] correlated with parameters reflecting airway inflammation. RESULTS: Exhaled [NO] was significantly correlated with symptom score, clinical severity, circulating eosinophil count, and the percentage of eosinophils in induced sputum in the steroid-naive asthmatics, but not in the steroid-treated asthmatics, although airway inflammation in this group was not well controlled, as evidenced by clinical symptoms and the higher percentage of eosinophils in induced sputum. Exhaled [NO] from the patients with COPD (6.2 +/- 0. 7 ppb) or bronchiectasis (5.4 +/- 1.3 ppb) was not significantly increased compared with the controls (6.0 +/- 1.0 ppb), and was significantly lower than in the asthmatic patients as a whole (19.0 +/- 2.0 ppb). CONCLUSIONS: Although exhaled [NO] is a useful marker of airway inflammation for differential diagnosis and evaluation of severity in steroid-naive patients with bronchial asthma, it may not be as useful in steroid-treated patients.

Adrenal Cortex Hormones↗