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Department of Environmental Health, Harvard School of Public Health, Boston, Massachsetts 02115; and Department of Anesthesiology and Department of Physiology and Biophysics, Mayo Clinic, Rochester, Minnesota 55905
Received 17 April 1996; accepted in final form 9 September 1996.
Fredberg, J. J., K. A. Jones, M. Nathan, S. Raboudi,
Y. S. Prakash, S. A. Shore, J. P. Butler, and G. C. Sieck. Friction in airway smooth muscle: mechanism, latch, and
implications in asthma. J. Appl.
Physiol. 81(6): 2703-2712, 1996.
In muscle,
active force and stiffness reflect numbers of actin-myosin interactions and shortening velocity reflects their turnover rates, but the molecular basis of mechanical friction is somewhat less clear. To
better characterize molecular mechanisms that govern mechanical friction, we measured the rate of mechanical energy dissipation and the
rate of actomyosin ATP utilization simultaneously in activated canine
airway smooth muscle subjected to small periodic stretches as occur in
breathing. The amplitude of the frictional stress is proportional to
E, where E is the tissue stiffness defined by the slope of the
resulting force vs. displacement loop and is the hysteresivity
defined by the fatness of that loop. From contractile stimulus onset,
the time course of frictional stress amplitude followed a biphasic
pattern that tracked that of the rate of actomyosin ATP consumption.
The time course of hysteresivity, however, followed a different
biphasic pattern that tracked that of shortening velocity. Taken
together with an analysis of mechanical energy storage and dissipation
in the cross-bridge cycle, these results indicate, first, that like
shortening velocity and the rate of actomyosin ATP utilization,
mechanical friction in airway smooth muscle is also governed by the
rate of cross-bridge cycling; second, that changes in cycling rate
associated with conversion of rapidly cycling cross bridges to slowly
cycling latch bridges can be assessed from changes of hysteresivity of
the force vs. displacement loop; and third, that steady-state force
maintenance (latch) is a low-friction contractile state. This last
finding may account for the unique inability of asthmatic patients to reverse spontaneous airways obstruction with a deep inspiration.
hysteresis; resistance; shortening velocity; cross bridge
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H. Yuan, E. P. Ingenito, and B. Suki Dynamic properties of lung parenchyma: mechanical contributions of fiber network and interstitial cells J Appl Physiol, November 1, 1997; 83(5): 1420 - 1431. [Abstract] [Full Text] [PDF]
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X. Shen, M. F. Wu, R. S. Tepper, and S. J. Gunst Pharmacological modulation of the mechanical response of airway smooth muscle to length oscillation J Appl Physiol, September 1, 1997; 83(3): 739 - 745. [Abstract] [Full Text] [PDF]
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J. Solway and J. J. Fredberg Perhaps Airway Smooth Muscle Dysfunction Contributes to Asthmatic Bronchial Hyperresponsiveness After All Am. J. Respir. Cell Mol. Biol., August 1, 1997; 17(2): 144 - 146. [Full Text]
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R. K. Lambert and P. D. Pare Lung parenchymal shear modulus, airway wall remodeling, and bronchial hyperresponsiveness J Appl Physiol, July 1, 1997; 83(1): 140 - 147. [Abstract] [Full Text] [PDF]
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D. Stamenovic, Z. Liang, J. Chen, and N. Wang Effect of the cytoskeletal prestress on the mechanical impedance of cultured airway smooth muscle cells J Appl Physiol, April 1, 2002; 92(4): 1443 - 1450. [Abstract] [Full Text] [PDF]
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N. Wang, I. M. Tolic-Norrelykke, J. Chen, S. M. Mijailovich, J. P. Butler, J. J. Fredberg, and D. Stamenovic Cell prestress. I. Stiffness and prestress are closely associated in adherent contractile cells Am J Physiol Cell Physiol, March 1, 2002; 282(3): C606 - C616. [Abstract] [Full Text] [PDF]
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