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PubMed1998

Cross sectional study of exhaled nitric oxide levels following lung transplantation.

BACKGROUND: The role of nitric oxide (NO) in the pathophysiology of graft dysfunction following lung transplantation remains unclear. To determine whether measurement of NO in the exhaled breath of lung transplant recipients provides useful information about graft pathology, a cross sectional study was performed on a cohort of recipients as they attended for review. METHODS: One hundred and four lung transplant recipients and 55 healthy non-smoking controls were included in the study. Each subject performed three consecutive single breath NO manoeuvres. In recipients NO levels were compared according to current clinical status, presence of any graft pathology, type of lung transplant procedure, indication for transplantation, and current level of immunosuppression. RESULTS: Mean (SE) exhaled NO levels were 6.5 (0.61) ppb in the control group, 5.3 (0.46) in clinically well recipients, 10.3 (1.4) in those with lymphocytic bronchiolitis, 10.5 (1.0) in recipients with infection, and 2.5 (0.6) in those with acute vascular rejection. There was no significant difference in NO levels between the control group and lung transplant recipients as a whole (mean difference 0.29 (95% CI -1.17 to 1.75), p = 0.7). Levels were increased significantly in the presence of lymphocytic bronchiolitis (4.98 (95% CI 1.6 to 8.36), p = 0.0002) and infection (5.28 (95% CI 2.9 to 7.56), p < 0.0001), but not in acute vascular rejection (2.76 (95% CI 0.97 to 4.55), p = 0.1) compared with exhaled NO in clinically well recipients. Recipients with obliterative bronchiolitis were subdivided according to the grade of their bronchiolitis obliterans syndrome (BOS). Exhaled NO levels in those with BOS grade 1 were 10.0 (1.3) ppb and in those with BOS grades 2 or 3 were 5.1 (0.7) ppb. Compared with those who were clinically well, NO levels were increased in those with BOS grade 1 (4.74 (95% CI 1.8 to 7.69), p < 0.0001) but not in those with BOS grades 2 or 3 (0.19 (95% CI -1.55 to 1.93), p = 0.82). CONCLUSIONS: Exhaled NO levels are increased in lung transplant recipients with lymphocytic bronchiolitis, early obliterative bronchiolitis, and infection. These conditions are all associated with the presence of airway inflammation within the graft. The findings suggest that exhaled NO measurements may have a role as a marker of pulmonary allograft dysfunction.

Breath Tests↗
PubMed1998

Raised levels of exhaled carbon monoxide are associated with an increased expression of heme oxygenase-1 in airway macrophages in asthma: a new marker of oxidative stress.

BACKGROUND: Chronic inflammatory diseases are associated with an increased production of oxidants. Induction of a stress protein, heme oxygenase (HO) HO-1, is a cytoprotective mechanism against oxidative cellular injury. HO-1 catabolises heme to bilirubin, free iron, and carbon monoxide (CO). METHODS: Exhaled CO and sputum bilirubin levels were measured and HO-1 protein expression in airway macrophages was determined by Western blotting in asthmatic patients as levels of oxidants are raised in asthma and may induce HO-1. RESULTS: Exhaled CO was significantly increased in 37 non-steroid treated asthmatic patients compared with 37 healthy subjects (5.8 (95% CI 5.20 to 6.39) ppm vs 2.9 (2.51 to 3.28) ppm; p < 0.0001) but was similar to normal in 25 patients who received corticosteroids (3.3 (95% CI 2.92 to 3.67) ppm; p > 0.05). In non-treated asthmatic patients more HO-1 protein was expressed in airway macrophages than in normal subjects. Bilirubin levels in induced sputum were also higher than in normal subjects. Inhalation of hemin, a substrate for HO, significantly increased exhaled CO from 3.8 (95% CI 2.80 to 4.87) ppm to 6.7 (95% CI 4.95 to 8.38 CI) ppm (p < 0.05) with a concomitant decrease in exhaled nitric oxide levels, suggesting an interaction between the two systems. CONCLUSIONS: Increased exhaled CO levels and HO-1 expression may reflect induction of HO-1 which may be inhibited by steroids. Measurement of exhaled CO, an index of HO activity in non-smoking subjects, may therefore be clinically useful in the detection and management of asthma and possibly other chronic inflammatory lung disorders.

Adult↗
PubMed1999

Effect of inhaled steroids on airway hyperresponsiveness, sputum eosinophils, and exhaled nitric oxide levels in patients with asthma.

BACKGROUND: Airway hyperresponsiveness, induced sputum eosinophils, and exhaled nitric oxide (NO) levels have all been proposed as non-invasive markers for monitoring airway inflammation in patients with asthma. The aim of this study was to compare the changes in each of these markers following treatment with inhaled glucocorticosteroids in a single study. METHODS: In a randomised, double blind, placebo controlled, parallel study 25 patients with mild asthma (19-34 years, forced expiratory volume in one second (FEV1) >75% predicted, concentration of histamine provoking a fall in FEV1 of 20% or more (PC20) <4 mg/ml) inhaled fluticasone propionate (500 microg twice daily) for four weeks. PC20 to histamine, sputum eosinophil numbers, and exhaled NO levels were determined at weeks 0, 2, and 4, and two weeks after completing treatment. Sputum was induced by inhalation of hypertonic (4.5%) saline and eosinophil counts were expressed as percentage non-squamous cells. Exhaled NO levels (ppb) were measured by chemiluminescence. RESULTS: In the steroid treated group there was a significant increase in PC20, decrease in sputum eosinophils, and decrease in exhaled NO levels compared with baseline at weeks 2 and 4 of treatment. Subsequently, each of these variables showed significant worsening during the two week washout period compared with week 4. These changes were significantly different from those in the placebo group, except for the changes in sputum eosinophils and exhaled NO levels during the washout period. There were no significant correlations between the changes in the three markers in either group at any time. CONCLUSIONS: Treatment of asthmatic subjects with inhaled steroids for four weeks leads to improvements in airway hyperresponsiveness to histamine, eosinophil counts in induced sputum, and exhaled nitric oxide levels. The results suggest that these markers may provide different information when monitoring anti-inflammatory treatment in asthma.

Administration, Inhalation↗
PubMed1983

Measurement of lung emptying patterns during slow exhalations.

Five subjects slowly inhaled a 200-ml bolus of sulfur hexafluoride (SF6) from residual volume (RV) followed by an O2-Ar mixture to total lung capacity, then exhaled to RV, either slowly or as rapidly as possible. Larger amounts of SF6 and N2 were recovered in fast than in slow exhalations. We calculated the gas volumes of the apical and basal halves of the parenchymal mass as functions of exhaled volume during slow exhalations from 1) the difference between SF6 recovered in slow and fast exhalations and 2) an estimate of the apex-to-base concentration profile of SF6 in the lung after inspiration. The maximal volume difference, where the apex contained 600 ml more gas than the base, occurred when 70% of the vital capacity had been exhaled. The same calculation, but using N2 data, gave unrealistically large volume differences. Apparently SF6 delivered as a bolus results in an apex-to-base gradient that is large relative to intraregional gradients, but dilution of the resident N2 by a non-N2 gas results in sizable intraregional gradients.

Humans↗
PubMed1993

Dynamics of soluble gas exchange in the airways. III. Single-exhalation breathing maneuver.

The exchange characteristics of a highly soluble gas with the pulmonary airways during a single-exhalation maneuver were analyzed using a mathematical model previously described by our group (M. E. Tsu et al. Ann. Biomed. Eng. 16: 547-571, 1988). The model integrates the simultaneous exchange of water, heat, and a soluble gas with the pulmonary airways. The purpose of this paper is to provide experimental data for model validation. Exhaled ethyl alcohol concentration profiles of human subjects were measured with an Intoxilyzer 5000 and were plotted against exhaled volume measured with a wedge spirometer. Each subject performed a series of breathing maneuvers in which exhalation flow rate was the only variable. Phase III has a positive slope (0.047 +/- 0.0089 mol alcohol in air.mol alcohol in alveolus-1.l-1) that is statistically independent (P > 0.05) of flow rate. Reducing the molecular diffusion coefficient of alcohol in the nonperfused tissue layer improves the fit of the model to the experimental data. The optimal diffusion coefficient of alcohol for all subjects was 12 +/- 5.3 (SD) x 10(-7) cm2/s, which is 8% of the diffusion coefficient of alcohol in water (1.6 x 10(-5) cm2/s). We concluded that the experimental data showing a positive slope of the exhaled alcohol profile are consistent with a reduced diffusivity of alcohol in the respiratory mucosa. The reduced diffusion coefficient enhances reabsorption of alcohol by the airways on exhalation and creates a positive phase III slope.

Adult↗
PubMed1995

Effect of a nitric oxide synthase inhibitor and a glucocorticosteroid on exhaled nitric oxide.

Nitric oxide (NO) is produced by a variety of cells within the respiratory tract, including inflammatory epithelial cells. NO has been detected in the exhaled air of normal human subjects, and its concentration is raised in asthmatic patients. To study whether exhaled NO arises from the respiratory tract, we administered a NO synthase (NOS) inhibitor, NG-monomethyl-L-arginine (L-NMMA), by inhalation (490 mg) in a double-blind randomized manner in nine normal and six asthmatic subjects. Because exhaled NO may arise from an inducible isoform of NO synthase that may be inhibited by glucocorticosteroids, we also studied the effects of oral prednisolone (30 mg orally for 3 d) in seven normal and six asthmatic subjects in a separate double-blind crossover study with matched placebo. After nebulized L-NMMA, there was a significant fall in peak exhaled NO compared with saline control values, with a mean fall of 43.6 +/- 5.6% in normal subjects (p < 0.01) and of 39.7 +/- 6.5% (p < 0.01) in asthmatic subjects, which persisted for 4 h. There were no effects of L-NMMA inhalation on heart rate, blood pressure, or FEV1 in either normal or asthmatic patients. Administration of oral prednisolone (30 mg) resulted in a fall in exhaled NO concentrations in asthmatic subjects by 21.6 +/- 5.0% at 48 h (p < 0.01) but no significant change in normal subjects. These data suggest that NOS inhibitors may be safely given in normal and asthmatic patients and that the increased exhaled NO seen in asthmatic patients is likely to be caused by induction of inducible NOS.

Adult↗
PubMed1996

Inhaled glucocorticoids decrease nitric oxide in exhaled air of asthmatic patients.

Exhaled nitric oxide (NO) is elevated in untreated patients with asthma but not in patients treated with inhaled glucocorticoids. This may reflect an inhibitory effect of glucocorticoids on the induction of the enzyme NO synthase in the respiratory tract. We have now studied the effect of an inhaled glucocorticoid (budesonide 800 micrograms twice daily via a dry powder delivery system for 3 wk) on exhaled NO in 11 patients with mild asthma in a double-blind crossover randomized-order placebo-controlled study. Exhaled NO was reduced from a baseline value of 203 +/- 29 parts per billion (ppb) to 120 +/- 26 ppb after 3 wk of treatment (p < 0.01), whereas there was no change after a matched placebo (169 +/- 20 at baseline compared with 184 +/- 16 ppb after 3 wk). A significant and progressive fall in exhaled NO was found from 1 to 3 wk. There was no significant change in FEV1 after inhaled steroids (although mean FEV1 was 92% predicted normal at baseline), although there was a reduction in airway responsiveness to methacholine (approximately 2.5 doubling dilutions). These results add further support to the view that the elevated levels of exhaled NO in asthma may derive from induction of an inducible isoform of NO synthase and indicate that exhaled NO may be a useful way of monitoring the anti-inflammatory effects of glucocorticoids and other anti-inflammatory treatments in asthma.

Administration, Inhalation↗
PubMed1996

Nasal contribution to exhaled nitric oxide at rest and during breathholding in humans.

We characterized the nasal contribution to exhaled nitric oxide (NO) at rest and during breathholding in humans. Exhaled NO was greater during nose breathing (141 +/- 17 nl/min/M2, mean +/- SEM) compared with mouth breathing (68 +/- 6 nl/min/M2, n = 8, p < 0.001). After voluntary closure of the soft palate (VCSP) to eliminate nasal NO, exhaled NO from the mouth decreased further (30 +/- 4 nl/min/M2, p < 0.001). Release of NO into nasal passages during VCSP (217 +/- 19 nl/min/M2) was greater than exhaled NO during nasal breathing (141 +/- 17 nl/min/m2, p < 0.001), suggesting that nasal NO is taken up by the respiratory tract. During mouth breathing or nose breathing, NO concentrations sampled with a bronchoscope were higher in the nasopharynx than at the epiglottis or in the trachea in five subjects. Increased peak exhaled NO after a breathhold (33 +/- 7 ppb) was reduced (10 +/- 4 ppb, p < 0.001) after balloon occlusion of the nasopharynx. NO concentration during breathholding increased to a greater extent in the nasopharynx than in the pharynx or trachea. We conclude that the majority of exhaled NO at rest and during a breathhold originates in the nasopharynx.

Adult↗
PubMed1998

Increased carbon monoxide in exhaled air of subjects with upper respiratory tract infections.

Viral infection may induce the expression of heme oxygenase, resulting in increased carbon monoxide (CO) formation. CO may be produced by various cells of the upper and lower respiratory tract and may be detected in the exhaled air. Therefore, exhaled CO concentrations were measured on a CO monitor by vital capacity maneuver in subjects with upper respiratory tract infections (URTIs) and in nonsmoking and smoking healthy control subjects. At the time of symptoms of URTI, exhaled CO concentrations were 5.6 +/- 0.4 ppm and decreased to 1.0 +/- 0.1 ppm during recovery. Recovery values of exhaled CO were similar to those in age-matched nonsmoking healthy control subjects (1.2 +/- 0.3 ppm). Smoking healthy control subjects had the highest levels of exhaled CO concentration among the groups (18.5 +/- 2.5 ppm). These findings suggest that symptomatic URTIs increase the concentration of CO in exhaled air. This may reflect the induction of heme oxygenase that has an antiviral effect in the airways.

Breath Tests↗
PubMed1998

Exhaled nitric oxide is higher both at day and night in subjects with nocturnal asthma.

Nitric oxide in exhaled air is thought to reflect airway inflammation. No data have been reported so far on circadian changes in NO in subjects with nocturnal asthma. To determine whether exhaled NO shows a circadian rhythm inverse to the circadian rhythm in airway obstruction in subjects with nocturnal asthma, we conducted a study involving six healthy controls, eight individuals without nocturnal asthma (4-h to 16-h variation in peak expiratory flow [PEF] <= 15%), and six individuals with nocturnal asthma (4-h to 16-h PEF variation > 15%). Smoking, use of corticosteroids, and recent respiratory infections were excluded. NO concentrations were measured at 12, 16, 20, and 24 h, and at 4, 8, and 12 h of the next day, using the single-breath method. At the same times, FEV1 and PEF were also measured. Mean NO concentrations were significantly higher in subjects with nocturnal asthma than in subjects without nocturnal asthma, and higher in both groups than in healthy controls at all time points. Mean exhaled NO levels over 24 h correlated with the 4-h to 16-h variation in PEF (r = 0.61, p < 0.01). Exhaled NO did not show a significant circadian variation in any of the three groups as assessed with cosinor analysis, in contrast to the FEV1 in both asthma groups (p < 0.05). At 4 h, mean +/- SD NO levels were higher than at 16 h in subjects with nocturnal asthma; at 50 +/- 20 ppb versus 42 +/- 15 ppb (p < 0.05); other measurements at all time points were similar. Differences in NO and FEV1 from 4 h to 16 h did not correlate with one another. We conclude that subjects with nocturnal asthma exhale NO at higher levels both at night and during the day, which may reflect more severe diurnal airway-wall inflammation. A circadian rhythm in exhaled NO was not observed. NO levels did not correspond to the circadian rhythm in airway obstruction. The small increase in NO at 4 h may indicate an aspect of inflammation, but it is not associated with increased nocturnal airway obstruction.

Adolescent↗
PubMed1999

Exhaled nitric oxide measurements in a population sample of young adults.

In epidemiologic studies of asthma there is a group with recent wheeze, but with no airway hyperresponsiveness (AHR), in whom it is unclear whether any significant airway abnormality exists. Exhaled nitric oxide (NO) has been proposed as a measure of airway inflammation. We measured exhaled NO in a population sample of 306 young adults who also underwent bronchial challenge with histamine or a bronchodilator test. Subjects blew into a 3-L Tedlar bag against a 2-mm-diameter resistance to close the soft palate and exclude nasal air. The NO content of expired gas from a single breath was analyzed by chemiluminescent analyzer. Exhaled NO was log-normally distributed in the population sample and duplicate measurements were highly reproducible (intraclass correlation coefficient = 0.98). Exhaled NO correlated significantly with airway responsiveness, measured as the dose-response ratio to histamine (r = 0.39, p < 0.001) and with peripheral blood eosinophils (r = 0.35, p < 0.001). Exhaled NO was significantly greater in asthmatic subjects (geometric mean, 22.2; 95% confidence intervals, 16.1 to 30. 7 ppb) than in normal subjects (7.8, 7.1 to 8.4, p < 0.001) or in subjects with wheeze but no AHR (8.8, 7.5 to 10.3, p < 0.001). We conclude that exhaled NO is log-normally distributed, is highly reproducible and discriminates well among subjects, suggesting that it is both a feasible and useful measurement for epidemiologic studies of asthma. The findings suggest that wheeze in the absence of AHR is unlikely to be associated with airway inflammation.

Adult↗
PubMed2000

Exhaled nitric oxide following repeated spirometry or repeated plethysmography in healthy individuals.

Subjects with asthma have higher concentrations of exhaled nitric oxide (NO) than normal individuals. It has been demonstrated that in asthmatics, repeated FVC maneuvers reduce NO. Although the cause of this phenomenon is not known, it has been hypothesized that deep breaths associated with FVC maneuvers reduce exhaled NO by affecting neural sources of NO, possibly via a mechanism related to the pathobiology of asthma. To establish whether FVC maneuvers influence NO concentrations in normal individuals, we measured exhaled NO at baseline values and after FVC maneuvers performed every 15 min for 1 h in subjects without asthma. To investigate the role of deep breaths in reducing exhaled NO, we compared these results with concentrations of exhaled NO after plethysmography. Repeated FVC maneuvers over 60 min produced a decrease in NO concentrations in mixed expired gas (F(E)NO; 24.6 +/- 5.1% decrease for F(E)NO, p < 0. 01 versus baseline). In contrast to the results after spirometry, repeated specific airway conductance (sGaw) maneuvers do not have a significant effect on F(E)NO (p = 0.16). These results, which demonstrate that in nonasthmatic subjects FVC maneuvers-but not panting maneuvers-produce a fall in NO, suggest that the mechanism responsible for the reduction in exhaled NO after FVC maneuvers is related to volume history of the lung rather than the pathobiology of asthma.

Adult↗
PubMed2000

Exhaled ethane is elevated in cystic fibrosis and correlates with carbon monoxide levels and airway obstruction.

Ethane is produced from lipid peroxidation and can be measured in the exhaled air. Cystic fibrosis (CF) is characterized by recurrent respiratory infections, release of reactive oxygen species by inflammatory cells, and increased oxidative stress. We measured exhaled ethane in 23 CF subjects (mean age +/- SEM, 21 +/- 4 yr; 10 male, FEV(1) 62 +/- 4%) and compared it with two other noninvasive markers of oxidative stress and inflammation, carbon monoxide (CO) and nitric oxide (NO). Exhaled ethane was collected during a flow and pressure-controlled exhalation into a reservoir discarding dead space air contaminated with ambient air. A sample (2 ml) of the expired air was analyzed by chromatography. Ethane levels were elevated in patients not on steroids (n = 13, 1.99 +/- 0.20 ppb) compared with steroid-treated patients (n = 10, 0.67 +/- 0.09 ppb, p < 0.01) and with 14 nonsmoking control (8 men, age 33 +/- 2.8 yr) subjects (0.82 +/- 0.40 ppb, p < 0.05). In patients not on steroid treatment ethane was correlated to airway obstruction as assessed by the ratio of residual volume to total lung capacity (RV/ TLC) (r = 0. 66, p < 0.05) and exhaled CO (r = 0.65, p < 0.05). CO concentrations were also higher in patients not on steroid treatment (3.4 +/- 0.2 ppm) than in steroid-treated patients (2.6 +/- 0.1 ppm, p < 0.05), whereas NO concentrations were not influenced by steroid treatment (3.0 +/- 0.4 ppm and 2.9 +/- 0.2 ppm, p > 0.05) and were lower than in a control group (7.0 +/- 0.4 ppb, p < 0.05). Exhaled ethane is elevated in CF, reduced in steroid-treated patients and correlates with CO and RV/TLC; therefore, it may be a useful noninvasive marker of oxidative stress.

Adult↗
PubMed2000

Exhaled ethane, a marker of lipid peroxidation, is elevated in chronic obstructive pulmonary disease.

Ethane is a product of lipid peroxidation and can be measured in the exhaled air as an index of oxidative stress. Oxidant/antioxidant imbalance is important in the pathogenesis of chronic obstructive pulmonary disease (COPD). Therefore, we measured exhaled ethane in 22 patients with COPD (mean age +/- SEM, 59 +/- 8 yr; 19 male) and compared it with other noninvasive markers of oxidative stress and inflammation such as carbon monoxide (CO), measured electrochemically, and nitric oxide (NO), measured by chemiluminescence. Exhaled ethane was collected during a flow and pressure-controlled exhalation into a reservoir, discarding dead space air contaminated with ambient air. A sample of the collected expired air was analyzed by chromatography. Compared with normal subjects (n = 14; eight men; age, 33 +/- 2.8 yr), patients with COPD not on steroid treatment (n = 12; FEV(1), 58 +/- 6%) had elevated levels of exhaled ethane (2.77 +/- 0.25 and 0.88 +/- 0.09 ppb, respectively, p < 0.05), CO (5.96 +/- 0.50 and 2.8 +/- 0.25 ppm, p < 0.05) and NO (11.86 +/- 0.53 and 6.77 +/- 0.50 ppb, p < 0.05) levels. Ethane was correlated to FEV(1) (r = -0.67, p < 0.05). Patients receiving steroid treatment (n = 10; FEV(1), 56 +/- 2%) had lower levels of ethane (0.48 +/- 0.05 ppb) than did steroid-treated patients, whereas CO (5.99 +/- 0.63 ppm) and NO (9.11 +/- 0.53 ppb) levels were similar in the two treatment groups. Exhaled ethane is elevated, correlates with FEV(1), and is significantly lower in patients treated with steroids, so it may be complementary to the use of NO and CO in assessing and monitoring oxidative stress in COPD.

Biomarkers↗
PubMed2000

Increased nitrotyrosine in exhaled breath condensate of patients with asthma.

The reaction of nitric oxide (NO) and superoxide anions (O(2)(-)) in the airway results in the formation of peroxynitrite, a highly reactive oxidant species. Peroxynitrite reacts with tyrosine residues in proteins to form the stable product nitrotyrosine. We investigated whether nitrotyrosine in exhaled breath condensates may be increased in patients with asthma. Four groups of nonsmoking subjects were studied. We measured exhaled NO, nitrotyrosine, and leukotrienes concentrations in breath condensate in healthy nonatopic subjects (n = 15) and in patients with mild asthma (steroid naive, n = 15), moderate asthma (inhaled steroid treatment, n = 12), and severe asthma (oral steroid treatment, n = 12). Exhaled NO was increased significantly in patients with mild (19.2 +/- 2.7 ppb, p < 0.01) and moderate asthma (14.0 +/- 1.53 ppb, p < 0.05), as compared with normal control (6.58 +/- 0.61 ppb). The levels of LTC(4)/D(4)/E(4) and LTB(4) were increased significantly in patients with moderate and severe asthma treated with steroids. Nitrotyrosine concentrations were detectable (6.3 +/- 0.8 ng/ml) in breath condensate of normal subjects, and were increased significantly in patients with mild asthma (15.3 +/- 2.0 ng/ml, p < 0.01). However, the levels of nitrotyrosine in exhaled condensate were lower in patients with moderate (5.0 +/- 0.6 ng/ml) and severe asthma (3.3 +/- 0.6 ng/ml, p < 0.05). There was a significant correlation between nitrotyrosine in breath condensate and exhaled NO in patients with mild asthma (r = 0.65, p < 0.05). We conclude that nitrotyrosine formation in exhaled breath condensates may be a marker of oxidative stress in airways of asthma.

Adult↗
PubMed1993

Endogenous nitric oxide in single exhalations and the change during exercise.

The concentrations of endogenous nitric oxide (NO) and CO2 were measured in exhaled air from healthy humans. During a single exhalation, NO concentrations peaked when the CO2 level reached its plateau. However, whereas CO2 levels remained at a plateau throughout the exhalation, NO concentrations declined after having peaked. After breathholding (5 to 60 s) NO peaked at a higher level than during normal breathing. Nitric oxide concentrations in exhaled air decreased during physical exercise (50 to 100 W). However, taking the increased ventilatory minute volume into account, excretion of NO markedly increased during exercise. The data are compatible with the hypothesis that the NO detected in exhaled air is formed preferentially in the terminal and respiratory bronchioles, and they suggest increased production of NO into exhaled air during exercise and during hyperventilation at rest.

Adult↗
PubMed1985

Flow resistance of exhalation valves and positive end-expiratory pressure devices used in mechanical ventilation.

We studied the flow-impeding characteristics of the exhalation valves and PEEP attachments commonly used in mechanical ventilation. To characterize these devices, the pressure difference across each mechanism was measured at a series of constant flows (5 to 160 L/min), and resistance-related energy dissipation was measured using mechanical models of passive and active exhalation. At ambient end-expiratory pressure, an inflatable diaphragm (mushroom) design commonly used to valve exhalation presented resistance comparable to that of an endotracheal tube with an internal diameter of 5 mm. The valve's energy dissipation increased further as PEEP was applied. By comparison, the servo-actuated scissor valve we tested presented less resistance during the passive deflation experiment but impeded the early phase of active exhalation. Spring-loaded PEEP attachments were prohibitively resistive in comparison with alternative methods using an underwater tube, a water column, a weighted spirometer, or an inflatable diaphragm to raise end-expiratory pressure. We conclude that the exhalation valves and PEEP attachments currently available for clinical use present significant impedance to air flow. Such resistance within the exhalation pathway may be clinically important for patients supported by mechanical ventilation during the hyperpneic or weaning phases of their illness.

Analysis of Variance↗
PubMed2002

Increased interleukin-4 and decreased interferon-gamma in exhaled breath condensate of children with asthma.

Exhaled breath condensate analysis for noninvasive quantification of airway inflammation in asthma is a potentially useful research tool in children. There is an imbalance between T-helper (Th)-2 cells, which secrete interleukin (IL)-4, and Th1 cells, which secrete interferon (IFN)-gamma, in asthma. We measured concentrations of IL-4 and IFN-gamma in breath condensates of 37 children (11 normal, 12 steroid-naive, and 14 steroid-treated children with asthma). Exhaled IFN-gamma was significantly lower in steroid-naive and steroid-treated children with asthma compared with normal control subjects (3.7 +/- 0.2 versus 5.1 +/- 0.4 pg/ml, p < 0.01 and 4.1 versus 5.1 pg/ml, p < 0.05). By contrast, mean exhaled IL-4 was elevated in asthma (53.7 +/- 4.2 pg/ml) compared with normal children (35.7 +/- 6.2 pg/ml, p < 0.05) and concentrations were lower with steroid treatment (37.5 +/- 5.6 pg/ml, p < 0.05). Exhaled IL-4 was significantly lower in children with asthma on more than 600 microg inhaled steroid/day. The IL-4/IFN-gamma ratio was significantly greater in children with asthma compared with control children and the children with asthma on inhaled steroid therapy. We have shown for the first time that IFN-gamma and IL-4 can be assayed in exhaled breath condensate and shows an increased ratio of IL-4/IFN-gamma, consistent with predominance of Th2 cells in airways of children with asthma. Exhaled breath condensate analysis may have a useful role in studying allergic inflammation in childhood asthma.

Adolescent↗