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PubMed1996

Reduced upper airway nitric oxide in cystic fibrosis.

Nitric oxide (NO) produced within the respiratory tract is detectable in exhaled and nasal air. Its synthesis may be induced by inflammatory cytokines and reduced by glucocorticoids. Increased concentrations have been found in asthma and bronchiectasis. In this study, NO concentrations were determined in 63 children with cystic fibrosis, of whom 13 were on inhaled steroids (mean age 13.3 years) and 50 were not (mean age 12.3 years); 57 normal children (mean age 12.2 years) were also studied. NO was measured by chemiluminescence analyser, exhaled NO following a relaxed vital capacity manoeuvre, and nasal NO with the breath held following a full inspiration. Mean concentration of exhaled NO in cystic fibrosis patients (no steroids) was 4.7 parts per billion (ppb) (95% confidence interval (CI) 4.0 to 5.3); this did not differ from values in normal children (mean 4.8 ppb, 95% CI 3.8 to 5.8) or in cystic fibrosis patients on inhaled steroids (mean 3.6 ppb, 95% CI 2.5 to 4.8). Nasal concentrations were significantly lower in cystic fibrosis patients, with or without inhaled steroids, than in normal children (cystic fibrosis, no inhaled steroids: 460 ppb, 95% CI 399 to 520; cystic fibrosis, inhaled steroids: 522 ppb, 95% CI 313 to 730, v normal children: 1024 ppb, 95% CI 896 to 1152, p < 0.0001). Considering the inflammatory nature of cystic fibrosis, it is surprising exhaled NO levels were not increased, but this may have been due to alteration in NO diffusion through thick mucus. The low nasal NO concentrations, which are probably the result of impaired flow from the paranasal sinuses, may contribute to the recurrent respiratory infections typical of cystic fibrosis.

Administration, Inhalation↗
PubMed1988

Acidic colonic microclimate--possible reason for false negative hydrogen breath tests.

About 5% of normal subjects fail to produce increased hydrogen breath concentration after ingestion of the non-digestible carbohydrate lactulose (low hydrogen producers). The existence of low hydrogen producers limits the diagnostic use of hydrogen (H2) breath tests. We studied the effects of lactulose and of magnesium sulphate (MgSO4) pretreatment on stool-pH and on hydrogen exhalation after oral loading with lactulose or lactose in 17 hydrogen producers and 12 low hydrogen producers. In seven hydrogen producers acidification of stool pH by lactulose pretreatment (20 g tid) decreased hydrogen exhalation and three of seven (43%) became low hydrogen producers. In contrast, after pretreatment of eight low hydrogen producers with magnesium sulphate (5 g twice daily) all eight produced hydrogen after a lactulose load. Similarly four lactose intolerant low hydrogen producers had abnormal lactose hydrogen breath tests after MgSO4 pretreatment. MgSO4 pretreatment neither resulted in false positive lactose hydrogen breath tests in five lactose tolerant hydrogen producers, nor increased the hydrogen exhalation in five additional hydrogen producing controls after ingestion of lactulose. The results of these studies confirm that hydrogen production from lactulose decreases when the colonic pH is lower (lactulose pretreatment), and increases when colonic pH is higher (MgSO4 pretreatment). In low hydrogen producers the lacking increase of H2 exhalation after ingestion of non-digestible carbohydrates can be overcome by MgSO4 pretreatment, thus increasing the sensitivity of the test by avoiding false negative hydrogen breath tests in low hydrogen producers with disaccharide malabsorption or maldigestion. The underlying mechanism of this remarkable effect of MgSO4 pretreatment warrants further investigation.

Breath Tests↗
PubMed2004

Current and future uses of breath analysis as a diagnostic tool.

The analysis of exhaled breath is a potentially useful method for application in veterinary diagnostics. Breath samples can be easily collected from animals by means of a face mask or collection chamber with minimal disturbance to the animal. After the administration of a 13C-labelled compound the recovery of 13C in breath can be used to investigate gastrointestinal and digestive functions. Exhaled hydrogen can be used to assess orocaecal transit time and malabsorption, and exhaled nitric oxide, carbon monoxide and pentane can be used to assess oxidative stress and inflammation. The analysis of compounds dissolved in the aqueous phase of breath (the exhaled breath condensate) can be used to assess airway inflammation. This review summarises the current status of breath analysis in veterinary medicine, and analyses its potential for assessing animal health and disease.

Animals↗
PubMed1998

Chronic hypoxia decreases nitric oxide production and endothelial nitric oxide synthase in newborn pig lungs.

To examine the effect of chronic hypoxia on nitric oxide (NO) production and the amount of the endothelial isoform of nitric oxide synthase (eNOS) in lungs of newborn piglets, studies were performed using 1- to 3-day-old piglets raised in room air (control) or 10% O2 (chronic hypoxia) for 10-12 days. Exhaled NO output and plasma nitrites and nitrates (collectively termed NOx-) were measured in anesthetized animals. NOx- concentrations were measured in the perfusate of isolated lungs. eNOS amounts were assessed in whole lung homogenates. In the intact piglets, exhaled NO outputs and plasma NOx- were lower in the chronically hypoxic (exhaled NO output = 0.2 +/- 0.1 nmol/min; plasma NOx- = 10.3 +/- 3.7 nmol/ml) than in control animals (exhaled NO output = 0.8 +/- 0.2 nmol/min; plasma NOx- = 22.3 +/- 4.3 nmol/ml). In perfused lungs, the perfusate accumulation of NOx- was lower in chronic hypoxia (1.0 +/- 0.3 nmol/min) than in control (2.6 +/- 0.6 nmol/min) piglets. The amount of whole lung homogenate eNOS from the chronic hypoxia piglets was 40 +/- 8% less than that from the control piglets. The reduced NO production observed in anesthetized animals or perfused lungs of chronically hypoxic newborn piglets is consistent with the finding of reduced lung eNOS protein amounts. Decreased NO production might contribute to the development of chronic hypoxia-induced pulmonary hypertension in newborns.

Animals↗
PubMed2006

Exercise-induced bronchoconstriction alters airway nitric oxide exchange in a pattern distinct from spirometry.

Exhaled nitric oxide (NO) is altered in asthmatic subjects with exercise-induced bronchoconstriction (EIB). However, the physiological interpretation of exhaled NO is limited because of its dependence on exhalation flow and the inability to distinguish completely proximal (large airway) from peripheral (small airway and alveolar) contributions. We estimated flow-independent NO exchange parameters that partition exhaled NO into proximal and peripheral contributions at baseline, postexercise challenge, and postbronchodilator administration in steroid-naive mild-intermittent asthmatic subjects with EIB (24-43 yr old, n = 9) and healthy controls (20-31 yr old, n = 9). The mean +/- SD maximum airway wall flux and airway diffusing capacity were elevated and forced expiratory flow, midexpiratory phase (FEF(25-75)), forced expiratory volume in 1 s (FEV(1)), and FEV(1)/forced vital capacity (FVC) were reduced at baseline in subjects with EIB compared with healthy controls, whereas the steady-state alveolar concentration of NO and FVC were not different. Compared with the response of healthy controls, exercise challenge significantly reduced FEV(1) (-23 +/- 15%), FEF(25-75) (-37 +/- 18%), FVC (-12 +/- 12%), FEV(1)/FVC (-13 +/- 8%), and maximum airway wall flux (-35 +/- 11%) relative to baseline in subjects with EIB, whereas bronchodilator administration only increased FEV(1) (+20 +/- 21%), FEF(25-75) (+56 +/- 41%), and FEV(1)/FVC (+13 +/- 9%). We conclude that mild-intermittent steroid-naive asthmatic subjects with EIB have altered airway NO exchange dynamics at baseline and after exercise challenge but that these changes occur by distinct mechanisms and are not correlated with alterations in spirometry.

Adaptation, Physiological↗
PubMed2002

Impact of axial diffusion on nitric oxide exchange in the lungs.

Nitric oxide (NO) appears in the exhaled breath and is a potentially important clinical marker. The accepted model of NO gas exchange includes two compartments, representing the airway and alveolar region of the lungs, but neglects axial diffusion. We incorporated axial diffusion into a one-dimensional trumpet model of the lungs to assess the impact on NO exchange dynamics, particularly the impact on the estimation of flow-independent NO exchange parameters such as the airway diffusing capacity and the maximum flux of NO in the airways. Axial diffusion reduces exhaled NO concentrations because of diffusion of NO from the airways to the alveolar region of the lungs. The magnitude is inversely related to exhalation flow rate. To simulate experimental data from two different breathing maneuvers, NO airway diffusing capacity and maximum flux of NO in the airways needed to be increased approximately fourfold. These results depend strongly on the assumption of a significant production of NO in the small airways. We conclude that axial diffusion may decrease exhaled NO levels; however, more advanced knowledge of the longitudinal distribution of NO production and diffusion is needed to develop a complete understanding of the impact of axial diffusion.

Diffusion↗
PubMed2004

A new and more accurate technique to characterize airway nitric oxide using different breath-hold times.

Exhaled nitric oxide (NO) arises from both airway and alveolar regions of the lungs, which provides an opportunity to characterize region-specific inflammation. Current methodologies rely on vital capacity breathing maneuvers and controlled exhalation flow rates, which can be difficult to perform, especially for young children and individuals with compromised lung function. In addition, recent theoretical and experimental studies demonstrate that gas-phase axial diffusion of NO has a significant impact on the exhaled NO signal. We have developed a new technique to characterize airway NO, which requires a series of progressively increasing breath-hold times followed by exhalation of only the airway compartment. Using our new technique, we determined values (means +/- SE) in healthy adults (20-38 yr, n = 8) for the airway diffusing capacity [4.5 +/- 1.6 pl.s(-1).parts per billion (ppb)(-1)], the airway wall concentration (1,340 +/- 213 ppb), and the maximum airway wall flux (4,350 +/- 811 pl/s). The new technique is simple to perform, and application of this data to simpler models with cylindrical airways and no axial diffusion yields parameters consistent with previous methods. Inclusion of axial diffusion as well as an anatomically correct trumpet-shaped airway geometry results in significant loss of NO from the airways to the alveolar region, profoundly impacting airway NO characterization. In particular, the airway wall concentration is more than an order of magnitude larger than previous estimates in healthy adults and may approach concentrations (approximately 5 nM) that can influence physiological processes such as smooth muscle tone in disease states such as asthma.

Adult↗
PubMed2006

[Role of oxidative stress in respiratory diseases and its monitoring].

Together with inflammation and subsequent remodeling of airways, an imbalance between oxidative and anti-oxidative agents is generated during the development of numerous pulmonary diseases. This process seems to be involved in both the pathogenesis and chronification of asthma, chronic obstructive pulmonary disease (COPD), SOAS, interstitial lung diseases and cystic fibrosis. Reactive oxygen species including superoxide anion, hidroxyl radicals and hydrogen peroxide (H2O2) are synthetised as a response of inflammatory cells and are responsible of the oxidation of nucleic acids, proteins and membrane lipids, leading to cell damage and enhanced inflammation. Until recently, it was difficult to quantify the airway production of reactive oxidative species (ROS). In fact, it has been only in the last few years when it has been possible to determine indirectly the levels of ROS in expired air and in tissue of asthmatic patients. The analysis of exhaled air is a single, reproducible and non-invasive technique which is useful in the study of volatile and non-volatile gases generated in different conditions. The determination of exhaled nitric oxide and carbon monoxide (CO) has a great usefulness in the assessment of asthma. Nitric oxide seems to be closely related to the physiopathology of asthma and COPD. In fact, it is correlated with the levels of sputum eosinophils and with the response to the treatment with steroids. Yet a correlation with the degree of airflow obstruction and the seriousness of the process has not been found. Exhaled CO is another indirect marker of inflammation and it is increased in asthma, COPD, cystic fibrosis and bronchectases. Even though numerous studies have shown its usefulness as a marker of inflammation and in the response to corticosteroids, its clinical application has limitations. In particular, it is not a specific and exclusive marker of oxidative stress and its levels are highly influenced by tobacco smoke. On the other hand, the association between exhaled CO and FEV1 is not clear and no relationship has been proved so far with the improvement of pulmonary function after steroid therapy and with the decrease of maximum expiratory flow at relapses. In this Review, we describe the advances in the knowledge of oxidative stress as a decisive factor in the pathogenesis of prevalent pulmonary diseases, as well as the methods allowing its analysis and monitoring.

Biomarkers↗
PubMed2003

Endogenous production of nitric oxide in endotoxemic piglets.

We sought to assess the relation between endotoxin-induced pulmonary hypertension and the production of nitric oxide (NO) in neonatal animals. Adult animals respond to endotoxin by increasing exhaled NO and plasma NO metabolites. The response of neonatal animals has not previously been reported. We administered 20 microg/kg of Escherichia coli lipopolysaccharide (LPS) to 12- to 18-day-old and to 5- to 7-week-old piglets. Pulmonary vascular resistance increased significantly in both age groups. Exhaled NO in the 12- to 18-day-old animals and in the 5- to 7-week-old piglets did not increase significantly. A similarly treated group of adult rats did show a significant increase in exhaled NO (2.6 +/- 1.0 to 109.5 +/- 54.3 ppb; p = 0.028). Plasma NO metabolite measurements followed the same pattern of no increase in both porcine groups, and a large increase in the rat group. However, immunostaining of lungs from 12- to 18-day-old piglets did reveal an increase in inducible NO synthase. These results suggest that piglets demonstrate a limited ability to modulate LPS-induced pulmonary hypertension by elevations in exhaled NO. They also demonstrate the differential response to LPS between species.

Animals↗
PubMed1996

Endogenous nitric oxide is decreased in asthmatic patients by an inhibitor of inducible nitric oxide synthase.

Exhaled nitric oxide (NO) may be derived from constitutive NO synthase (NOS) in normal airways, but the increased concentration in asthma is likely to be derived from inducible NOS expressed in inflamed airways. To investigate this, we administered a nonselective NOS inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), and a selective inhibitor of inducible NOS, aminoguanidine, by nebulization in a double-blind, placebo-controlled manner in both normal subjects and subjects with asthma. L-NAME resulted in a significant reduction in exhaled NO compared with saline control in eight normal subjects (maximum fall from baseline, 53 +/- 7.6% versus 8.9 +/- 6.5%; P < 0.05) and in seven patients with asthma (maximum fall, 67 +/- 7.4% versus 10 +/- 7.4% versus 10 +/- 9.3%; p < 0.05). Aminoguanidine at the same molar concentration decreased exhaled NO in subjects with asthma (maximum fall, 53 +/- 7.2% versus 7.1 +/- 10.4%; p < 0.05), but caused no significant change in normal volunteers (maximum fall, 28 +/- 9.3 versus 15 +/- 11). No rise in blood pressure, fall in FEV1, or adverse effects were observed in either subject group. We have demonstrated that NOS inhibitors can safely be given by inhalation in a single does in normal subjects and subjects with asthma. The raised exhaled NO concentration in patients with asthma may be attributable to induction of NOS, with that in normal subjects reflecting basal constitutive NOS activity.

Administration, Inhalation↗
PubMed1998

Allergen-induced early and late asthmatic responses are not affected by inhibition of endogenous nitric oxide.

Endogenous exhaled nitric oxide (NO) is increased during the late response to inhaled allergen in patients with asthma and may be bronchoprotective in asthma or have a deleterious effect when generated in excess under inflammatory conditions. To investigate this, we evaluated the effect of inhibiting endogenous NO production with nebulized NG-nitro-L-arginine methyl ester (L-NAME), a nonselective NO synthase (NOS) inhibitor, on early and late asthmatic responses to inhaled allergen in patients with mild allergic asthma. After a screening allergen challenge (AC), 22 male patients attended two visits conducted in a double-blind, randomized, placebo-controlled, crossover manner. Twelve patients demonstrating an early asthmatic response only (single responders) inhaled either L-NAME 170 mg or 0.9% saline 20 min before AC, with exhaled NO and FEV1 measured for 3 h. Ten patients demonstrating both early and late asthmatic responses (dual responders) were studied in a similar fashion but inhaled two further doses of L-NAME or placebo 3.5 and 7 h after the initial dose, with exhaled NO and FEV1 measured for 10 h. L-NAME reduced exhaled NO levels by 77 +/- 5% (p < 0.01) and 71 +/- 7% (p < 0.01) in single and dual responders, respectively, but had no significant effect on early or late asthmatic responses. Following AC in single responders, the mean (+/- SEM) maximum fall in FEV1 after L-NAME and saline was 21.2 +/- 2.9% and 23.8 +/- 3.0%, respectively, and in dual responders, 31.2 +/- 4.5% and 31.8 +/- 5. 8% during the early asthmatic responses, and 27.4 +/- 3.9% and 30.6 +/- 4.5% during the late asthmatic responses, respectively. Area under the curve (AUC) did not significantly differ. AUC0-2 h in single responders after L-NAME and saline was 20.2 +/- 3.9 and 24.9 +/- 4.4 Delta% FEV1/h, and in dual responders, 37.6 +/- 8.4 and 36.7 +/- 8.4 Delta% FEV1/h, respectively, and 106.2 +/- 18.9 and 117.1 +/- 22.4 Delta% FEV1/h, respectively, for the AUC4-10 h. This study suggests that in mild allergic asthma, endogenous NO neither protects against nor contributes to the processes underlying airway responses to inhaled allergen.

Adult↗
PubMed1999

Effect of inhaled budesonide on lung function and airway inflammation. Assessment by various inflammatory markers in mild asthma.

In a double-blind, cross-over study, we examined the effect of inhaled budesonide (800 microgram twice daily via Turbohaler) on lung function and various markers of airway inflammation including airway responsiveness to methacholine (PC20), exhaled nitric oxide (NO), eosinophils in induced sputum, bronchoalveolar lavage (BAL), and airway biopsies from 14 patients with mild asthma needing beta2- agonist therapy only. After inhaled steroids, there was a significant increase in FEV1 and PC20, and reduction in exhaled NO. Eosinophils in induced sputum and airway biopsy sections were also significantly decreased, although BAL eosinophil counts remained unchanged. At baseline, significant correlations were observed between exhaled NO and PC20 methacholine (r = 0.64, p < 0.05), exhaled NO and peak expiratory flow rate (PEFR) variability (r = 0. 65, p < 0.05), sputum eosinophils and FEV1 (r = -0.63, p = 0.05), and sputum eosinophils and log PC20 methacholine (r = -0.67, p < 0. 05). After treatment with inhaled steroids, there was a significant correlation between eosinophils in biopsy sections, and BAL, with log PC20 methacholine. It is likely that these parameters represent different aspects of the inflammatory process, which are all inhibited by inhaled steroids.

Administration, Inhalation↗
PubMed2000

No effect of inhaled budesonide on the response to inhaled ozone in normal subjects.

Inhalation of ozone in normal subjects causes a neutrophilic inflammatory response in the airways. Pretreatment with inhaled corticosteroids reduces the inflammatory response to inhaled ozone in dogs. We undertook a double-blind, randomized, placebo-controlled, crossover study to investigate the effects of 2 wk of treatment with inhaled budesonide 800 microg twice daily or placebo prior to ozone exposure in humans. Fifteen (six male; mean age, 31.1 +/- 2.1 yr) healthy nonsmokers were exposed to 400 parts per billion (ppb) ozone for 2 h with intermittent exercise. Spirometry, exhaled carbon monoxide (CO) and nitric oxide (NO) levels, measurement of methacholine reactivity, and collection of exhaled air condensate and induced sputum samples were performed at baseline, preexposure, and at intervals up to 24 h postexposure. Ozone exposure led to significant decreases in spirometry and increased methacholine reactivity and sputum neutrophils and myeloperoxidase (MPO). There were no changes in exhaled NO and CO levels, or exhaled breath nitrite after ozone exposure. There were no differences in any of the parameters after treatment with budesonide compared with placebo, and no differences in the response to ozone between treatment groups. We conclude that a high dose of inhaled corticosteroid does not protect against the effects of ozone exposure in normal subjects.

Administration, Inhalation↗
PubMed2000

Interrelation between oxygen tension and nitric oxide in the respiratory system.

To understand the relationship between oxygen tension and nitric oxide (NO) function, one animal and two human studies were designed. In the animal study, the effect of NO in inducing the relaxation of aortic specimens was significantly lower by 68% under 480 mm Hg of oxygen tension than under 28 mm Hg, indicating that oxygen tension has an important role in determining the biological effects of NO. In a clinical analysis with nonsmokers (n = 23), the alveolar-to-arterial difference for oxygen (A-aDO(2)) was reciprocally correlated with exhaled NO concentrations (r = 0.53). Because NO concentration in the lower respiratory zone depends partly on the amount of inspirable NO originating in the upper airway, a well-ventilated area, requiring much perfusion, could receive greater amounts of NO than a poorly ventilated one. Thus, the reciprocal relation of A-aDO(2) with the concentration of exhaled NO is not necessarily incompatible with the effect of hypoxic pulmonary vasoconstriction in ventilation-to-perfusion (V'A/Q') imbalance. In our third experiment, with nonsmokers (n = 21), pure oxygen inhalation during mechanical ventilation significantly decreased the concentration of exhaled NO and enhanced A-aDO(2), indicating a relationship between NO and oxygen similar to that observed in the animal experiment. These findings led us to conclude that a positive relation between exhaled NO and blood oxygenation efficiency exists in the respiratory system, and further, that oxygen might affect this relationship. Thus, the relative balance of NO and oxygen concentrations may be another factor for consideration in respiratory function.

Adult↗
PubMed2001

Effect of imposed inflation time on respiratory frequency and hyperinflation in patients with chronic obstructive pulmonary disease.

Decreases in ventilator inflation time (TI,vent) can cause tachypnea, probably as a response to lung inflation. The response may differ in chronic obstructive pulmonary disease (COPD) because time-constant inhomogeneities could foster overdistention of some lung units during early inflation, causing neural inspiratory time to be shorter than in healthy subjects. We tested the hypothesis that a decrease in TI,vent causes tachypnea, prolongation of exhalation, and a decrease in intrinsic positive end-expiratory pressure (PEEP(i)). Ten patients with stable COPD received assist-control ventilation through a mouthpiece. Decreases in TI,vent, achieved through increases in flow from 30 to 90 L/min, increased frequency, from 16.1 +/- 1.0 (SE) to 20.8 +/- 1.5 breaths/min (p < 0.001), time for exhalation, from 2.1 +/- 0.2 to 2.3 +/- 0.2 s (p < 0.025), and decreased PEEP(i), from 7.0 +/- 1.3 to 6.4 +/- 1.1 cm H(2)O (p < 0.01). Decreases in TI,vent, achieved by decreasing inspiratory pause from 2 to 0 s, increased frequency, from 12.9 +/- 0.8 to 18.1 +/- 1.6 breaths/min (p < 0.001), time for exhalation, from 2.0 +/- 0.2 to 2.6 +/- 0.3 s (p < 0.001), and decreased PEEP(i), from 6.4 +/- 1.1 to 5.5 +/- 0.9 cm H(2)O (p < 0.01). In both experiments, decreases in TI,vent reduced inspiratory effort (p < 0.01). In conclusion, strategies to reduce TI,vent in patients with COPD caused tachypnea, yet prolonged the time for exhalation with consequent decrease in PEEP(i).

Aged↗
PubMed1989

Effect of cystic fibrosis on inhaled aerosol boluses.

An aerosol bolus undergoes changes in shape between its inspiration and expiration. In comparison with the inhaled bolus, the exhaled bolus is more spread because of convective mixing, may have a shift in the location of the mode caused by asymmetries of filling and emptying of lung units, and contains fewer particles because of particle deposition. We hypothesized that the extent of these changes is related to lung health. To examine this, 11 patients with cystic fibrosis (CF) and 11 healthy subjects inhaled 70 cm3 boluses containing 1 micron monodisperse particles that were inspired to volumetric penetrations (Vp) of 100 to 700 cm3. As each bolus was expired, we measured spreading (volumetric width at one-half aerosol concentration peak height), modal shift, and particle deposition. Patients with CF exhaled boluses that were broader than those exhaled by normal subjects at all penetrations examined. At a Vp of 600 cm3, patients had a mean bolus half-width that was 68% greater than that of healthy subjects (p less than 0.0001), and they exhaled the bolus mode 20% earlier (p less than 0.0002). Particle deposition was increased compared with that in normal subjects at all Vp. For example, mean deposition at a Vp of 600 cm3 was 46.2 +/- 2.6% (SE) for the patients versus 25.8 +/- 1.6% for the normal subjects (p less than 0.0001). Among the patients with CF, pulmonary function parameters indicating obstruction were significantly correlated with bolus spreading and aerosol deposition: the percent predicted FEV1/FVC was inversely correlated with spreading (r = -0.88, p less than 0.0004) and deposition (r = -0.84, p less than 0.0008).(ABSTRACT TRUNCATED AT 250 WORDS)

Aerosols↗
PubMed1980

Alveolar gas compression in smokers and asthmatics.

To correlate the degree of alveolar gas compression with the severity of airway obstruction, we plotted separately exhaled and plethysmographic maximal-expiratory-flow-volume (MEFV) curves in each of 4 healthy nonsmokers, 4 asymptomatic smokers, and 4 asymptomatic asthmatics. Spirometry, lung volumes, single breath nitrogen plateau (Phase III), and closing volumes (Phase IV) were normal in the smokers and nonsmokers, and there were either normal or showed evidence of mild airway obstruction in the asthmatics. MEFV curves were plotted by using exhaled flow (VE) against exhaled volume (VE), and by using plethysmographic flow (VL) against plethysmographic volume (VL). These curves were utilized to construct isovolume-pressure-flow (IVPF) curves of esophageal pressure (Pes) against VE and against VL for each subject. Differences in the flow (VL minus VE) were calculated from these curves at 75% vital capacity (VC), 50% VC, and 25% VC at the same Pes in all 3 groups. At 75% VC, the mean flow difference in the asthmatic group was significantly higher than in normals (P less than 0.05); at 50% VC, it was significantly higher both in the asthmatics and the smokers (P less than 0.05); at 25% VC, there was no significant difference among the 3 groups. The mean plethysmographic forced vital capacity (FVC) exceeded exhaled FVC in all 3 groups, but the difference was significantly higher in smokers and asthmatics than in nonsmokers (P less than 0.05). These findings suggest that significant alveolar gas compression may occur at 75% VC in mild asthmatics, whereas in smokers it occurs at the middle portion of the VC.

Adult↗
PubMed1984

Overestimation of the single-breath carbon monoxide diffusing capacity in patients with air-flow obstruction.

It has been previously shown that conventional methods of measuring the single-breath diffusing capacity of the lung for carbon monoxide (DLCOsb) overestimate diffusion in normal subjects when the expiratory flow rate is reduced, when the collection of the exhaled alveolar gas sample is delayed, and/or when too large an alveolar gas sample is collected. Conventional methods use a single breathholding equation to analyze the entire single-breath maneuver, which consists of inhalation, breathholding, and exhalation. We previously developed a method of calculating DLCOsb using 3 separate equations, one for each phase of the single-breath maneuver. Using this method, DLCOsb measurements are unaffected by changes in expiratory flow rate or by the size and timing of the alveolar gas sample, as these parameters are analytically included in the analysis. We hypothesized that in patients with air-flow obstruction, conventional methods of measuring DLCOsb would overestimate diffusion. We examined the effects of measuring DLCOsb using rapid inhalation and exhalation maneuvers in a group of normal subjects and in 3 groups of patients with emphysema, asthma, and cystic fibrosis, respectively. First, we found that, whereas conventional methods specify 750 ml or 1 L of gas to be used for dead space washout, the washout volumes, as measured from a continuous monitor of the helium concentration in the exhaled gas in the single-breath maneuver, exceeded 1 L in 26% of the study group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗