Mechanoelectric feedback has been described in isolated cells and intact ve
ntricular myocardium, but the mechanical stimulus that governs mechanosensi
tive channel activity in intact tissue is unknown. To study the interaction
of myocardial mechanics and electrophysiology in multiple dimensions, we u
sed a finite element model of the rabbit ventricles to simulate electrical
propagation through passively loaded myocardium. Electrical propagation was
simulated using the collocation-Galerkin finite element method. A stretch-
dependent current was added in parallel to the ionic currents in the Beeler
-Reuter ventricular action potential model. We investigated different mecha
nical coupling parameters to simulate stretch-dependent conductance modulat
ed by either fiber strain, cross-fiber strain, or a combination of the two.
In response to pressure loading, the conductance model governed by fiber s
train alone reproduced the epicardial decrease in action potential amplitud
e as observed in experimental preparations of the passively loaded rabbit h
eart. The model governed by only cross-cider strain reproduced the transmur
al gradient in action potential amplitude as observed in working canine hea
rt experiments, but failed to predict a sufficient decrease in amplitude at
the epicardium. Only the model governed by both fiber and cross-fiber stra
in reproduced the epicardial and transmural changes in action potential amp
litude similar to experimental observations. In addition, dispersion of act
ion potential duration nearly doubled with the same model. These results su
ggest that changes in action potential characteristics may be due not only
to length changes along the long axis direction of the myofiber, but also d
ue to deformation in the plane transverse to the fiber axis. The model prov
ides a framework for investigating how cellular biophysics affect the funct
ion of the intact ventricles. (C) 2001 Biomedical Engineering Society.