Literature DB >> 10515404

Dynamic hyperinflation and flow limitation during methacholine-induced bronchoconstriction in asthma.

C Tantucci1, M Ellaffi, A Duguet, M Zelter, T Similowski, J P Derenne, J Milic-Emili.   

Abstract

Although persistent activation of the inspiratory muscles and narrowing of the glottic aperture during expiration have been indicated as relevant mechanisms leading to dynamic hyperinflation in acute asthma, expiratory flow limitation (EFL) has recently been proposed as a possible triggering factor for increasing endexpiratory lung volume (EELV). To establish whether the attainment of maximal flow rate during tidal expiration could elicit dynamic elevation of EELV, breathing pattern, change in EELV by measuring inspiratory capacity (IC) and occurrence of EFL by the negative expiratory pressure (NEP) method were monitored in 10 stable asthmatic subjects during methacholine-induced, progressive bronchoconstriction in seated position. Change in dyspnoea was scored using the Borg scale. At maximum response forced expiratory volume in one second (FEV1) fell on average by 45+/-2% (p<0.001 versus control), while IC decreased 29+/-2%, (by 0.89+/-0.07 L, (p<0.01 versus control)). Only 2 subjects exhibited EFL at the end of methacholine challenge. In 7 subjects EELV started to increase before the occurrence of EFL. Dyspnoea, which increased from 0.2+/-0.1 to 5.5+/-1.0 (Borg scale) at maximum response (p<0.001), was significantly related to the level of bronchoconstriction as assessed by change in (delta)FEV1 (r=0.72; p<0.001) and to dynamic hyperinflation as measured by deltaIC (r=0.50; p<0.001). However, for both deltaFEV1 and deltaIC the slope of the relationship with increasing dyspnoea was highly variable among the subjects. It is concluded that in acute methacholine-induced bronchoconstriction, dynamic hyperinflation may occur in the absence of expiratory flow limitation and that expiratory flow limitation does not represent the triggering factor to generate dynamic hyperinflation. In these circumstances, dyspnoea appears to be related to the increase in end-expiratory lung volume and not to the onset of expiratory flow limitation.

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Year:  1999        PMID: 10515404     DOI: 10.1183/09031936.99.142

Source DB:  PubMed          Journal:  Eur Respir J        ISSN: 0903-1936            Impact factor:   16.671


  15 in total

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3.  Regional pulmonary perfusion, inflation, and ventilation defects in bronchoconstricted patients with asthma.

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4.  Hypoxic Pulmonary Vasoconstriction Does Not Explain All Regional Perfusion Redistribution in Asthma.

Authors:  Vanessa J Kelly; Kathryn A Hibbert; Puja Kohli; Mamary Kone; Elliot E Greenblatt; Jose G Venegas; Tilo Winkler; R Scott Harris
Journal:  Am J Respir Crit Care Med       Date:  2017-10-01       Impact factor: 21.405

5.  Effects of altered airway function on exercise ventilation in asthmatic adults.

Authors:  Matthew J Rossman; Susan Nader; Dustin Berry; Francesca Orsini; Andrew Klansky; Hans Christian Haverkamp
Journal:  Med Sci Sports Exerc       Date:  2014-06       Impact factor: 5.411

6.  Chemokines mediate ethanol-induced exacerbations of murine cockroach allergen asthma.

Authors:  J C Bouchard; D R Beal; J Kim; L J Vaickus; D G Remick
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Review 7.  Diagnostic Insights from Plethysmographic Alveolar Pressure Assessed during Spontaneous Breathing in COPD Patients.

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8.  Methods for Assessing Expiratory Flow Limitation during Tidal Breathing in COPD Patients.

Authors:  Nickolaos G Koulouris; Georgios Kaltsakas; Anastasios F Palamidas; Sofia-Antiopi Gennimata
Journal:  Pulm Med       Date:  2012-09-02

9.  Vital capacity and inspiratory capacity as additional parameters to evaluate bronchodilator response in asthmatic patients: a cross sectional study.

Authors:  Karen S Azevedo; Ronir R Luiz; Patricia Rm Rocco; Marcus B Conde
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10.  Expiratory flow limitation definition, mechanisms, methods, and significance.

Authors:  Claudio Tantucci
Journal:  Pulm Med       Date:  2013-03-28
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