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This Article Full Text Full Text (PDF) All Versions of this Article: 297/2/L362    most recent 00095.2009v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Bates, J. H. T. Articles by Lauzon, A. -M. Search for Related Content PubMed PubMed Citation Articles by Bates, J. H. T. Articles by Lauzon, A. -M.

Transient oscillatory force-length behavior of activated airway smooth muscle

¹Vermont Lung Center, University of Vermont College of Medicine, Burlington, Vermont; ²Meakins-Christie Laboratories, McGill University, Montreal, Quebec, Canada; ³Department of Mathematics, University of Auckland, Auckland, New Zealand; and ⁴Division of Sleep Medicine, University of Pennsylvania, Philadelphia, Pennsylvania

Submitted 23 March 2009 ; accepted in final form 11 June 2009

Airway smooth muscle (ASM) is cyclically stretched during breathing, even in the active state, yet the factors determining its dynamic force-length behavior remain incompletely understood. We developed a model of the activated ASM strip and compared its behavior to that observed in strips of rat trachealis muscle stimulated with methacholine. The model consists of a nonlinear viscoelastic element (Kelvin body) in series with a force generator obeying the Hill force-velocity relationship. Isometric force in the model is proportional to the number of bound crossbridges, the attachment of which follows first-order kinetics. Crossbridges detach at a rate proportional to the rate of change of muscle length. The model accurately accounts for the experimentally observed transient and steady-state oscillatory force-length behavior of both passive and activated ASM. However, the model does not predict the sustained decrement in isometric force seen when activated strips of ASM are subjected briefly to large stretches. We speculate that this force decrement reflects some mechanism unrelated to the cycling of crossbridges, and which may be involved in the reversal of bronchoconstriction induced by a deep inflation of the lungs in vivo.

crossbridge kinetics; viscoelasticity; deep lung inflation; computational model; rat trachealis; deep inspiration