60 research outputs found
Tidal Volume Single Breath Washout of Two Tracer Gases - A Practical and Promising Lung Function Test
Small airway disease frequently occurs in chronic lung diseases and may cause ventilation inhomogeneity (VI), which can be assessed by washout tests of inert tracer gas. Using two tracer gases with unequal molar mass (MM) and diffusivity increases specificity for VI in different lung zones. Currently washout tests are underutilised due to the time and effort required for measurements. The aim of this study was to develop and validate a simple technique for a new tidal single breath washout test (SBW) of sulfur hexafluoride (SF(6)) and helium (He) using an ultrasonic flowmeter (USFM)
Reproducibility of exhaled nitric oxide in smokers and non-smokers: relevance for longitudinal studies
<p>Abstract</p> <p>Background</p> <p>Currently, there is much interest in measuring fractional exhaled nitric oxide (<b>FE<sub>NO</sub></b>) in populations. We evaluated the reproducibility of <b>FE<sub>NO </sub></b>in healthy subjects and determined the number of subjects necessary to carry out a longitudinal survey of <b>FE<sub>NO </sub></b>in a population containing smokers and non-smokers, based on the assessed reproducibility.</p> <p>Methods</p> <p>The reproducibility of <b>FE<sub>NO </sub></b>was examined in 18 healthy smokers and 21 non-smokers. <b>FE<sub>NO </sub></b>was assessed once at 9 AM on five consecutive days; in the last day this measurement was repeated at 2 PM. Respiratory symptoms and medical history were assessed by questionnaire. The within- and between-session repeatability of <b>FE<sub>NO </sub></b>and log-transformed <b>FE<sub>NO </sub></b>was described. The power of a longitudinal study based on a relative increase in <b>FE<sub>NO </sub></b>was estimated using a bilateral t-test of the log-transformed <b>FE<sub>NO </sub></b>using the between-session variance of the assay.</p> <p>Results</p> <p><b>FE<sub>NO </sub></b>measurements were highly reproducible throughout the study. <b>FE<sub>NO </sub></b>was significantly higher in males than females regardless of smoking status. <b>FE<sub>NO </sub></b>was positively associated with height (p < 0.001), gender (p < 0.034), smoking (p < 0.0001) and percent FEV<sub>1</sub>/FVC (p < 0.001) but not with age (p = 0.987). The between-session standard deviation was roughly constant on the log scale. Assuming the between-session standard deviation is equal to its longitudinal equivalent, either 111 or 29 subjects would be necessary to achieve an 80% power in detecting a 3% or a 10% increase in <b>FE<sub>NO </sub></b>respectively.</p> <p>Conclusion</p> <p>The good reproducibility of <b>FE<sub>NO </sub></b>is not influenced by gender or smoking habits. In a well controlled, longitudinal study it should allow detecting even small increases in <b>FE<sub>NO </sub></b>with a reasonable population size.</p
Capability of a neck worn device to measure sleep/wake, airway position, and differentiate benign snoring from obstructive sleep apnea
Effect of acetylcholine aerosols on diffusing capacity in asthmatic and normal subjects.
Mechanisms of chronic airway obstruction in smokers
AbstractStudies over the past few decades have showed a clear association between cigarette smoking and the development of chronic airway obstruction. Yet, only a minority of smokers is affected so that in many, even heavy, smokers, pulmonary function remains within normal limits. While carcinogens have been well characterized, there is only limited information about the constituents of cigarette smoke responsible for inducing chronic airway obstruction. In addition, the associated risks factors for airway obstruction in smokers have not been totally identified. The present paper is a review of the recently accumulated facts concerning the intimate action of cigarette smoke at the level of large and small airways and lung parenchyma. The role of classical inflammatory cells such as neutrophils and alveolar macrophages is reviewed, but emphasis is put on recent evidence indicating the involvement of CD8+ T-lymphocytes and possibly eosinophils in the genesis of the structural changes leading to airways obstruction. The mechanisms by which airway inflammation and remodelling cause airway narrowing and airflow limitation are discussed, along with the associated loss of lung elasticity secondary to destructive emphysema. Other biological, epidemiological, physiopathological, and clinical aspects are analyzed, stressing such fundamental aspects as the defence mechanisms, the morpho-functional correlations, the identification of susceptible smokers, and the early detection of airway obstruction, both in specialized laboratories and in primary care
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