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Airway obstruction in asthma: does the response to a deep inspiration matter?

Authors
Publisher
BioMed Central
Publication Date
Source
PMC
Keywords
  • Commentary
Disciplines
  • Medicine

Abstract

com m entary review reports research article ASM = airway smooth muscle; DI = deep inspiration. Available online http://respiratory-research.com/content/2/5/273 Introduction Smooth muscle surrounding the airway shortens when it is activated, and as the muscle shortens the airway narrows. In normal individuals subjected to challenge with non-spe- cific contractile agonists, the extent of airway narrowing is limited and this limited response is reflected by a plateau of the dose–response curve corresponding to only modest levels of airway narrowing. Asthmatic individuals, by con- trast, are hyperresponsive. Compared with the response in the normal subject, the plateau of the dose–response curve in the asthmatic is markedly elevated, or abolished altogether, indicating that airway smooth muscle (ASM) shortening is limited only by airway closure. It is the marked elevation of this plateau, or its absence altogether, that makes asthma such a serious disease [1]. It is presently unclear if the elevated or absent plateau in asthma is attributable to fundamental changes in the phenotype of the smooth muscle, structural and/or mechanical changes in the non-contractile elements within the airway wall, or alterations in the mechanical coupling of the airway wall to the surrounding lung parenchyma. Current evidence suggests that ASM has the force-gener- ating capacity to close every airway, even in the normal lung [2,3]. Given the modest level of the plateau response in the normal lung, it follows that there must be mecha- nisms at work that act to limit smooth muscle shortening. Furthermore, it follows that those mechanisms might become compromised in the asthmatic lung, thereby accounting for an elevated plateau. Might the response of the airway to a deep inspiration (DI) fit into this picture? Maximally activated ASM is subjected to time-varying mechanical strains associated with tidal lung inflations and spontaneous DIs. Consequently, acti- vated ASM must become equilibrated within a dyn

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