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The present study was undertaken to examine propagation in long single chains, in which the cells were connected by varying numbers of gj-channels, and to compare the propagation velocity with the measured cable properties, such as the length constant ( λ). Transverse propagation also occurred by the same EF mechanism between adjacent parallel chains that were closely packed. This EF action is accentuated when the junctional membranes contain fast Na + channels at a higher density than that in the surface sarcolemma. The mechanism proposed was the relatively large electric field (EF) that develops in the narrow junctional clefts when the prejunctional membrane fires an AP. Propagation of excitation occurred at near-physiological speeds even when there were no gj-channels connecting between the longitudinally-oriented cells. In previous studies on simulated myocardial cells, propagation of action potentials (APs) was examined in short chains of cells (e.g., 10 cells long) and in 2-dimensional sheets (e.g., 10 × 10 and 20 × 10), with the number of gj-channels varied from zero to 10,000. The PSpice simulation studies suggest that too many gj-channels (e.g., more than 100 channels per junction) causes the propagation velocity to exceed the physiological range. Although the presence of gj-channels is not essential for propagation of excitation in the heart, when hearts do contain gj-channels, propagation velocity is speeded up. In biological studies on connexon43 knockout mice, absent in gj-channels in their hearts, propagation velocity was only slowed and not blocked. For a 10 nm (100 Å) cleft width and 50 % of the I Na channels located in the junctional membranes, they found that conduction still occurred at a velocity of about 20 cm/sec when cell coupling was reduced to 10 % of normal and at about 10 cm/sec when coupling was only 1 % of normal. determined how conduction velocity varied with the fraction of fast I Na channels located in the junctional membranes. In a simulation study of cardiac muscle, Kucera et al.
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The fact that the junctional membranes (i.e., the intercalated disks) have a higher concentration (density) of fast Na + channels than the surface sarcolemma should cause them to be more excitable than the surface membrane. As was stated in the 1977 paper of Sperelakis and Mann, for the EF mechanism to work successfully, the junctional membrane must be more excitable than the contiguous surface sarcolemma. This has been demonstrated to be possible in theoretical and modeling studies by Sperelakis and colleagues, and has been confirmed by other laboratories. Successful transmission of excitation from one myocardial cell to the next contiguous cell can occur without the necessity of gj-channels between the cells. θ ov became very non-physiological at 300 gj-channels or higher. The effect of increasing the number of gj-channels on increasing λ was relatively small compared to the larger effect on θ ov. When there were many gj-channels (e.g., 300, 1000, 3000), there was an exponential decay of voltage on either side of the injected cell, with the length constant ( λ) increasing at higher numbers of gj-channels.
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When there were no or only few gj-channels (namely, 0, 10, or 30), the voltage change (ΔV m) in the two contiguous cells (#50 & #52) to the cell injected with current (#51) was nearly zero, i.e., there was a sharp discontinuity in voltage between the adjacent cells. The end-effect was more pronounced at longer chain lengths and at greater number of gj-channels. Increasing the number of gj-channels produced an increase in θ ov and caused the firing order to become more uniform. In contrast, when the local-circuit current mechanism was dominant (100 gj-channels or more), θ ov was slightly slowed with lengthening of the chain.
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There seems to be no simple explanation for this phenomenon. When the electric field (EF) mechanism was dominant (0, 1, and 10 gj-channels), the longer the chain length, the faster the overall velocity ( θ ov). Simulations were carried out using the PSpice program as previously described.