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PubMed2005

Increased heme catabolism in critically ill patients: correlation among exhaled carbon monoxide, arterial carboxyhemoglobin, and serum bilirubin IXalpha concentrations.

It has been reported that exhaled carbon monoxide (CO) concentrations and arterial carboxyhemoglobin (CO-Hb) concentration in blood may be increased in critically ill patients. However, there was no study that examined correlation among amount of CO in exhaled air, CO-Hb concentrations in erythrocytes, and bilirubin IXalpha (BR) in serum, i.e., the three major indexes of heme catabolism, within the same subject. Here, we examined CO concentrations in exhaled air, CO-Hb concentrations in arterial blood, and BR levels in serum in 29 critically ill patients. Measurements of exhaled CO, arterial CO-Hb, and serum total BR have been done in the intensive care unit. As control, exhaled CO concentration was also measured in eight healthy volunteers. A median exhaled CO concentration was significantly higher in critically ill patients compared with control. There was significant correlation between CO and CO-Hb and CO and total BR level. We also found CO concentrations correlated with indirect BR but not direct BR. Multivariate linear regression analysis for amount of exhaled CO concentrations also showed significant correlation with CO-Hb and total BR, despite the fact that respiratory variables of study subjects were markedly heterogeneous. We found no correlation among exhaled CO, patients' severity, and degree of inflammation, but we found a strong trend of a higher exhaled CO concentration in survivors than in nonsurvivors. These findings suggest there is an increased heme breakdown in critically ill patients and that exhaled CO concentration, arterial CO-Hb, and serum total BR concentrations may be useful markers in critically ill conditions.

Aged↗
PubMed2005

Measuring airway exchange of endogenous acetone using a single-exhalation breathing maneuver.

Exhaled acetone is measured to estimate exposure or monitor diabetes and congestive heart failure. Interpreting this measurement depends critically on where acetone exchanges in the lung. Health professionals assume exhaled acetone originates from alveolar gas exchange, but experimental data and theoretical predictions suggest that acetone comes predominantly from airway gas exchange. We measured endogenous acetone in the exhaled breath to evaluate acetone exchange in the lung. The acetone concentration in the exhalate of healthy human subjects was measured dynamically with a quadrupole mass spectrometer and was plotted against exhaled volume. Each subject performed a series of breathing maneuvers in which the steady exhaled flow rate was the only variable. Acetone phase III had a positive slope (0.054+/-0.016 liter-1) that was statistically independent of flow rate. Exhaled acetone concentration was normalized by acetone concentration in the alveolar air, as estimated by isothermal rebreathing. Acetone concentration in the rebreathed breath ranged from 0.8 to 2.0 parts per million. Normalized end-exhaled acetone concentration was dependent on flow and was 0.79+/-0.04 and 0.85+/-0.04 for the slow and fast exhalation rates, respectively. A mathematical model of airway and alveolar gas exchange was used to evaluate acetone transport in the lung. By doubling the connective tissue (epithelium+mucosal tissue) thickness, this model predicted accurately (R2=0.94+/-0.05) the experimentally measured expirograms and demonstrated that most acetone exchange occurred in the airways of the lung. Therefore, assays using exhaled acetone measurements need to be reevaluated because they may underestimate blood levels.

Acetone↗
PubMed1997

Decreased concentration of exhaled nitric oxide (NO) in patients with cystic fibrosis.

Nitric oxide (NO) is produced by various cell types in the human respiratory tract. Endogenously produced nitric oxide is detectable in the exhaled air of healthy individuals. Exhaled NO has been shown to be increased in airway inflammation, most probably due to cytokine-mediated activation of NO synthases. To assess whether NO can serve as a marker of inflammation in cystic fibrosis (CF) lung disease, we measured exhaled NO in CF patients with a chemiluminescence analyser. Single breath measurements were performed in 27 stable CF patients (age range, 6-40 years) and 30 non-smoking controls (age range, 6-37 years). Exhaled NO concentrations were 9.1 +/- 3.6 ppb in the controls and 5.9 +/- 2.6 ppb (P < 0.001) in CF patients. To account for room air NO concentrations on the measurement of exhaled NO, we also calculated the difference between exhaled NO and ambient NO concentrations. Difference values were also significantly lower in CF compared with controls (P < 0.0001). In CF patients there was a positive correlation between exhaled NO and forced vital capacity (r = 0.43, P = 0.033), suggesting that exhaled NO is lower in patients with severe lung disease than in those with mild disease. We conclude that measurements of exhaled NO in CF does not reflect activity of CF airway inflammation. The decreased concentrations of exhaled NO may be due to inhibitory effects of inflammatory cytokines on NO syntheses in the airways and alveolar epithelial cells or to increased retention in airway secretions.

Adolescent↗
PubMed2006

Exhaled nitric oxide in severe obesity: effect of weight loss.

Exhaled nitric oxide (NO) is a recognized biomarker in the lower respiratory tract. The effect of large variation in body mass on exhaled NO in the same individuals is not well known. The aim of the study was to evaluate both the effect of severe obesity and the influence of weight reduction on exhaled NO. A consecutive series of 24 uncomplicated obese patients (OB), who had laparoscopic adjustable gastric banding (LAGB) and 15 healthy controls (HC) were studied. Body mass index (BMI), exhaled NO and respiratory function tests were assessed. Exhaled NO was lower in obese in comparison to HC (12.0+/-3.6ppb versus 15.8+/-4.0ppb, p=0.0035). A significant positive correlation was found between exhaled NO and BMI in HC, which was not evident in OB. Among the respiratory indexes, functional residual capacity was significantly associated to exhaled NO. After 1 year, 12 obese patients undergone to LAGB were re-evaluated. Mean BMI (kg/m(2)) decreased from 44.8 before surgery to 32.3 post-operatively. The exhaled NO increased from 11.8+/-3.2ppb before surgery to 14.9+/-3.1ppb 1 year post-operatively (p=0.0023, n=12). In conclusion exhaled NO is consistently reduced in severe obesity and it is restored after weight reduction. The relationship between exhaled NO, large body mass excess and decrease of resting lung volume in severe obesity deserves further studies.

Adult↗
PubMed2000

Acute hypoxia and reoxygenation impairs exhaled nitric oxide release and pulmonary mechanics.

OBJECTIVE: Changes in exhaled nitric oxide levels often accompany conditions associated with elevated pulmonary vascular resistance and altered lung mechanics. However, it is unclear whether changes in exhaled nitric oxide reflect altered vascular or bronchial nitric oxide production. This study determined the effects of acute hypoxia and reoxygenation on pulmonary mechanics, plasma nitrite levels, and exhaled nitric oxide production. METHODS: Ten piglets underwent 90 minutes of hypoxia (fraction of inspired oxygen = 12%), 1 hour of reoxygenation on cardiopulmonary bypass, and 2 hours of recovery. Five additional animals underwent bypass without hypoxia. Exhaled nitric oxide, plasma nitrite levels, and pulmonary mechanics were measured. RESULTS: Exhaled nitric oxide decreased to 36% of baseline by end hypoxia (34 +/- 14 vs 12 +/- 9 ppb, P =.005) and declined further to 20% of baseline at end recovery (7 +/- 6 ppb). Aortic nitrite levels decreased from baseline during hypoxia (from 102 +/- 13 to 49 +/- 7 micromol/L, P =.05) but returned to baseline during recovery. Pulmonary arterial nitrite also decreased during hypoxia (from 31.4 +/- 7.8 to 22.9 +/- 9.5 micromol/L, P =.04) and returned to baseline at end recovery. Decreased production of exhaled nitric oxide was associated with impaired gas exchange (alveolar-arterial gradient = 32 mm Hg at baseline and 84 mm Hg at end recovery), decreased pulmonary compliance (6.6 +/- 0.9 mL/cm H(2)O at baseline, 5.0 +/- 0.7 mL/cm H(2)O at end hypoxia, and 5.4 +/- 0.7 mL/cm H(2)O at end recovery), and increased inspiratory airway resistance (41 +/- 4 cm H(2)O. L(-1). s(-1) at baseline, 56 +/- 4.9 cm H(2)O. L(-1). s(-1) at end hypoxia, and 50 +/- 5 cm H(2)O. L(-1). s(-1) at end recovery). CONCLUSIONS: A decrease in exhaled nitric oxide persisted after hypoxia, and plasma nitrite levels returned to baseline on reoxygenation, indicating that alterations in exhaled nitric oxide during hypoxia-reoxygenation might be unrelated to plasma nitrite levels. Furthermore, decreased exhaled nitric oxide corresponded with altered pulmonary mechanics and gas exchange. Reduced exhaled nitric oxide after hypoxia-reoxygenation might reflect bronchial epithelial dysfunction associated with acute lung injury.

Acute Disease↗
PubMed2004

Exhaled nitric oxide before and after cardiac surgery with cardiopulmonary bypass--response to acetylcholine and nitroglycerin.

BACKGROUND: Pulmonary endothelial dysfunction may occur after ischaemia-reperfusion injury and can be revealed as a reduced vasodilatory response upon administration of acetylcholine (ACh). ACh also releases the endothelium-derived vasodilator nitric oxide but direct measurements of this gas are difficult to perform in vivo. We wanted to study the effects of i.v. administration of ACh and the endothelium-independent vasodilator nitroglycerin on exhaled nitric oxide in relation to pulmonary endothelial dysfunction after open-heart surgery and cardiopulmonary bypass (CPB). METHODS: Basal exhaled nitric oxide and the response in exhaled nitric oxide to i.v. injections of ACh and nitroglycerin were measured with chemiluminescence in 10 patients before and after open-heart surgery. RESULTS: Exhaled nitric oxide decreased significantly after CPB. I.V. bolus injections of ACh induced a reproducible and dose-dependent increase in exhaled nitric oxide that was unaltered after CPB. In contrast, the increase in exhaled nitric oxide evoked by nitroglycerin was attenuated after CPB. The response in pulmonary vascular resistance index (PVRI) to an infusion of ACh decreased after CPB, indicating endothelial dysfunction. The decrease in PVRI response to ACh correlated to the duration of CPB. CONCLUSIONS: Interestingly, pulmonary vascular dysfunction after CPB was accompanied by a reduction in the exhaled nitric oxide response to nitroglycerin and lower levels of basal exhaled nitric oxide. The ACh-induced responses in exhaled nitric oxide were unchanged, which could indicate nitric oxide-independent mechanisms behind the endothelial dysfunction in this study. The possibility of using exhaled nitric oxide dynamics to investigate pulmonary endothelial dysfunction merits further studies.

Acetylcholine↗
PubMed1981

Desaturation of exhaled air in camels.

We have found that camels can reduce the water loss due to evaporation from the respiratory tract in two ways: (1) by decreasing the temperature of the exhaled air and (2) by removal of water vapour from this air, resulting in the exhalation of air at less than 100% relative humidity (r.h.). Camels were kept under desert conditions and deprived of drinking water. In the daytime the exhaled air was at or near body core temperature, while in the cooler night exhaled air wat at or near ambient air temperature. In the daytime the exhaled air was fully saturated, but at night its humidity might fall to approximately 75% r.h. The combination of cooling and desaturation can provide a saving of water of 60% relative to exhalation of saturated air at body temperature. The mechanism responsible for cooling of the exhaled air is a simple heat exchange between the respiratory air and the surfaces of the nasal passageways. On inhalation these surfaces are cooled by the air passing over them, and on exhalation heat from the exhaled air is given off to these cooler surfaces. The mechanism responsible for desaturation of the air appears to depend on the hygroscopic properties of the nasal surfaces when the camel is dehydrated. The surfaces give off water vapour during inhalation and take up water from the respiratory air during exhalation. We have used a simple mechanical model to demonstrate the effectiveness of this mechanism.

Air↗
PubMed2006

The effect of allergic rhinitis on adenosine concentration in exhaled breath condensate.

BACKGROUND: Patients with allergic rhinitis (AR) frequently develop asthma. This initiating inflammation in the lower airways may result in increased levels of inflammatory mediators such as adenosine in the exhaled breath. OBJECTIVE: We compared adenosine levels in exhaled breath condensate (EBC) and both exhaled and nasal nitric oxide (NO) levels of AR patients and healthy control subjects. We also tested whether inhalation through inflamed nasal cavity during EBC sampling influences adenosine concentrations in exhaled air. METHODS: Exhaled and nasal NO levels were measured and EBC samples (at oral inhalation) were collected from 27 patients and 15 healthy controls. EBC collection was repeated after 15 min with subjects inhaling through their nose. Adenosine was measured by HPLC and NO was determined by chemiluminescence. RESULTS: The concentration of EBC adenosine was higher in patients with AR than in healthy controls (12.4+/-1.3 nM vs. 6.5+/-0.7 nM, P=0.0019) and this was accompanied by an increase in the concentration of exhaled NO (10.2+/-1.3 ppb vs. 5.3+/-0.5 ppb; P=0.0099, respectively). No difference in nasal NO was detected. EBC adenosine concentration showed a significant positive correlation with the level of exhaled NO. In contrast to healthy control subjects, patients with rhinitis had higher levels of exhaled adenosine when inhaling via the nose instead of the mouth (17.7+/-2.8 nM, P=0.007). CONCLUSION: When compared with healthy subjects, patients with AR exhibit an increased concentration of exhaled adenosine and a related increase in exhaled NO concentration. EBC adenosine is further increased when rhinitis patients inhale through their nose than via their mouth. Our data suggest that non-asthmatic patients with rhinitis may have subclinical inflammation in their lower airways.

Adenosine↗
PubMed2002

Dose-dependent onset and cessation of action of inhaled budesonide on exhaled nitric oxide and symptoms in mild asthma.

BACKGROUND: Dose dependent anti-inflammatory effects of inhaled corticosteroids in asthma are difficult to demonstrate in clinical practice. The anti-inflammatory effect of low dose inhaled budesonide on non-invasive exhaled markers of inflammation and oxidative stress were assessed in patients with mild asthma. METHODS: 28 patients entered a double blind, placebo controlled, parallel group study and were randomly given either 100 or 400 micro g budesonide or placebo once daily, inhaled from a dry powder inhaler (Turbohaler), for 3 weeks followed by 1 week without treatment. Exhaled nitric oxide (NO), exhaled carbon monoxide (CO), nitrite/nitrate, S-nitrosothiols, and 8-isoprostanes in exhaled breath condensate were measured four times during weeks 1 and 4, and once a week during weeks 2 and 3. RESULTS: A dose-dependent speed of onset and cessation of action of budesonide was seen on exhaled NO and asthma symptoms. Treatment with 400 micro g/day reduced exhaled NO faster (-2.06 (0.37) ppb/day) than 100 micro g/day (-0.51 (0.35) ppb/day; p<0.01). The mean difference between the effect of 100 and 400 micro g budesonide was -1.55 ppb/day (95% CI -2.50 to -0.60). Pretreatment NO levels were positively related to the subsequent speed of reduction during the first 3-5 days of treatment. Faster recovery of exhaled NO was seen after stopping treatment with budesonide 400 micro g/day (1.89 (1.43) ppb/day) than 100 micro g/day (0.49 (0.34) ppb/day, p<0.01). The mean difference between the effect of 100 and 400 micro g budesonide was 1.40 ppb/day (95% CI -0.49 to 2.31). Symptom improvement was dose-dependent, although symptoms returned faster in patients treated with 400 micro g/day. A significant reduction in exhaled nitrite/nitrate and S-nitrosothiols after budesonide treatment was not dose-dependent. There were no significant changes in exhaled CO or 8-isoprostanes in breath condensate. CONCLUSION: Measurement of exhaled NO levels can indicate a dose-dependent onset and cessation of anti-inflammatory action of inhaled corticosteroids in patients with mild asthma.

Administration, Inhalation↗
PubMed1998

Influence of atmospheric nitric oxide concentration on the measurement of nitric oxide in exhaled air.

BACKGROUND: Measurement of nitric oxide (NO) in exhaled air shows promise as a non-invasive method of detecting lung inflammation. However, variable concentrations of NO are measured in environmental air. The aim of this study was to verify a possible relationship between exhaled NO and atmospheric NO values during high atmospheric NO days. METHOD: Exhaled air from 78 healthy non-smokers of mean age 35.3 years was examined for the presence of NO using a chemiluminescence NO analyser and NO levels were expressed as part per billion (ppb). The exhaled air from all the subjects was collected into a single bag and into two sequential bags. Before each test atmospheric NO was measured. RESULTS: The mean (SE) concentration of exhaled NO collected into the single bag was 17.1 (0.6) ppb while the mean values of exhaled NO in bags 1 and 2 were 16.7 (1.3) ppb and 13.8 (1.2) ppb, respectively. The atmospheric NO concentrations registered before each test varied from 0.4 to 71 ppb. There was a significant correlation between exhaled NO in the single bag and atmospheric NO (r = 0.38, p = 0.001). The atmospheric NO concentration also correlated with exhaled NO both in bag 1 (r = 0.44, p = 0.0001) and in bag 2 (r = 0.42, p = 0.0001). These correlations disappeared with atmospheric NO concentrations lower than 35 ppb. CONCLUSIONS: These results indicate a relationship between atmospheric NO and NO levels measured in exhaled air, therefore exhaled NO should not be measured on very high atmospheric NO days.

Adult↗
PubMed1998

Nitrite levels in breath condensate of patients with cystic fibrosis is elevated in contrast to exhaled nitric oxide.

BACKGROUND: Nitric oxide (NO) is released by activated macrophages, neutrophils, and stimulated bronchial epithelial cells. Exhaled NO has been shown to be increased in patients with asthma and has been put forward as a marker of airways inflammation. However, we have found that exhaled NO is not raised in patients with cystic fibrosis, even during infective pulmonary exacerbation. One reason for this may be that excess airway secretions may prevent diffusion of gaseous NO into the airway lumen. We hypothesised that exhaled NO may not reflect total NO production in chronically suppurative airways and investigated nitrite as another marker of NO production. METHODS: Breath condensate nitrite concentration and exhaled NO levels were measured in 21 clinically stable patients with cystic fibrosis of mean age 26 years and mean FEV1 57% and 12 healthy normal volunteers of mean age 31 years. Breath condensate was collected with a validated method which excluded saliva and nasal air contamination and nitrite levels were measured using the Griess reaction. Exhaled NO was measured using a sensitive chemiluminescence analyser (LR2000) at an exhalation rate of 250 ml/s. Fourteen patients with cystic fibrosis had circulating plasma leucocyte levels and differential analysis performed on the day of breath collection. RESULTS: Nitrite levels were significantly higher in patients with cystic fibrosis than in normal subjects (median 1.93 microM compared with 0.33 microM). This correlated positively with circulating plasma leucocytes and neutrophils (r = 0.6). In contrast, exhaled NO values were not significantly different from the normal range (median 3.8 ppb vs 4.4 ppb). There was no correlation between breath condensate nitrite and lung function and between breath condensate nitrite and exhaled NO. CONCLUSIONS: Nitrite levels in breath condensate were raised in stable patients with cystic fibrosis in contrast to exhaled NO. This suggests that nitrite levels may be a more useful measure of NO production and possibly airways inflammation in suppurative airways and that exhaled NO may not reflect total NO production.

Adult↗
PubMed1996

Rate of nitric oxide release in the lung and factors influencing the concentration of exhaled nitric oxide.

The level of nitric oxide (NO) in exhaled air fluctuates in normal individuals depending on the physiological conditions. We evaluated the effects of duration of exhalation and breath-holding on the exhaled concentrations of NO in 16 normal human volunteers. Exhaled gas corresponding to vital capacity was collected in 6-liter Tedlar bags and analyzed by chemiluminescence. The NO concentration in exhaled gas increased significantly in proportion to the duration of exhalation [P = 0.009 +/- 0.011 (SD)] and was increased after breath-holding. There was no significant difference in the exhaled NO concentration among 10-s phases of a 30-s exhalation, as determined from multiple breath collections. The NO released from the airways is presumably unaffected by fluctuation of exhalation speed. The NO release rate, calculated from a single regression analysis between the NO concentration and the duration of exhalation, was 39 +/- 29 pmol/s, a value which was about fourfold greater in nine patients with bronchial asthma.

Adult↗
PubMed1980

Effect of ventilation and diffusion nonuniformity on DLCO (exhaled) in a lung model.

Recent studies have shown that diffusing capacities measured at multiple intervals during a single exhalation [DLCO(exhaled)] remained constant with lung volume in normal subjects, but decreased with decreasing lung volume in patients who may have had diffusion nonuniformity. We have examined the theoretical basis of these results by determining what factors affected DLCO(exhaled) in a computerized lung model in which diffusion in each compartment remained constant with lung volume. DLCO(exhaled) decreased with decreasing lung volume when a small lung region lacked diffusion. However, the change in DLCO(exhaled) with lung volume was also affected by nonuniform ventilation and these effects could not be eliminated by correcting the carbon monoxide decay and the simultaneous decay of helium. DLCO(exhaled) values were also influenced by the exhaled flow rate in the presence of nonuniform ventilation and/or nonuniform diffusion. However, prolonging the period of breath holding prior to exhalation reduced DLCO(exhaled) values at all lung volumes when non-uniform diffusion was simulated, but did not affect DLCO(exhaled) when only nonuniform ventilation was simulated.

Carbon Dioxide↗
PubMed1998

Single-exhalation profiles of NO and CO2 in humans: effect of dynamically changing flow rate.

Endogenous production of nitric oxide (NO) in the human lungs has many important pathophysiological roles and can be detected in the exhaled breath. An understanding of the factors that dictate the shape of the NO exhalation profile is fundamental to our understanding of normal and diseased lung function. We collected single-exhalation profiles of NO and CO2 from normal human subjects after inhalation of ambient air (approximately 15 parts/billion) and examined the effect of a 15-s breath hold and exhalation flow rate (VE) on the following features of the NO profile: 1) series dead space, 2) average concentration in phase III with respect to time and volume, 3) normalized slope of phase III with respect to time and volume, and 4) elimination rate at end exhalation. The dead space is approximately 50% smaller for NO than for CO2 and is substantially reduced after a breath hold. The concentration of exhaled NO is inversely related to VE, but the average NO concentration with respect to time has a stronger inverse relationship than that with respect to volume. The normalized slope of phase III NO with respect to time and that with respect to volume are negative at a constant VE but can be made to change signs if the flow rate continuously decreases during the exhalation. In addition, NO elimination at end exhalation vs. VE produces a nonzero intercept and slope that are subject dependent and can be used to quantitate the relative contribution of the airways and the alveoli to exhaled NO. We conclude that exhaled NO has an airway and an alveolar source.

Adult↗
PubMed1997

Increased carbon monoxide in exhaled air of asthmatic patients.

Exhaled carbon monoxide (CO) concentrations were measured on a CO monitor by vital capacity maneuvers in asthmatic patients receiving or not receiving inhaled corticosteroids and in nonsmoking and smoking healthy control subjects. CO was detectable and measured reproducibly in the exhaled air of all subjects. The exhaled CO concentrations were higher in asthmatic patients not receiving inhaled corticosteroids (5.6+/-0.6 ppm, p < 0.001) and similar in asthmatic patients receiving inhaled corticosteroids (1.7+/-0.1 ppm) compared with those in nonsmoking healthy control subjects (1.5+/-0.1 ppm). Smoking healthy control subjects had the highest levels of exhaled CO concentration among the groups (21.6+/-2.8 ppm, p < 0.001). To examine whether inhaling corticosteroids reduce exhaled CO concentration in a given asthmatic patient, 12 patients with symptomatic asthma who were being treated by inhaled beta2-agonists alone underwent measurements of exhaled CO concentration before and 4 wk after the initiation of inhaled corticosteroid treatment. All patients had reductions in exhaled CO concentration (p < 0.001) and eosinophil cell counts in sputum (p < 0.01) that were accompanied by an improvement in airway obstruction. Changes in exhaled CO concentration were significantly related to those in the eosinophil cell counts in sputum (p < 0.001). The present study shows an elevation of exhaled CO in asthmatic patients that decreases with corticosteroid therapy. Increases in the exhaled CO levels therefore may reflect inflammation in the asthmatic lung.

Administration, Inhalation↗
PubMed1999

Effect of natural grass pollen exposure on exhaled nitric oxide in asthmatic children.

Exhaled nitiric oxide (NO) is increased in exhaled breath of asthmatic patients. The aim of this study was to investigate the longitudinal changes of exhaled NO outside and during the pollen season in pollen-allergic asthmatic children. Twenty-one children (age 6 to 16 yr), with a seasonal allergic asthma sensitive to grass pollen, underwent measurements of exhaled NO and pulmonary function before (March), during (May), and after (November) the pollen season. Exhaled NO was measured by a tidal breathing method with a chemiluminescence analyzer and NO steady-state levels were recorded. The timing of the measurements during the pollen season was based on the atmospheric pollen count. Exhaled NO values of asthmatic children were compared with those of 21 sex- and age-matched healthy children. Pulmonary function and symptoms of asthma were also evaluated at each visit. The mean value of exhaled NO before the grass season was 12.7 +/- 5.1 ppb (mean +/- SD), significantly higher when compared with controls (7.8 +/- 2.7 ppb, p < 0.001). In the pollen season there was a significant (p < 0.001) twofold increase in exhaled NO (21.4 +/- 7.6 ppb) that, after the season, returned to values similar (12.8 +/- 5.8 ppb, p = NS) to those found before the season. There were no significant changes in FEV1 before and during the season (98.6% predicted versus 101% predicted, p = NS). We conclude that natural allergen exposure is related to an increase of exhaled NO in asthmatic grass pollen-allergic children even in absence of significant changes in airways function. We speculate that measurement of exhaled NO could be a sensitive noninvasive marker of asthma disease activity.

Adolescent↗
PubMed2001

Acute changes in bronchoconstriction influences exhaled nitric oxide level.

In previous studies the exhaled nitric oxide (NO) level of asthma patients was investigated only in association with bronchial inflammation, and whether the degree of bronchoconstriction itself influences the exhaled NO level has never been investigated. We therefore evaluated the effect of inhalation of a bronchoconstrictor (methacholine) or a bronchodilator (salbutamol) on the exhaled NO level of healthy volunteers and asthma patients. The exhaled NO level of the healthy volunteers decreased after methacholine inhalation. The exhaled NO level of patients with mild or moderate persistent asthma, who had no asthma attacks on the day of measurement, increased after salbutamol inhalation, and the exhaled NO level of asthma patients during asthma attacks increased after salbutamol inhalation followed by intravenous drip infusion of aminophylline. It is suspected that large amounts of NO are trapped in the lung distal to the constricted airway, contributing little to the exhaled NO level at the mouth. However, we expect that the trapped NO is exhaled at a larger fraction after the dilatation of the constricted small airway, thereby increasing the exhaled NO level at the mouth. In conclusion, the results of this study suggest that acute changes in bronchoconstriction themselves influence the exhaled NO level independently of the change in NO synthase activity associated with airway inflammation.

Adult↗
PubMed1999

[Exhaled and nasal nitric oxide in patients with Japanese cedar pollinosis and effects of nasal steroids].

INTRODUCTION: Nitric oxide (NO) is produced by the action of NO synthase (NOS) using L-arginine as a substrate in various cells and found in air exhaled by humans. Previous studies suggest that almost all exhaled NO is derived from the upper airways and increases in patients with untreated asthma and allergic rhinitis. Exhaled NO is inhibited by treatment with inhalation of steroids that may be caused by inhibition of inducible nitric oxide synthase (iNOS). The purpose of this study is to determine whether exhaled and nasal NO increases in patients with Japanese cedar pollinosis compared with nonallergic healthy subjects, and whether it is affected by treatment with nasal steroids. Furthermore, we investigated its relation to nasal function and allergic rhinitis. SUBJECTS AND METHODS: 10 patients with Japanese cedar pollinosis and 5 healthy normal subjects were tested. All subjects had no history of respiratory infection for at least 2 weeks and did not smoke. Exhaled NO was collected in a sampling bag from oral and nasal breathing, and nasal NO was sampled directly from the nasal cavity. Both were measured by a chemiluminescence NO analyzer, ML9841, at a detection limit of 1 part per billion (ppb). Subjects used nasal steroids for 2 weeks and were measured similarly afterwards. RESULTS: NO concentrations in nasal air and air exhaled from the nose in patients with Japanese cedar pollinosis (277.9 +/- 59.5 ppb, 34.4 +/- 3.9 ppb, n = 10) were higher than the normal subjects (153.3 +/- 30.6 ppb, 19.9 +/- 3.4 ppb, n = 5) (p < 0.05). NO exhaled from the mouth was not significantly different between patients (20.5 +/- 4.9 ppb) and normal subjects (23.7 +/- 2.6 ppb). In patients with Japanese cedar pollinosis, the concentration of nasal NO and nasal exhaled NO were significantly decreased after treatment with nasal steroids (144.0 +/- 21.0 ppb, 26.1 +/- 3.0 ppb) (p < 0.01, p < 0.05), but there was no change in oral exhaled NO (17.2 +/- 3.3 ppb). In normal subjects, oral (22.5 +/- 5.3 ppb), nasal exhaled NO (19.1 +/- 2.3 ppb), and nasal NO (151.2 +/- 24.8 ppb) were not changed. CONCLUSION: In patients with Japanese cedar pollinosis, nasal NO was increased and decreased by nasal steroids. These results suggest that increased nasal NO in patients with allergic rhinitis is produced by induction of iNOS and that nasal NO produces the symptoms of nasal obstruction and rhinorrhea.

Administration, Intranasal↗