About this Journal Submit a Manuscript Table of Contents
Journal of Allergy
Volume 2012 (2012), Article ID 156909, 5 pages
http://dx.doi.org/10.1155/2012/156909
Review Article

Accumulating Evidence for Increased Velocity of Airway Smooth Muscle Shortening in Asthmatic Airway Hyperresponsiveness

1Meakins-Christie Laboratories, McGill University, 3626 St. Urbain Street, Montreal, QC, Canada H2X 2P2
2Department of Medicine, McGill University, 687 Pine Avenue, Montreal, QC, Canada H3A 1A1
3Department of Biomedical Engineering, McGill University, 3775 University Street, Montreal, QC, Canada H3A 2B4
4Department of Physiology, McGill University, 3655 Promenade Sir William Osler, Montreal, QC, Canada H3G 1Y6

Received 31 August 2012; Accepted 6 December 2012

Academic Editor: Ynuk Bossé

Copyright © 2012 Gijs Ijpma et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

It remains unclear whether airway smooth muscle (ASM) mechanics is altered in asthma. While efforts have originally focussed on contractile force, some evidence points to an increased velocity of shortening. A greater rate of airway renarrowing after a deep inspiration has been reported in asthmatics compared to controls, which could result from a shortening velocity increase. In addition, we have recently shown in rats that increased shortening velocity correlates with increased muscle shortening, without increasing muscle force. Nonetheless, establishing whether or not asthmatic ASM shortens faster than that of normal subjects remains problematic. Endobronchial biopsies provide excellent tissue samples because the patients are well characterized, but the size of the samples allows only cell level experiments. Whole human lungs from transplant programs suffer primarily from poor patient characterization, leading to high variability. ASM from several animal models of asthma has shown increased shortening velocity, but it is unclear whether this is representative of human asthma. Several candidates have been suggested as responsible for increased shortening velocity in asthma, such as alterations in contractile protein expression or changes in the contractile apparatus structure. There is no doubt that more remains to be learned about the role of shortening velocity in asthma.