From the Cardiology Section of the Department of Medicine and the
Department of Physiology, Gazes Cardiac Research Institute Medical University
of South Carolina and the Veterans Administration Medical Center, Charleston
(M.R.Z., K.R., J.M.B., M.K., B.A.C., G.C.), and the Department of
Bioengineering, Clemson University, Clemson (M.R.Z., K.R., M.K.C., V.G.,
G.C.), SC.
Background—The purpose of this study
was to determine whether changes in the constitutive properties of the
cardiac muscle cell play a causative role in the development of
diastolic dysfunction.
Methods and Results—Cardiocytes from normal and
pressure-hypertrophied cats were embedded in an agarose gel, placed on
a stretching device, and subjected to a change in stress (
Conclusions—Changes in viscous damping and myofilament activation
in combination may cause pressure-hypertrophied cardiocytes to
resist changes in shape during diastole and contribute to
diastolic dysfunction.
© 1998 American Heart Association, Inc.
Basic Science Reports
Constitutive Properties of Adult Mammalian Cardiac Muscle Cells
), and
resultant changes in cell strain (
) were measured. These
measurements were used to examine the passive elastic spring, viscous
damping, and myofilament activation. The passive elastic spring was
assessed in protocol A by increasing the on the agarose gel at a
constant rate to define the cardiocyte -versus-
relationship. Viscous damping was assessed in protocol B from the loop
area between the cardiocyte -versus- relationship during
an increase and then a decrease in . In both protocols, myofilament
activation was minimized by a reduction in
[Ca2+]i. Myofilament activation effects were
assessed in protocol C by defining cardiocyte versus
during an increase in with physiological
[Ca2+]i. In protocol A, the
cardiocyte -versus- relationship was similar in normal
and hypertrophied cells. In protocol B, the loop area was greater in
hypertrophied than normal cardiocytes. In protocol C, the
-versus- relation in hypertrophied cardiocytes was
shifted to the left compared with normal cells.
Key Words: hypertrophy • myocytes • diastole • elasticity • heart failure
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