Friction in airway smooth muscle: mechanism, latch and implications
in asthma.
Fredberg, J. J., K. A. Jones, Madhavi Nathan, S Raboudi, Y. S.
Prakash, S. A. Shore, J. P. Butler, G. C. Sieck.
Department of Environmental Health, Harvard School of Public
Health, Boston, MA, Department of Anesthesiology and Department of
Physiology and Biophysics, Mayo Clinic, Rochester, MN
APStracts 3:0453A, 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 hE where E is the tissue stiffness defined
by the slope of the resulting force vs. displacement loop and h 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 crossbridge 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 crossbridge 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 asthmatics to reverse spontaneous airways obstruction
with a deep inspiration.
Received 17 April 1996; accepted in final form 9 September 1996.
APS Manuscript Number A366-6.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 5 November 1996