Home
For authors
Submission status

Archive
Archive (English)
Current
   Volumes 113-120
   Volumes 93-112
      Volume 112
      Volume 111
      Volume 110
      Volume 109
      Volume 108
      Volume 107
      Volume 106
      Volume 105
      Volume 104
      Volume 103
      Volume 102
      Volume 101
      Volume 100
      Volume 99
      Volume 98
      Volume 97
      Volume 96
      Volume 95
      Volume 94
      Volume 93
Search
VOLUME 100 (2014) | ISSUE 5 | PAGE 390
Two models of anisotropic propagation of cardiac excitation wave
DOI: 10.7868/S0370274X14170123
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 \mus, which is close to the characteristic values of synaptic delay.