Abstract:
Propagation of the action potential in the real heart is
direction-dependent (anisotropic).
We propose two general physical models explaining this anisotropy on the
cellular level. The first, “delay” model
takes into account the frequency of the cell–cell transitions
in different directions of propagation, assuming each transition
requires some small time interval.
The second model relies on the assumption that the action potential
transmits to the next cell
only from the area at the pole of the previous cell.
We estimated parameters of both models by doing optical mapping and
fluorescent staining
of cardiac cell samples grown on polymer fiber substrate.
Both models gave reasonable estimations, but predicted different behavior
of anisotropy ratio (ratio of largest and smallest wave velocities)
after addition of sodium channels supressor like lidocaine.
The results of the experiment on lidocaine effect on anisotropy ratio
was in favor of the first, “delay” model.
Estimated average cell–cell transition delay was
$240\pm80\,\mu$s, which is close to the characteristic values of synaptic
delay.
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