Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Exhalation”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 235 records · Page 13Linked to original sources
PubMed1987

Elevated lipid peroxidation in rats induced by dietary lipids and N-nitrosodimethylamine and its inhibition by indomethacin monitored via ethane exhalation.

The effect of dietary lipids alone or in combination with an administered carcinogen, N-nitrosodimethylamine (NDMA), on whole body lipid peroxidation was studied in rats in vivo. Groups of rats were fed diets containing 2%, 12.5%, or 25% of either saturated or polyunsaturated fat. Lipid peroxidation in individual animals was determined by measuring the concentration of ethane in exhaled air. Increased ethane exhalation was found in rats when the amount of dietary fat was increased from 2% to 12.5%, but animals receiving 12.5% or 25% fat in the diet exhaled ethane at similar rates. Rats consuming polyunsaturated fat exhaled more ethane than those eating saturated fat. In all groups, NDMA administration drastically increased ethane exhalation. Indomethacin completely blocked the increase in ethane exhalation caused by dietary lipids.

Animals↗
PubMed2002

Nasal and oral contribution to inhaled and exhaled nitric oxide: a study in tracheotomized patients.

Nitric oxide (NO) is produced at different sites in the human airways and may have several physiological effects. Orally-produced NO seems to contribute to the levels found in exhaled air. Autoinhalation of nasal NO increases oxygenation and reduces pulmonary artery pressure in humans. The aim of this study was to measure the concentration and output of NO during nasal, oral and tracheal controlled exhalation and inhalation. Ten tracheotomized patients and seven healthy subjects were studied. The mean+/-SEM fraction of exhaled NO from the nose, mouth and trachea was 56+/-8, 14+/-4 and 6+/-1 parts per billion (ppb), respectively. During single-breath nasal, oral and tracheal inhalation the fraction of inhaled NO was 64+/-14, 11+/-3 and 4+/-1, respectively. There was a marked flow dependency on nasal NO output in the healthy subjects, which was four-fold greater at the higher flow rates, during inhalation when compared to exhalation. There is a substantial contribution of nasal and oral nitric oxide during both inhalation and exhalation. Nasal nitric oxide output is markedly higher during inhalation, reaching levels similar to those that are found to have clinical effects in the trachea. These findings have implications for the measurement of nitric oxide in exhaled air and the physiological effects of autoinhaled endogenous nitric oxide.

Adult↗
PubMed2002

Exhaled nitric oxide measurements with dynamic flow restriction in children aged 4-8 yrs.

Fractional exhaled nitric oxide concentration (FENO) depends on exhalation flow; however, children often are unable to perform controlled flow procedures. Therefore, a device was developed for off-line FENO sampling, with dynamic flow restriction (DFR). The authors compared off-line with on-line FENO, assessed feasibility, and obtained normal values for FENO in children aged 4-8 yrs. Subjects inhaled nitric oxide (NO)-free air and exhaled into the device, where DFR kept exhalation flow constant at 50 mL x s(-1). Dead space air was discarded. Exhaled air was collected in a 150 mL mylar balloon. On-line measurements were performed and values compared with off-line FENO in 19 adult volunteers. Seventy-nine children performed off-line sampling. All samples were analysed with a chemiluminescence NO-analyser. Normal values were obtained in 34 healthy children. There was an excellent correlation between on- and off-line values. Bland and Altman plots showed good agreement between on- and off-line FENO. Seventy-four out of 79 children were able to perform a correct off-line procedure. Geometric mean+/-SEM FENO in healthy children was 4.9+/-1.2 parts per billion (ppb) for male children and 7.6+/-1.1 ppb for female children. It can be concluded that off-line fraction of exhaled nitric oxide measurements with dynamic flow restriction are feasible in young children and correspond to on-line values.

Adult↗
PubMed2003

Exhaled NO and plasma cGMP increase after endotoxin infusion in healthy volunteers.

Nitric oxide (NO) is believed to be involved in the pathophysiology of sepsis. This study evaluated the activity of the NO pathway in a human endotoxin model. At baseline and after endotoxin, on-line measurements of exhaled NO (eNO) were made using a chemiluminescence technique with a single-breath method. NO-free air was inhaled prior to exhalation against a resistance. NO in orally and nasally exhaled air and in rectal gas was investigated. Plasma nitrite, nitrate, and guanosine 3', 5'-monophosphate (cGMP) and the events after diclophenac administration were also studied. Endotoxin infusion resulted in tachycardia and fever. An early increase in oral eNO concentration was observed and oral eNO decreased after diclophenac administration. NO exhaled nasally, NO in rectum gas and nitrite/nitrate levels remained unchanged over the study period, cGMP increased after 4 h. These findings suggest an early increase in nitric oxide production from the lungs, probably due to increased activity of the constitutive nitric oxide synthase upon endotoxin stimulation. In contrast, nitric oxide production in the upper airways, measured as nasally exhaled nitric oxide and nitric oxide in rectal gas, remained unchanged. Further studies will elucidate if exhaled nitric oxide is a valuable marker of sepsis-induced lung injury and if monitoring of treatment is possible.

Adult↗
PubMed1995

Increased nitric oxide in exhaled air of normal human subjects with upper respiratory tract infections.

Viral infection may induce the expression of nitric oxide (NO) synthase, resulting in increased NO formation that has an antiviral effect. NO may be produced by various cells of the upper and lower respiratory tract, and may be detected in the exhaled air. We have studied the levels of exhaled NO in 18 normal subjects during symptomatic upper respiratory tract infections and during recovery 3 weeks later. Exhaled NO was measured using a modified chemiluminescence analyser. At the time of symptoms of upper respiratory tract infection, the peak exhaled NO values were 315 +/- 57 ppb (mean +/- SEM) and decreased to 87 +/- 9 ppb during recovery. Recovery values of exhaled NO were similar to those reported in age-matched normal control subjects (88 +/- 3 ppb, n = 72). These findings suggest that symptomatic upper respiratory tract infections markedly increase the concentration of NO in exhaled air. This may reflect the induction of nitric oxide synthase (NOS) in upper and lower respiratory tract, and may be relevant to viral exacerbations of asthma.

Adult↗
PubMed1996

Changes in the dose of inhaled steroid affect exhaled nitric oxide levels in asthmatic patients.

An increased concentration of nitric oxide (NO) in the exhaled air of asthmatic patients may reflect inflammation of the airways, and exhaled NO may, therefore, be useful in monitoring asthma control and the optimal use of anti-inflammatory treatment. We have studied the effect of reducing and then increasing the dose of inhaled steroid on exhaled NO, lung function and symptoms in 14 asthmatic patients treated with twice daily budesonide. Baseline measurements were made at the end of a 2 week run-in period, 2 weeks after the daily dose of budesonide was reduced by 200 micrograms daily, and 2 weeks after the dose was then increased by 200 micrograms daily. Exhaled NO increased significantly compared with baseline after the dose was reduced by 200 micrograms daily (from 122 +/- 13 to 246 +/- 52 ppb); whereas, there was no significant decrease in spirometry or change in peak flow variability. There was also a significant increase in symptoms at night, but no change during the day or in the number of rescue doses of inhaled beta 2-agonist. The level of exhaled NO decreased when the dose of inhaled steroids was increased, and this was associated with a reduction in diurnal variability of peak expiratory flow, and in nocturnal symptoms. Our study suggests that exhaled nitric oxide may be a useful means of monitoring control of asthma. Further longitudinal studies in patients of differing asthma severity are now indicated.

Administration, Inhalation↗
PubMed1996

Exhaled nitric oxide during acute changes of airways calibre in asthma.

It has been shown that endogenous nitric oxide (NO), measured in exhaled air, is increased in asthmatic subjects and after allergen challenge in sensitized animals. NO is also a paracrine molecule with some, though weak, bronchodilator effects. However, whether the amount of endogenous NO that originates in the lungs can reflect the degree of bronchial tone and airways calibre in asthmatic subjects has not yet been investigated. The aim of this study was, therefore, to determine whether NO production could be modified by acute changes of airways calibre in mild, nonatopic, asthmatic subjects. NO output was measured in the exhaled air of 14 steroid-free asthmatics, 8 steroid-treated asthmatics and 21 control subjects. In seven steroid-free asthmatics, exhaled NO was measured after methacholine challenge, and then after salbutamol-induced bronchial dilatation. Exhaled tidal breathing was collected for 30 s and NO in the exhaled air was measured with a chemiluminescence analyser. Both NO concentration and its output were significantly higher in the steroid-free asthmatic patients (15.6 +/- 1.5 parts per billion (ppb) and 6.3 +/- 0.7 nmol.min-1, respectively) as compared with the control subjects (8.9 +/- 1.0 ppb and 3.5 +/- 0.3 nmol.min-1, respectively; p < 0.001 for both) and with the steroid-treated asthmatic patients (11.3 +/- 3.3 ppb and 3.7 +/- 0.9 nmol.min-1, respectively; p < 0.05 for both). Neither methacholine-induced bronchial obstruction nor salbutamol-induced bronchial dilatation caused a significant change in exhaled NO. We conclude that NO production is higher in steroid-free than in steroid-treated asthmatics and in control subjects. Furthermore, NO production is not affected by acute pharmacologically-induced changes of airways calibre in asthmatic subjects. Our results suggest that NO production is a marker of airways inflammation rather than an endogenous modulator of bronchial tone in asthma.

Adult↗
PubMed1996

Nitric oxide in exhaled air.

Much interest is now being focused on measurements of nitric oxide (NO) in exhaled air. In healthy subjects exhaled NO seems to originate mainly in the nasal airways, whereas the contribution from the lower respiratory tract is low. In certain inflammatory airway disorders, the excretion of NO into the airways is altered resulting in changes in the levels of NO in exhaled air. New techniques have been developed to measure NO release at different levels of the airways: asthmatics show increased orally-exhaled NO levels, whereas patients with cystic fibrosis or Kartagener's syndrome exhibit a marked reduction in nasal release of NO. It has been suggested that measurements of exhaled NO may be clinically useful in noninvasive diagnosis and monitoring of inflammatory airway diseases. To further evaluate the potential clinical usefulness of measurement of exhaled NO, it is vital to explore how airway NO production is normally regulated and what factors influence airway NO excretion.

Breath Tests↗
PubMed2003

Oxygenation using tidal volume breathing after maximal exhalation.

UNLABELLED: We compared, in volunteers, the oxygenation achieved by tidal volume breathing (TVB) over a 3-min period after maximal exhalation with that achieved by TVB alone. Twenty-three healthy volunteers underwent the two breathing techniques in a randomized order. A circle absorber system with an oxygen flow of 10 L/min was used. The end-expiratory oxygen concentration (EEO(2)) was monitored at 15-s intervals up to 3 min. TVB after maximal exhalation produced EEO(2) values of 68% +/- 5%, 75% +/- 5%, and 79% +/- 4% at 30, 45, and 60 s, respectively, which were significantly larger (P < 0.05) than the corresponding values obtained with TVB alone (58% +/- 5%, 66% +/- 6%, and 71% +/- 5%, respectively). In both techniques, the EEO(2) increased exponentially, with time constants of 35 s during TVB after maximal exhalation versus 58 s during TVB without prior maximal exhalation. In conclusion, maximal exhalation before TVB can hasten preoxygenation by decreasing the nitrogen content of the functional residual capacity, with a consequent increase of EEO(2) to approximately 70% in 30 s and 80% in 60 s. IMPLICATIONS: Oxygenation by using maximal exhalation before tidal volume breathing produced a significantly faster increase in end-expiratory oxygen concentration than oxygenation with tidal volume breathing alone.

Adult↗
PubMed1999

Increased exhaled nitric oxide and impaired oxygen uptake (VO2) kinetics during exercise in patients with chronic heart failure.

Vascular endothelial function is abnormal in patients with congestive heart failure (CHF). Exhaled nitric oxide (NO) output is a marker of pulmonary endothelial NO release. The present study examined the relation between exhaled NO output and oxygen uptake (VO2) kinetics at the onset of exercise, which reflects blood flow response. Sixteen patients with CHF and 7 volunteers underwent constant bicycle exercise. Oxygen deficit and time constant for VO2 increment at the onset of exercise were analyzed. Exhaled NO concentration was measured by a chemiluminescence analyzer and exhaled NO output was calculated by multiplexing ventilation. Exhaled NO output was significantly greater in the CHF group than in the control group at rest (86+/-65 nl min(-1) m(-2) vs 298+/-135 nl min(-1) m(-2), p<0.001) and during exercise (152+/-98 nl min(-1) m(-2) vs 455+/-190 nl min(-1) m(-2), p<0.001). However, the %increase of NO output was significantly smaller in the CHF group than in the control group (70+/-26% vs 109+/-85%, p<0.05). Oxygen deficit was significantly greater in the CHF group than in the control group (240+/-70 ml vs 372+/-107 ml, p<0.01) and the time constant for VO2 increment was also significantly prolonged in the CHF group (35.1+/-8.0 s vs 50.1+/-16.3 s, p<0.05). Exhaled NO output during exercise significantly correlated with oxygen deficit (r=0.67, p<0.001) and the time constant for VO2 increment (r=0.74, p<0.001). Increased NO output played a counter-regulatory role in the impaired blood flow in CHF.

Adult↗
PubMed2003

Increased exhaled 8-isoprostane in childhood asthma.

STUDY OBJECTIVE: To quantify lung oxidative stress in asthmatic children by measuring concentrations of 8-isoprostane, a marker of oxidative stress, in exhaled breath condensate (EBC), which is a noninvasive method of sampling airway secretions. Secondary objectives were as follows: (1) to measure levels of exhaled prostaglandin (PG) E(2), since impaired PGE(2) production has been implicated in the pathogenesis of asthma in adults; and (2) to measure levels of fractional exhaled nitric oxide (FeNO), which is a marker of airway inflammation. DESIGN: Single-center, cross-sectional study. PATIENTS: Twelve healthy children, 12 steroid-naïve asthmatic children, and 30 children in stable condition with mild-to-moderate persistent asthma who were being treated with inhaled corticosteroids (ICSs) [average dose, 300 micro g per day] were studied. INTERVENTIONS: Subjects attended the outpatient clinic on one occasion for the collection of EBC and FeNO measurements. MEASUREMENTS AND RESULTS: 8-Isoprostane and PGE(2) concentrations in EBC were measured with specific radioimmunoassays. FeNO was measured online by a chemiluminescence analyzer. 8-Isoprostane was detectable in the EBC of healthy children (mean [+/- SEM], 34.2 +/- 4.5 pg/mL), and its concentrations were increased in both steroid-naïve asthmatic children (mean, 56.4 +/- 7.7 pg/mL; p < 0.01) and steroid-treated asthmatic children (mean, 47.2 +/- 2.3 pg/mL; p < 0.05). There was no difference in exhaled 8-isoprostane concentrations between the two groups of asthmatic children (p = 0.14). By contrast, exhaled PGE(2) concentrations were similar among the three study groups (p = 0.56). FeNO levels were higher in steroid-naïve children with asthma (49.2 +/- 9.6 parts per billion [ppb]; p < 0.05) and, to a lesser extent, in steroid-treated asthmatic children (37.8 +/- 6.6 ppb; p < 0.05) compared with healthy children (15.2 +/- 1.7 ppb). CONCLUSIONS: Lung oxidative stress is increased in children who are in stable condition with asthma, as reflected by increased exhaled 8-isoprostane concentrations. This increase seems to be relatively resistant to treatment with ICSs. Decreased PGE(2) lung production is unlikely to play a pathophysiologic role in childhood asthma.

Adolescent↗
PubMed1997

Nitric oxide in single-breath exhalation in humans.

This study was performed to test the hypothesis that the amount of nitric oxide (NO) in exhaled air (VNO) is the net result of both NO formation in the conducting airway and its clearance by diffusion in the alveoli. It's so difficult to collect the gas in the alveoli in volunteers that we made the following consideration from the profile of CO2 fraction (FECO2): the late fraction of exhaled air coming mainly from the alveoli while the early fraction representing mixed gas from both the conducting airway and/or the transition zone, and the alveoli. We compared the FECO2, NO concentration, and VNO in the early and late fractions of exhaled air after subjects inspiring either NO-free gas or NO-containing gas (510 ppb) using a single-breath technique (n = 5). After inspiring both the NO-free and NO-containing gases, NO appeared in a significantly lower concentration and amount in the late fraction of exhaled air than those in the early fraction. If NO was not cleared by diffusion in the alveoli or the transition zone, exhaled NO in the late fraction should not differ significantly from that in the early fraction. The results suggest that: 1) NO is constantly formed in the conducting airway and/or the transition zone, and is acquired by both inhaled and exhaled air; and 2) NO is cleared by diffusion in the alveoli.

Adult↗
PubMed1997

Endogenous nitric oxide in exhaled air from patients with liver cirrhosis.

BACKGROUND: The aim of this study was to investigate the potential effects of liver insufficiency on nitric oxide concentrations in exhaled air. METHODS: Nitric oxide concentrations in the exhaled air from 13 patients with liver cirrhosis and 11 healthy control subjects was examined by the single-breath technique. RESULTS: There was a clear correlation between Child-Pugh score and NO in exhaled air (peak after 15 sec of breathholding, R = 0.623, P = 0.023). Similarly, there were significant correlations in peak NO concentrations and alkaline phosphatase, bilirubin, aspartate and alanine aminotransferase, and albumin. The most severely ill patient in our study had the highest NO concentrations in her exhaled air. On recovery from her liver illness the concentration of NO in her exhaled air decreased. There was no correlation between circulating levels of the endogenous NO synthase inhibitors asymmetric and symmetric N(G), N(G)-dimethyl-arginine and exhaled NO concentrations. CONCLUSIONS: The present data show a correlation between endogenous NO formation in the respiratory system and liver dysfunction. This might contribute to the understanding of the pathophysiology in pulmonary vasodilatation in liver disease.

Breath Tests↗
PubMed2001

[Exhalation of I-131 after radioiodine therapy (RIT): time dependence and chemical form].

AIM: The change of both amount and chemical forms of radioiodine exhaled in the air of rooms with patients on the therapy ward should be investigated depending on radioactivity applied, time after application, and kind of thyroid disease. METHODS: The air of ward-rooms of 62 patients with thyroid carcinoma, Graves' Disease, and autonomy which received different therapy doses, was investigated with an portable constant air flow sampler. Different chemical iodine species (organic, elemental, aerosol bound) were collected during 8 hr in various filters until 3 days after application of the radioiodine capsule, according to their chemical form. The radioactivity in the filters was measured with a well counter on defined time points after application. RESULTS: The radioactivity exhaled was between 0.008 and 0.03% related to activity of radioiodine applied. The percentage of radioiodine exhaled related to the activity applied, differed significantly depending on disease and changed as follows: Grave's Disease > autonomy > carcinoma. The exhalation of radioiodine became stronger with increasing applied activities and showed an exponential decrease with time. The most part of radioiodine was present in organic bound form. This organic portion decreased with time in favour of the other iodine species. CONCLUSION: The degree of accumulation of radioiodine orally applied within thyroid seems to be in direct proportion to the extend of its exhalation. Further measurements directly in the breathing air of RIT-patients are necessary, in order to clarify the relationship between degree of thyroid uptake and quantity as well as chemical form of radioiodine exhaled.

Air Pollutants, Radioactive↗
PubMed2002

[Changes of exhaled nitrogen-monoxide concentration in acute ischemia-reperfusion injury of the lung].

INTRODUCTION: Nitric oxide (NO) plays an important role in both the physiological control of the pulmonary vascular bed and in the pathophysiology of several lung diseases. Though our knowledge regarding NO has became wider several aspects are still a matter of debate. The technical developments allowing direct measurements of NO in the expired air have provided an opportunity to evaluate NO production and consumption in the clinical setting and exhaled NO has become a diagnostic and monitoring tool in acute and chronic lung diseases. AIMS: The aim of our study was to evaluate the severity of different levels of ischaemia-reperfusion related lung injury by measuring nitric oxide in the exhaled air. After presenting our data regarding exhaled NO in ischaemia-reperfusion related acute lung injury associated with cardiothoracic surgery we discuss the physiology of exhaled NO and the technical aspects of measuring NO in the expired breath. METHODS: Comparing basal and GTN-induced exhaled NO data after two types of heart and lung surgery--routine open-heart surgery utilizing CPB and lung transplantation--we studied the effects of different levels of lung ischaemia on NO production. RESULTS: Following transient and incomplete lung ischaemia in the clinical setting of routine cardiac surgery utilizing cardiopulmonary bypass (CPB) both the airway epithelial and the vascular endothelial function remained preserved. However, prolonged and complete lung ischaemia during lung transplantation was associated with severe dysfunction resulted in a marked reduction of both the endogen and the induced levels of exhaled NO.

Acute Disease↗
PubMed2004

[Examination of exhaled breath condensate in patients with asthma and chronic obstructive pulmonary diseases].

Considerable interest of specialists all over the world has focused on the measurement of the markers of inflammation and oxidative stress in the exhaled breath condensate in patients with asthma or chronic obstructive pulmonary diseases recently. Use of exhaled condensate is based on the hypothesis that aerosol particles exhaled in human breath reflect the composition of the bronchoalveolar extracellular lining fluid. The standard collection of the material requires condensation of exhaled air and the samples have to be kept in biologically inert containers. Measurement of the very low concentrations of selected substances requires very sensitive analytical methods. The examination of exhaled breath condensate is absolutely non-invasive method, which can be repeated as often as needed and it is extremely well tolerated both by children and seniors. Markers in the condensate enable detection and quantification of the inflammation process, the disease monitoring, and assessment of the response to the treatment. The breath condensate diagnostics is a new progressive method and in the patients with asthma and chronic obstructive pulmonary disease it can bring complementary information to the very sensitive method of determination of exhaled nitric oxide.

Asthma↗
PubMed1997

Hydrogen peroxide in exhaled air is increased in stable asthmatic children.

Exhaled air condensate provides a noninvasive means of obtaining samples from the lower respiratory tract. Hydrogen peroxide (H2O2) in exhaled air has been proposed as a marker of airway inflammation. We hypothesized that in stable asthmatic children the H2O2 concentration in exhaled air condensate may be elevated as a result of airway inflammation. In a cross-sectional study, 66 allergic asthmatic children (of whom, 41 were treated with inhaled steroids) and 21 healthy controls exhaled through a cold trap. The resulting condensate was examined fluorimetrically for the presence of H2O2. All subjects were clinically stable, nonsmokers, without infection. The median H2O2 level in the exhaled air condensate of the asthmatic patients was significantly higher than in healthy controls (0.60 and 0.15 micromol, respectively; p<0.05), largely because of high values in the stable asthmatic children who did not use anti-inflammatory treatment (0.8 micromol; p<0.01 compared to controls). We conclude that hydrogen peroxide is elevated in exhaled air condensate of children with stable asthma, and may reflect airway inflammation.

Adult↗
PubMed2004

Effect of inhaled N-acetylcysteine on hydrogen peroxide exhalation in healthy subjects.

N-acetylcysteine (NAC) has antioxidant properties and its oral administration decreased H(2)O(2) exhalation in patients with chronic obstructive pulmonary disease. In this study we tested whether inhaled NAC could suppress H(2)O(2) levels in exhaled breath condensate (EBC) of eight healthy subjects that have never smoked (never-smokers). Original NAC solution (ACC vial, 300 mg NAC in 3 ml solvent), NAC-placebo (vehicle), sterile 0.9% NaCl or distilled water were nebulized via the pneumatic De Vilbiss nebulizer once daily every 7 days and H(2)O(2) and thiols exhalation was measured just before, 30 min and 3 h after the end of drug administration. Additional in vitro experiments were performed to evaluate NAC stability during nebulization, reactivity with H(2)O(2) and possible H(2)O(2) generation in aqueous NAC solutions. NAC almost completely abolished H(2)O(2) exhalation 30 min after inhalation (0.02+/-0.04 vs. 0.21+/-0.09 microM, p<0.001). However, 3 h later the H(2)O(2) levels raised 1.8-fold from baseline (p<0.01). Other inhaled solutions did not affect H(2)O(2) levels. Mean thiol concentration in EBC rose (p<0.05) after treatment with NAC and reached 1.03+/-0.48 microM at 3 h. Although, 25 and 50 mM NAC completely inhibited H(2)O(2)-peroxidase-luminol-dependent chemiluminescence, detectable amounts of H(2)O(2) were generated in NAC solutions. It was accompanied by moderate loss of -SH groups. Catalase and ascorbic acid prevented H(2)O(2) formation in NAC solutions. In conclusion inhaled NAC revealed biphasic effect on H(2)O(2) exhalation in healthy subjects, which depends on direct H(2)O(2) scavenging and H(2)O(2) generation related to drug oxidation. The net result of these processes may determine anti- or pro-oxidant action of inhaled NAC.

Acetylcysteine↗