Published ahead of print on July 29, 2005, doi:10.1165/rcmb.2005-0183OC Am. J. Respir. Cell Mol. Biol., Volume 33, Number 5, November 2005, 500-504 A more recent version of this article appeared on November 1, 2005
Submitted on May 13, 2005 The Role of Airway Smooth Muscle During an Attack of Asthma Simulated in vitroBrent E McParland1,1 Department of Medicine, University of British Columbia, Vancouver, BC, Canada; The James Hogg iCAPTURE Center for Cardiovascular and Pulmonary Research, University of British Columbia, St. Paul's Hospital/Providence Health Care, Vancouver, BC, Canada, 2 The James Hogg iCAPTURE Center for Cardiovascular and Pulmonary Research, University of British Columbia, St. Paul's Hospital/Providence Health Care, Vancouver, BC, Canada, 3 Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, BC, Canada; The James Hogg iCAPTURE Center for Cardiovascular and Pulmonary Research, University of British Columbia, St. Paul's Hospital/Providence Health Care, Vancouver, BC, Canada * To whom correspondence should be addressed. E-mail: cseow{at}mrl.ubc.ca.
Rationale: Excessive narrowing of airways in response to contractile agonists is a characteristic feature of asthma. We hypothesized that airway smooth muscle (ASM) adaptation to short lengths could contribute to exaggerated airway narrowing during an acute attack of asthma by allowing the muscle to regain its ability to generate maximal force at a shortened length. To test this hypothesis we mimicked, in vitro, the sequence of contractile events that would occur during a spontaneous attack of asthma. Methods: Trachealis muscle was challenged with carbachol (300 nM, submaximal dose) and allowed to shorten to ~ half of its original length. After 30 minutes of adaptation at the shortened length in the presence of carbachol, muscle force, amount and rate of shortening in response to electrical stimulation were compared to corresponding values obtained from control experiments during which the ASM was not adapted to the short length. Results: After adaptation at the shortened length the developed force, amount and rate of shortening increased by 1.93±0.08, 1.57±0.12, and 1.75±0.2 fold, respectively. Conclusion: Shortening of ASM in response to contractile agonists can lead to adaptation of the muscle to the shortened length that in turn can result in further shortening and the potential for airway closure.
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