PubMed HealthSearch

Biomedical subjects

G Bylin

Publications and source records attributed to G Bylin.

At least 19 recordsLinked to original sources

Variability in airway conductance and lung volume in subjects with asthma.

Variability in airway conductance (Gaw) and lung volume (TGV) was studied in 26 subjects with moderately severe asthma during a 9-week period. Specific airway conductance (SGaw) was calculated as Gaw:TGV. There was considerable inter-individual variability in airway conductance, and a smaller variability in TGV. Airway conductance (SGaw) showed an eight-fold difference and TGV a three-fold difference between smallest and largest values. The intra-individual variability was less, with a range of +/- 55% (SGaw) and +/- 12% (TGV) of the grand mean, respectively. The error of the method contributed only marginally to the variations in airway conductance. These data for spontaneous variability of conductance facilitate, for example, the assessment of the clinical importance of changes in lung function seen after exposure to air pollutants in chamber studies. Furthermore, the substantial inter-individual variability in conductance argues against comparing samples of asthmatic subjects in polluted and non-polluted areas, and in favour of prospective studies of cohorts of subjects with asthma.

Airway Resistance

Added external resistance reduces oropharyngeal deposition and increases lung deposition of aerosol particles in asthmatics.

Mouth and throat, and regional lung deposition was estimated in fifteen asthmatic subjects for 3.6-microns (aerodynamic diameter) radiolabeled polytetrafluoroethylene (Teflon) particles inhaled at 0.5 L/s with and without added external resistance. Radioactivity was measured by a profile scanner. Behavior of the pharynx and larynx was assessed by fiberoptic laryngoscopy. Mean mouth and throat deposition was 22% (range, 13 to 47%) and 33% (range, 12 to 84%) with and without resistance (p < 0.05), respectively. A marked reduction in mouth and throat deposition (range, 20 to 44%), with a corresponding increase in lung deposition, was observed especially in the six subjects with mouth and throat deposition values > 30% at inhalation without resistance. Furthermore, a small (mean 8%) but significant (p < 0.05) increase in peripheral lung deposition, estimated as retention at 24 h, was found at inhalation with increased resistance. The fiberoptic examination showed wide intersubject variability in the pharynx and larynx, with tendencies toward higher mouth and throat deposition with pharyngeal narrowing, and significantly (p < 0.05) lower lung retention with laryngeal narrowing. Our results show that an external resistance reduces mouth and throat deposition and increases deposition and retention of aerosol particles in the lungs in asthmatic individuals.

Adult

Deposition of inhaled particles in the mouth and throat of asthmatic subjects.

We previously studied the deposition of inhaled particles in the mouth and throat of asthmatic patients, and found large, reproducible differences among subjects. In the present study, we examined whether anatomical and/or functional differences in the pharynx and larynx could underlie this interindividual variation. Deposition in the mouth and throat, and in the lung was estimated in 16 asthmatic subjects after inhalation of 3.6 microns (aerodynamic diameter) monodisperse Teflon particles labelled with 111In. The particles were inhaled at a flow rate of 0.5 l.s-1 with maximally deep breaths. Radioactivity was measured by external scanning over head and neck, lungs and stomach, immediately after the inhalation. Radioactivity in the lungs was also measured 24 h later. A measure of the total amount of particles deposited in the mouth and throat was obtained from the added activities in mouthwash, head and neck, and stomach, immediately after the inhalation of the test particles. Pharynx and larynx function was examined by fibreoptic laryngoscopy performed during a corresponding inhalation procedure. Deposition in the mouth and throat varied widely among the subjects, ranging 9-76% (median 12%). We found two subpopulations, 13 subjects in the range 9-34%, and 3 subjects with > 70% deposition. Deviations in pharyngeal configuration during inhalation were significantly related to high mouth and throat deposition, whereas functional differences in the larynx were not. Our study shows that mouth and throat deposition may be extremely high in some asthmatics, and that pharyngeal configuration affects deposition of particles in the mouth and throat.

Adult

Relationships among gas exchange, spirometry and symptoms in asthma.

OBJECTIVES: The severity of asthma is usually evaluated by clinical examination and spirometry. In a small study of asthmatics considerable ventilation/perfusion (VA/Q) inequality was found, however, despite essentially normal flow rates. These findings prompted the current study. METHODS: We prospectively examined symptoms, spirometry and VA/Q inequality in 26 patients with chronic, symptomatic asthma once a week for 9 consecutive weeks. VA/Q measurements were made using a less invasive approach of the multiple inert gas elimination technique and symptoms were scored. RESULTS: Correlation coefficients between indices for VA/Q inequality (log SDQ), spirometry (FEV1.0/VC, MEF25) and symptom scores were only in the range 0.24-0.29. CONCLUSION: We conclude that even at the individual level, symptoms, spirometry and VA/Q inequality are so poorly correlated that one cannot evaluate any of these aspects of asthma without measuring each. The data support the notion that spirometric and gas exchange abnormalities in asthma are caused by different pathophysiologic events.

Asthma

Regional deposition of 3.6-micron particles and lung function in asthmatic subjects.

In a group of moderately severe asthmatic subjects, regional deposition of 3.6-microns (aerodynamic diameter) monodispersed Teflon particles labeled with 111In was studied twice. The particles were inhaled with maximally deep inhalation at 0.5 l/s. Lung retention was measured at 0, 6, 24, and 48 h by use of a profile scanner equipped with two 13 x 5-cm NaI crystals. The retentions at 24 (Ret24) and 48 h were highly correlated (r = 0.96 with a slope of the regression line close to 1). There was a poor correlation between retention at 6 h and Ret24 (r = 0.54). The Ret24 values at the two exposures were well correlated (r = 0.86). There were significant correlations between airway resistance as well as single-breath nitrogen test phase III and Ret24 (r = 0.70 and 0.67, respectively). The correlation between single-breath nitrogen test phase III and Ret24 persisted also when only subjects within a narrow interval of airway resistance were included. The study indicates that regional deposition can be studied by measurements of Ret24 in subjects with moderately severe asthma and that it is dependent on changes in both large and small airways.

Administration, Inhalation

Ambient nitrogen dioxide concentrations increase bronchial responsiveness in subjects with mild asthma.

Twenty subjects with mild asthma were exposed at rest in a body plethysmograph, to NO2 at 0, 260, 510 and 1,000 micrograms.m3, for 30 min on four separate days. Bronchial responsiveness (histamine inhalation test) was measured after each exposure session. Airway resistance (Raw), thoracic gas volume (TGV) and specific airway resistance (sRaw) were measured before, during and after exposure, and the breathing pattern was monitored during the whole session. Bronchial responsiveness increased significantly after 30 min exposure to 510 micrograms.m3 NO2 (p less than 0.01). There were also tendencies to an increased bronchial responsiveness after exposure to 260 and 1,000 micron.m3 NO2, but these changes were not statistically significant. Effects on airway resistance and breathing pattern were not demonstrated by exposure to 0-1,000 micrograms.m3 NO2. We conclude that short-term NO2 exposure at about 500 micrograms.m3 slightly affects human bronchial responsiveness in subjects with mild asthma.

Adult

Reproducibility of the multiple inert gas elimination technique.

Although measurement errors in the multiple inert gas elimination technique have a coefficient of variation of approximately 3%, small biological fluctuations in ventilation, blood flow, or other variables must contribute additional variance to this method of assessing ventilation-perfusion (VA/Q) mismatch. To determine overall variance of computed indices of VA/Q mismatch, an analysis of variance was carried out using a total of 400 duplicate pairs of inert gas samples obtained from canine (N = 118) and human (N = 282) studies in the past 2 years. In both sets VA/Q mismatch ranged from minimal (2nd moment of ventilation and blood flow distributions, log SDV and log SDQ, respectively approximately equal to 0.3 each) to severe (log SDV and log SDQ approximately equal to 2.0). Differences between duplicate log SD values were computed and found to be a constant fraction of the mean log SD of each duplicate pair, averaging 13% for both canine and human ventilation and blood flow data. The resultant coefficient of variation for a single measurement of log SD about its mean averaged 8.6% for all data combined. This analysis demonstrates excellent reproducibility of these dispersion indices over a wide range of conditions, and if the mean of duplicate values is used, thus reducing variability by square root 2 to 6.1%, log SD can be estimated with an approximately 95% confidence limit of +/- 12%.

Animals

Ventilation-perfusion inequality in chronic asthma.

The prevalence and variability of ventilation-perfusion (VA/Q) inequality was examined in 26 stable, symptomatic, asthmatic subjects (mean FEV1/FVC, 79% predicted; mean FEF75, 43% predicted) studied once a week for 9 consecutive weeks. We used a recent modification of the multiple inert gas elimination technique allowing frequent serial studies without the need for sampling arterial blood. The VA/Q inequality was expressed as log SD (the second moment) of the distributions of blood flow (Q) and ventilation (V) on a log scale. Log SDQ averaged 0.74, and in every patient log SDQ exceeded the 95% upper limit of normal (0.60) in 2 wk or more. In only 5 patients was mean log SDQ less than 0.6. The ventilation distribution was less abnormal, with mean log SDV exceeding the 95% normal upper limit in only 4 patients. Bimodal blood-flow distributions containing low VA/Q units were observed at some point in 24 of 26 subjects, but occurrence was variable, and in only one third of all measurements was bimodality found. Analysis of variance showed that 70 to 75% of the total variance of log SD was due to intersubject differences, about 20% was due to random changes over time, and the remaining 7 to 9% was not explained by either and was due mostly to experimental error. Arterial PO2 measured 3 times in each subject was inversely related to log SDQ (r = 0.76), but only 60% of the variance in PaO2 was explained by VA/Q mismatch, the rest being due presumably to variation in mixed venous PO2 and similar extrapulmonary factors.(ABSTRACT TRUNCATED AT 250 WORDS)

Asthma

No influence of acetylcysteine on gas exchange and spirometry in chronic asthma.

Non-smoking patients (n:25) with stable symptomatic asthma were investigated with regard to the pulmonary effects of N-acetylcysteine (NAC), peroral dose 200 mg three times daily, in a crossover double-blind study. They were studied once a week for 9 weeks, with a run-in period and periods with NAC and placebo (3 weeks each). Functional residual capacity and specific airway resistance were 19 and 53% larger, respectively, and forced expiratory variables (FEV%, MEF25) were 20 and 53% lower than reference values. Distribution of ventilation-perfusion ratios (VA/Q), assessed by multiple inert gas elimination technique with peripheral venous sampling, was abnormal, although arterial PO2 and PCO2 were within normal limits. NAC medication had no effect on any spirometric, lung mechanic or gas exchange variable, nor on the frequency of pulmonary symptoms.

Acetylcysteine

Effects of short-term exposure to ambient nitrogen dioxide concentrations on human bronchial reactivity and lung function.

Eight normal and 8 asthmatic subjects were exposed to NO2 in a modified body box for plethysmography during 20 min at 0,230,460 and 910 micrograms/m3 on 4 separate days. Bronchial reactivity (histamine inhalation test) was measured after exposure to air alone and to 910 micrograms/m3NO2. Airway resistance (Raw), thoracic gas volume (TGV) and specific airway resistance (SRaw) were measured before, during and after exposure. The bronchial reactivity of the asthmatic subjects increased significantly (p = 0.04) by 20 min exposure to 910 micrograms/m3 NO2. In the non-asthmatic group the airway resistance increased significantly (p = 0.03) after 20 min exposure to 460 micrograms/m3 NO2 and decreased significantly (p = 0.01) after 20 min exposure to 910 micrograms/m3 NO2. In the asthmatic group the trend in airway resistance was the same but not statistically significant. In the latter group TGV was significantly decreased (p = 0.02) during exposure to 910 micrograms/m3 NO2. Short term NO2-exposure in concentrations even below 1000 micrograms/m3 seems to have effects on human bronchial reactivity and lung function.

Adolescent