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PubMed1994

Exhaled nitric oxide as a marker for organic nitrate tolerance.

BACKGROUND: This study was designed to demonstrate the development of biochemical tolerance to organic nitrates by measuring levels of exhaled gaseous nitric oxide (NO) in lambs given intravenous (IV) nitroglycerin or sodium nitroprusside. METHODS AND RESULTS: IV injections of nitroglycerin or sodium nitroprusside produced dose-dependent and sustained increases in the exhaled levels of nitric oxide measured by chemiluminescence in awake lambs with tracheostomies. After a 6-hour IV infusion of 25 micrograms.kg-1.min-1 nitroglycerin, peak exhaled NO levels were significantly reduced (-53.6 +/- 4.9%, mean +/- SEM, P < .001) and systemic hypotensive responses were attenuated (-52.6 +/- 5.9%, P < .001) after an IV challenge of nitroglycerin but not sodium nitroprusside. After a subsequent 12-hour nitroglycerin-free period, there was complete recovery of NO excretion in exhaled breath and a return to baseline of systemic hypotensive changes on administration of IV nitroglycerin boluses. For IV sodium nitroprusside challenges, pulmonary NO excretion and systemic hypotensive responses remained constant throughout the study. Challenges with IV nitroglycerin but not sodium nitroprusside during a 12-hour nitroglycerin-free period resulted in delayed biochemical recovery with various exhaled NO levels and systemic hypotensive responses to challenges with IV nitroglycerin. CONCLUSIONS: Measurements of exhaled NO provide in vivo, noninvasive evidence for the development of biochemical tolerance to nitroglycerin. There was reduced NO release into exhaled gas from the pulmonary vasculature concomitant with evidence of tolerance to nitroglycerin vasodilation in the systemic circulation.

Animals↗
PubMed1995

Elevated levels of exhaled nitric oxide in bronchiectasis.

Bronchiectasis is characterized by chronic inflammation in one or more bronchi, but the extent of inflammation is difficult to monitor. The concentration of nitric oxide (NO) in exhaled air is increased in asthmatic patients, possibly as a result of the chronic inflammatory process. We have measured exhaled NO in patients with documented bronchiectasis and investigated whether the concentration of exhaled NO is related to the extent of disease as defined by computed tomography (CT) and lung function. In 20 patients with bronchiectasis who were not taking inhaled steroids, the peak concentration of NO in exhaled air, measured by a modified chemiluminescence analyzer, was significantly elevated (285 +/- 49.0 ppb) as compared with values for 79 normal subjects (89 +/- 2.7 ppb, p < 0.01) and 19 patients with bronchiectasis treated with inhaled steroids (88 +/- 13.4 ppb, p < 0.01). Thin-section CT was used to quantify the extent of bronchiectasis in the 19 patients. There was a significant correlation between the CT score and FEV1 (r = 0.73, p < 0.01). In patients not treated with inhaled steroids there was a significant relationship between CT score and peak exhaled NO (r = 0.81, n = 12, p < 0.02), but this was not the case for patients treated with regular inhaled steroids (n = 7). We conclude that untreated bronchiectasis is associated with an increase in exhaled NO, and that this is correlated with disease severity, whereas patients treated with inhaled steroids have levels of exhaled NO within the normal range.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Agonists↗
PubMed1995

Acute and chronic effects of cigarette smoking on exhaled nitric oxide.

Cigarette smoking is associated with an increased risk of respiratory tract infections, chronic airway disease, and cardiovascular diseases, all of which may be modulated by endogenous nitric oxide (NO). We have investigated whether cigarette smoking reduces the production of endogenous NO. We compared exhalations of 41 current cigarette smokers with normal lung function and 73 age-matched non-smoking controls. Peak exhaled NO levels were measured by a modified chemiluminescence analyzer. The effects of inhaling a single cigarette in smokers were also measured. In control subjects we also measured the effects of inhalation of NO itself and carbon monoxide, both constituents of tobacco smoke. Peak exhaled NO concentrations were significantly reduced in smokers (42 +/- 3.9 compared with 88 +/- 2.7 parts per billion in nonsmokers, p < 0.01), with a significant relation between the exhaled NO and cigarette consumption (r = 0.77, p < 0.001). Smoking a single cigarette also significantly (p < 0.02), but transiently, reduced exhaled NO. Inhalation of carbon monoxide and NO had no effect on exhaled NO in normal subjects. Cigarette smoking decreased exhaled NO, suggesting that it may inhibit the enzyme NO synthase. Since endogenous NO is important in defending the respiratory tract against infection, in counteracting bronchoconstriction and vasoconstriction, and in inhibiting platelet aggregation, this effect may contribute to the increased risks of chronic respiratory and cardiovascular disease in cigarette smokers.

Administration, Inhalation↗
PubMed1996

Increased exhaled nitric oxide in asthma is mainly derived from the lower respiratory tract.

Nitric oxide (NO) is detectable in the exhaled air of human subjects, and its concentration is increased in patients with asthma. We have investigated the origin of the increase in exhaled NO in asthmatic patients by using different expiratory maneuvers and by direct sampling from the upper and lower respiratory tracts. Exhaled NO was measured by a chemiluminescence analyzer. Concentrations of NO measured during expiration against the resistance of the analyzer with exhaled flow of 1 L/min, were 78 +/- 3 ppb in normal subjects (n = 46) and significantly elevated in patients with asthma (301 +/- 26 ppb, n = 30, p < 0.001). Values of exhaled NO were lower when measured during unobstructed expiration with a flow of 5 L/min with sampling from a side-arm (7 +/- 1 ppb), but again were elevated in patients with asthma (46 +/- 6 ppb, p < 0.001). Breath-holding for 20 s resulted in an initial peak of NO, but end-expiration values similar to the unobstructed expiration. The concentration of NO in the nose was considerably greater than in expired air (996 +/- 39 ppb) and was elevated in patients with asthma (1,390 +/- 71 ppb, p < 0.002). Direct sampling from trachea and right middle lobe bronchus via a fiberoptic bronchoscope gave similar values in five normal and 15 asthmatic subjects to the values recorded during unobstructed expiration, and there was a good correlation between values in expired air and direct sampling (trachea r = 0.91, right middle lobe r = 0.87, p < 0.001). We conclude that exhaled NO measured in an unobstructed breath reflects concentrations in the lower respiratory tract, but that breath-holding or expiration against resistance is contaminated by residual NO derived from the upper respiratory tract. We also provide evidence that the elevated levels of exhaled NO in asthmatic patients are derived predominantly from the lower respiratory tract.

Adult↗
PubMed2001

Increased nitrosothiols in exhaled breath condensate in inflammatory airway diseases.

Nitrosothiols (RS-NOs) are formed by interaction of nitric oxide (NO) with glutathione and may limit the detrimental effect of NO. Because NO generation is increased in airway inflammation, we have measured RS-NOs in exhaled breath condensate in patients with asthma, cystic fibrosis, or chronic obstructive pulmonary disease (COPD). We also measured exhaled NO and nitrite (NO(2-)) in the same subjects. RS-NOs were detectable in exhaled breath condensate of all subjects. RS-NOs were higher in subjects with severe asthma (0.81 +/- 0.06 microM) when compared with normal control subjects (0.11 +/- 0.02 microM, p < 0.01) and with subjects with mild asthma (0.08 +/- 0.01 microM, p < 0.01). Elevated RS-NOs values were also found in patients with cystic fibrosis (0.35 +/- 0.07 microM, p < 0.01), in those with COPD (0.24 +/- 0.04 microM, p < 0.01) and in smokers (0.46 +/- 0.09 microM, p < 0.01). In current smokers there was a correlation (r = 0.8, p < 0.05) between RS-NOs values and smoking history (pack/year). We also found elevated concentrations of NO(2-) in patients with severe asthma, cystic fibrosis, or COPD, but not in smokers or patients with mild asthma. This suggests that exhaled NO(2-) is less sensitive than exhaled RS-NOs. This study has shown that RS-NOs are detectable in exhaled breath condensate of healthy subjects and are increased in patients with inflammatory airway diseases. As RS-NOs concentrations in exhaled breath condensate vary in the different airway diseases and increase with the severity of asthma, their measurement may have clinical relevance as a noninvasive biomarker of nitrosative stress.

Adult↗
PubMed2002

Exhaled nitric oxide and bronchial responsiveness in healthy subjects exposed to organic dust.

Inhalation of organic dust from swine houses causes an intense inflammatory reaction in the respiratory tract, and increased bronchial responsiveness to methacholine in healthy subjects. The aims of the present study were to investigate whether exhaled nitric oxide (NO) is a marker of the inflammation caused by exposure to organic dust (swine dust), whether there is a relationship between an increase in exhaled NO and bronchial responsiveness, and also whether wearing a half-mask influences the airway reaction (assessed by exhaled NO) and the increased bronchial responsiveness. Thirty-three healthy nonatopic, nonsmoking subjects were exposed during 3 h of light work in a swine confinement building. Eleven of the subjects were wearing a half-mask and 22 were unprotected. Lung function, bronchial responsiveness and exhaled NO were measured before and after exposure. The provocative concentration causing a 20% fall in forced expiratory volume in one second fell by 2.7 (2.1-4.1) (median (25th-75th percentiles)) doubling concentration steps in subjects without a half-mask and by 1.5 (0.9-2.9) doubling concentration steps in subject wearing a mask. Exhaled NO increased from 7.5 (5.7-13.7) parts per billion (ppb) before to 13.4 (10.5-17.5) ppb after exposure in the unprotected group and was unaltered (8.3 (6.1-14.1) to 8.6 (6.6-14.6) ppb) in the group wearing a half-mask. There was no correlation between NO increase and provocative dose causing a 20% fall in the forced expiratory volume in one second decrease. In conclusion, bronchial responsiveness and exhaled nitric oxide increased after exposure to a swine confinement facility. Half-mask abolished the increase in exhaled nitric oxide levels, but influenced the increase in bronchial responsiveness to a minor extent. These results indicate that these two outcome measures reflect different aspects of airway inflammation induced by exposure to a farming environment.

Adult↗
PubMed1998

Relationship between exhaled nitric oxide and airway hyperresponsiveness following experimental rhinovirus infection in asthmatic subjects.

Exhaled nitric oxide (NO) is elevated in asthmatics, and varies with disease severity. We postulated that a respiratory virus infection increases exhaled NO levels in asthma, and examined the relationship between the virus-induced changes in exhaled NO and in airway hyperresponsiveness to histamine. In a parallel study, seven patients underwent experimental rhinovirus 16 (RV16) inoculation at days 0 and 1, whilst seven patients received placebo. Exhaled NO was measured at baseline (day 0) and at days 1, 2 and 3 after inoculation. Histamine challenges were performed prior to (day -7) and after inoculation (day 3), and were expressed as provocative concentration causing a 20% fall in forced expiratory volume in one second (FEV1) (PC20). Following RV16 infection there was a significant increase in NO at days 2 and 3 as compared to baseline (median change (range): 4.2 (7.5) parts per billion (ppb), p=0.03, and 3.0 (10.1) ppb, p=0.02, respectively). Furthermore, PC20 decreased significantly following RV16 infection (mean+/-SD change in doubling dose: -0.65+/-0.54, p=0.02), whereas PC20 did not change in the placebo group (p=0.1). There was a significant correlation between the RV16-induced changes in exhaled NO levels at day 2 and the accompanying changes in PC20 at day 3 (rank correlation coefficient (rs): 0.86, p=0.01). Hence, the greater the increase in exhaled NO, the smaller the decrease in PC20. We conclude that rhinovirus infection increases exhaled nitric oxide levels in asthmatics, and that this increase is inversely associated with worsening of airway hyperresponsiveness to histamine. These results suggest that viral induction of nitric oxide synthase within the airways may play a protective role in exacerbations of asthma.

Adult↗
PubMed1998

Hydrogen peroxide in exhaled air of healthy children: reference values.

An increased content of hydrogen peroxide (H2O2), a marker of inflammation, has been described in the condensate of exhaled air from adults and children with inflammatory lung disorders, including asthma. However, the normal range of [H2O2] in the exhaled air condensate from healthy children has not been established. Therefore, the aim of this study was to determine the reference range of exhaled [H2O2] in healthy school-aged children. Ninety-three healthy nonsmoking children (48 female and 45 male, mean age 10 yrs, range 8-13 yrs), with a negative history for allergy, eczema or respiratory disease and with a normal lung function, participated. Exhaled air condensate was examined fluorimetrically for the presence of H2O2. In addition, the reproducibility of [H2O2] within subjects and between days and the stability of [H2O2] during storage at -20 degrees C were assessed. The median [H2O2] in the exhaled air condensate of all children was 0.13 microM, with a 2.5-97.5% reference range of <0.01-0.48 microM. No significant difference existed between males and females. There was no correlation between exhaled [H2O2] and age or lung function. Repeated [H2O2] measurements on 2 consecutive days showed satisfactory within-subject reproducibility and [H2O2] in stored samples remained stable for at least 1 month at -20 degrees C. In conclusion, this study provides reference data for exhaled hydrogen peroxide in a large group of healthy children. The observed levels were lower than those reported previously for healthy adults and were independent of age, sex and lung function.

Breath Tests↗
PubMed1999

Sampling of exhaled nitric oxide in children: end-expiratory plateau, balloon and tidal breathing methods compared.

The aim of this study was to compare exhaled nitric oxide concentrations obtained during controlled slow exhalation, presently considered as the method of choice, with two sampling methods that are easily performed by children: blowing air into a balloon and tidal breathing through a mouthpiece. One hundred and one well controlled, stable allergic asthmatic children (median age 11.7 yrs) performed the following tasks in duplicate: 1) exhalation from total lung capacity through a mouthpiece against a resistor with a standardized flow rate of 20% of the subject's vital capacity per second, using a biofeedback system; 2) a single deep exhalation into an NO-impermeable mylar balloon; and 3) tidal breathing through a low resistance mouthpiece over 2 min. NO was measured using a chemiluminescence analyser. Twenty-nine children (29%) were not able to perform a constant-flow exhalation of at least 3 s. All children performed the balloon and tidal breathing methods without difficulty. NO concentrations (means +/-SEM) were 5.3+/-0.2 parts per billion (ppb) at the end-expiratory plateau, 5.2+/-0.3 ppb in balloons (intraclass correlation coefficient (r(i)) = 0.73) and 8.0+/-0.4 ppb during tidal breathing (p<0.001, r(i) = 0.53 compared to plateau values). Mean values of NO during tidal breathing increased significantly with time, suggesting increasing contamination with nasal air. It was concluded that, in asthmatic children, the end-expiratory plateau concentration of nitric oxide during exhalation at 20% of the vital capacity per second is similar to the values obtained with the balloon method, with satisfactory agreement, but differs from values obtained during tidal breathing. The balloon method is cheap, simple and offers the interesting possibility to study exhaled nitric oxide in young children independently of the presence of a nitric oxide analyser.

Adolescent↗
PubMed2002

Exhalation behavior of four organic substrates and water absorbed by human skin.

The simultaneous measurement of several volatile organic compounds and water released from the human skin can be achieved successfully by using a modified gas chromatographic system. After the thumb of each subject was dipped in aqueous solution containing acetone, diethyl ether, ethanol, and toluene, it was dried in the air. Then the thumb attached to the sampling probe for measuring the released gases. It is found that 90% of all these chemical substrates were desorbed after 20 min. The initial exhalation rate factor for each chemical substrate was determined in every subject. Correlation factors of the linear relationships between the initial exhalation rate for hydrophilic substrates (acetone and ethanol) and the total amount of water (TAW) released from the skin were 0.94 and 0.92, respectively. However, the rate of hydrophobic toluene was not dependent on the TAW. Therefore, the exhalation rate of substrates is greatly influenced by both their hydrophilicity and TAW. Additionally, an interesting personal specific character among the 6 subjects was observed on plotting the exhalation rate of organic substrates and water during the elapsed time. With the released water mostly due to insensible perspiration, the exhalation rate of all simultaneous organic substrates decreased monotonically over the elapsed time. On the contrary, when subjects sweated emotionally, the exhalation rate of organic substrates showed some variation, namely a higher of exhalation rate compared to the case of mostly due to insensible perspiration. Therefore, emotionally-induced sweating can enhance the release of organic substrates.

Acetone↗
PubMed1997

Exhaled pentane levels in acute asthma.

BACKGROUND: Exhaled pentane, a product of lipid peroxidation, has been proposed as an objective, nonspecific, and noninvasive marker of active inflammation. Reactive oxygen species, which elicit lipid peroxidation, are increased in asthma and contribute to airway dysfunction. OBJECTIVE: To determine whether exhaled pentane levels are increased in acute asthma, and whether they decrease once acute asthma subsides. METHODS: Expired air was collected through a mouthpiece into a pentane-impermeable collection bag from 12 patients (40+/-5 years; mean+/-SEM) presenting to the emergency department of the University of Illinois Hospital in Chicago with acute asthma. Exhaled air was also collected after discharge from the hospital once acute asthma subsided. Eleven patients with stable asthma (40+/-5 years) and 17 healthy volunteers (31+/-5 years) served as control subjects. Exhaled air and ambient room air were analyzed for pentane content by gas chromatography. Peak expiratory flow rates were determined in each subject. RESULTS: Peak expiratory flow rates were 202+/-29 L/min during acute asthma and 327+/-26 L/min once acute asthma subsided (p<0.05). Exhaled pentane levels were 8.4+/-2.9 nmol/L during acute asthma and decreased significantly to 3.5+/-0.5 nmol/L once acute asthma subsided (p<0.05). Exhaled pentane levels were similar in patients with stable asthma and normal control subjects (3.6+/-0.4 nmol/L and 2.6+/-0.2 nmol/L, respectively; p>0.05). No pentane was detected in ambient air. CONCLUSION: Exhaled pentane levels are increased in patients with acute asthma and decrease significantly once acute asthma subsides.

Acute Disease↗
PubMed1997

Exhaled pentane and nitric oxide levels in patients with obstructive sleep apnea.

BACKGROUND: Upper airway inflammation is present in patients with obstructive sleep apnea (OSA). OBJECTIVE: To determine whether exhaled pentane and nitric oxide (NO) levels, two nonspecific markers of inflammation, are increased in patients with OSA. METHODS: Exhaled nasal and oral pentane and NO levels were determined before and after sleep in 20 patients with OSA (apnea-hypopnea index, 48+/-7; mean+/-SEM) and eight healthy control subjects. RESULTS: In patients with OSA, exhaled nasal and oral pentane levels after sleep were significantly higher than presleep values (6.1+/-1.2 nM vs 3.4+/-0.4 nM, and 7.0+/-1.3 nM vs 4.2+/-0.4 nM, respectively; p<0.05). Likewise, exhaled nasal and oral NO levels after sleep were significantly higher than presleep values in patients with OSA (39.7+/-3.8 ppb vs 28.4+/-2.9 ppb and 10.9+/-1.5 ppb vs 6.6+/-0.8 ppb, respectively; p<0.05). By contrast, there were no significant differences in exhaled nasal and oral pentane, and nasal NO levels before and after sleep in control subjects. Exhaled oral NO levels were significantly increased after sleep in comparison to presleep values in control subjects (p<0.05). CONCLUSION: Exhaled nasal pentane and NO levels are increased after sleep in patients with moderate-severe OSA. These data suggest that upper airway inflammation is present in these patients after sleep.

Adult↗
PubMed2000

Nasal and exhaled nitric oxide is reduced in adult patients with cystic fibrosis and does not correlate with cystic fibrosis genotype.

STUDY OBJECTIVES: Inducible nitric oxide synthase (iNOS) is upregulated in a number of inflammatory lung conditions, and exhaled nitric oxide (NO) concentration is increased. However, previous studies in children with cystic fibrosis (CF) have shown that exhaled NO is reduced. The purpose of this investigation was to study exhaled NO concentration in adults with CF, and to investigate the effect of CF genotype and respiratory tract infection on this measurement. DESIGN: Exhaled and nasal NO levels were measured in 54 adult CF subjects and 37 healthy nonsmoking age-matched subjects using a chemiluminesence analyzer. Spirometry (FEV(1) and FVC), CF genotype, and bacterial colonization were also recorded. SETTING: This study was conducted at a national CF center. RESULTS: The mean age of patients was 26.9 years, and the mean FEV(1) was 50.5% predicted (range, 17 to 104%). Nasal NO in the CF patients (mean, 520 parts per billion [ppb]; confidence interval [CI], 452 to 588) was significantly lower (p < 0.001) than in control subjects (987 ppb; CI, 959 to 1,015). Exhaled NO was significantly lower (p < 0. 001) in CF patients (5.0 ppb; CI, 4.1 to 6.1) than in control subjects (7.3 ppb; CI, 6.8 to 7.8). FEV(1) did not correlate with nasal or exhaled NO. No association was observed between genotype and NO values or colonization with Pseudomonas aeruginosa. CONCLUSIONS: Despite the airway inflammation that is characteristic of CF, both nasal and exhaled NO were reduced. There was no association with genotype or infection status. As NO has bacteriostatic effects and may augment mucociliary clearance, this observation may be of clinical importance.

Adolescent↗
PubMed2002

Exhaled and sputum nitric oxide in bronchiectasis: correlation with clinical parameters.

STUDY OBJECTIVES: Although there has been tremendous attention on endogenous nitric oxide (NO) production in many respiratory and systemic diseases, little is known on NO production in bronchiectasis. DESIGN AND SETTING: We determined exhaled and sputum NO levels in 109 patients with stable bronchiectasis (71 women; mean +/- SD age, 58.2 +/- 14.1 years) and 78 control subjects (39 women; mean age, 56.7 +/- 12.1 years) by using an automatic chemiluminescence analyzer. MEASUREMENTS AND RESULTS: There was no significant difference in exhaled NO between patients with bronchiectasis and control subjects (p = 0.11). Bronchiectasis patients with Pseudomonas aeruginosa infection had a significantly lower exhaled, but not sputum, NO levels than their counterparts and control subjects (p = 0.04 and p = 0.009, respectively). Exhaled NO correlated with 24-h sputum volume in P aeruginosa-infected patients (r = - 0.36; p = 0.002). After adjustment for sputum volume and number of bronchiectatic lung lobes, P aeruginosa-infected patients still had lower exhaled NO levels than their counterparts (p = 0.01). There was no correlation between exhaled NO with FEV(1), FVC, and the number of bronchiectatic lung lobes (p > 0.05). Sputum NO levels were not different between patients and control subjects (p = 0.64), and had no correlation with clinical parameters. CONCLUSION: Exhaled NO appears to be reduced among bronchiectasis patients with P aeruginosa infection independent of other clinical parameters, and further studies on the potential mechanisms and pathogenetic implications of this reduction should be pursued.

Adult↗
PubMed2003

Prospective evaluation of the validity of exhaled nitric oxide for the diagnosis of asthma.

STUDY OBJECTIVE: Exhaled nitric oxide (NO) levels are significantly elevated in patients with inflammatory airways disorders such as asthma, and the measurement of exhaled NO has been proposed as a noninvasive marker of airways inflammation. The aim of this study was to assess the accuracy of exhaled NO levels for the diagnosis of asthma. METHODS: Two hundred forty consecutive, nonsmoking, steroid-naive patients, who were referred to our outpatient clinic with symptoms suggestive of obstructive airways disease, were investigated. Asthma was diagnosed in 160 patients on the basis of the presence of significant airways reversibility (DeltaFEV(1) > 12% predicted) and/or airways hyperresponsiveness (provocative concentration of histamine causing a 20% fall in FEV(1) < or = 8 mg/mL). Prior to lung function measurements, exhaled NO was measured during a single-breath exhalation, according to European Respiratory Society and American Thoracic Society guidelines. RESULTS: The measurement of exhaled NO in our study population showed, at a cutoff level of 16 parts per billion, a specificity for the diagnosis of asthma of 90% and a positive predictive value of > 90%. CONCLUSIONS: These findings suggest that the simple and absolutely noninvasive measurement of exhaled NO can be used as an additional diagnostic tool for the screening of patients with a suspected diagnosis of asthma.

Adolescent↗
PubMed2004

Increased exhaled nitric oxide following autologous peripheral hematopoietic stem-cell transplantation: a potential marker of idiopathic pneumonia syndrome.

BACKGROUND: Increased production of nitric oxide (NO) and oxidative stress following bone marrow transplantation may play a role in the pathogenesis of idiopathic pneumonia syndrome (IPS). We hypothesize that patients who received high-dose chemotherapy followed by autologous peripheral hematopoietic stem-cell transplantation (APHSCT) have increased exhaled NO. METHOD: We measured exhaled lower respiratory tract NO concentration with a chemiluminescent NO analyzer during a slow vital capacity maneuver against a positive pressure of 16 cm H(2)O at an expiratory flow rate of 50 mL/s in 20 female patients who received high-dose chemotherapy (cyclophosphamide, carmustine, and cisplatin) followed by APHSCT for the treatment of stage III or IV breast carcinoma. Pulmonary function tests were performed, and exhaled NO measurements and clinical and laboratory data were obtained before transplantation and at every 6-week visit after transplantation for 24 weeks. RESULTS: All study patients had evidence of IPS with dyspnea and reduction in diffusion capacity of the lung for carbon monoxide (DLCO). Lower respiratory tract exhaled NO was significantly higher after APHSCT and during the 6 months of follow-up. Mean (+/- SD) exhaled NO increased from (mean +/- SD) 12.54 +/- 1.32 parts per billion (ppb) before APHSCT to 21.26 +/- 1.94 ppb at 6 weeks (p = 0.099), 21.26 +/- 1.94 ppb (p = 0.006) at 12 weeks, 24.62 +/- 2.55 ppb (p = 0.012) at 18 weeks, and 25.28 +/- 3.31 ppb (p = 0.013) at 24 weeks (all p values were compared to baseline). There was a strong negative correlation between DLCO and exhaled NO (regression coefficient - 0.60, p = 0.01). CONCLUSION: Lower respiratory tract concentration of exhaled NO is significantly increased following APHSCT and correlates with reduction in DLCO. Increase in lower respiratory tract concentration of NO is a potential marker of IPS.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1993

Increased amount of nitric oxide in exhaled air of asthmatics.

The presence of nitric oxide (NO) in the exhaled air of humans has recently been described. We wanted to assess at what level exhaled NO originates in normal airways, and to determine whether airway inflammation induces changes in the levels of exhaled NO. Exhaled NO was continuously measured by chemiluminescence technique during normal tidal breathing through the nose or mouth, with a detection limit of 1 part per billion (ppb). Twelve control subjects were compared to eight patients with mild atopic asthma and rhinitis caused by occupational allergen. In control subjects, the major part of NO in exhaled air (up to 30 ppb) seemed to originate in the nasal airways, with only minor contribution from the lower airways and the oral cavity. However, in mild asthmatics, the level of exhaled NO during oral breathing, indicating the involvement of the lower airways, was increased 2-3 fold. Since increased production of NO in the lower airways may involve activated macrophages or neutrophils, we suggest that exhaled NO may be used to instantly monitor ongoing bronchial inflammation, at least when involving inducible NO synthase.

Adult↗
PubMed2006

Comparison between effects of intravenous and nebulized histamine in guinea pigs: correlation between changes in respiratory mechanics and exhaled nitric oxide.

Nitric oxide (NO) is a marker of airway inflammation in humans, despite not having effects on basal bronchial tone. Inhibition of NO synthesis can lead to enhanced airway reactivity in humans and it is therefore of importance to understand how bronchial provocation can affect endogenous NO. Presently, we have studied the role of exhaled nitric oxide in airway reactivity by measuring changes in pulmonary mechanics in response to histamine in anaesthetized guinea pigs. Two groups were challenged i.v. and four groups were challenged by aerosol at different doses. One of the i.v. and one of the aerosol groups received an inhibitor of NO synthesis, N(omega)-nitro-L-arginine methyl ester (L-NAME), to reduce endogenous production of NO before histamine challenge. All animals with intact NO production showed a decrease in exhaled nitric oxide after challenge. There were positive correlations between the peak in exhaled nitric oxide and pulmonary resistance, and between the decrease in exhaled nitric oxide and lung compliance. L-NAME pretreatment increased the reactivity to aerosolized histamine but not to i.v. histamine. We conclude that the different ways of administration elicit different response patterns of exhaled nitric oxide, resistance, and compliance, even when compared at similar insufflation pressure changes. The effects of L-NAME suggest that, although different mechanisms might be responsible for the changes in pulmonary mechanics, inhibition of endogenous NO enhances decrements in pulmonary function when histamine is administered in an aerosol. The close relationship between changes in exhaled nitric oxide and changes in lung compliance and pulmonary resistance merits further studies on the relationship between NO and airway reactivity.

Administration, Inhalation↗