![]() We have modeled APs in cardiac muscle using the PSpice program for circuit design and analysis, and we have corroborated our earlier reports that the EF developed in the junctional cleft is sufficiently large to allow the transfer of excitation without the requirement for a gap junction. Propagation in the heart still occurs in connexin-43 and Cx40 knockout mice, but it is slowed, as predicted by our PSpice simulation study. Fast Na + channels are localized in the junctional membranes of the intercalated disks in cardiac muscle, a requirement for the EF mechanism to work. Propagation has been shown to be discontinuous (or saltatory) in cardiac muscle. This results in a staircase-shaped propagation, the surface sarcolemma of each cell firing almost simultaneously. The total propagation time consists primarily of the summed junctional delays. This results in excitation of the postjunctional cell after a brief junctional delay. In a computer simulation study of propagation in cardiac muscle, it was shown that the electric field (EF) generated in the narrow junctional clefts when the prejunctional membrane fires an action potential (AP) depolarizes the postjunctional membrane to its threshold. There are no low-resistance connections between the cells in several different cardiac muscle and smooth muscle preparations. 1000 or 10,000), the transmission of excitation was produced by local-circuit current flow from one cell to the next through the gj-channels. 100 A) when the prejunctional membrane fires an AP. the negative junctional cleft potential, that is generated in the narrow junctional clefts (e.g. When there were no gj-channels, or only a few, the transmission of excitation between cells was produced by the electric field (EF), i.e. The velocity of propagation (θ, in cm/s) was calculated from the measured total propagation time (TPT, the time difference between when the AP rising phase of the first cell and the last cell crossed -20 mV, assuming a cell length of 150 μm. The shunt resistance across the junctions produced by the gj-channels (R gj) was varied from 100,000 M? (0 gj-channels) to 10,000 M? (1 gj-channel), to 1,000 M? (10 channels), to 100 M? (100 channels), and 10 M? (1000 channels). The propagation of complete APs was studied in a chain (strand) of 10 cardiac muscle cells, in which various numbers of gap-junction (gj) channels (assumed to be 100 pS each) were inserted across the cell junctions. This produced repolarization of the AP, not by activation of K + conductance, but by deactivation of the Na + conductance. This second BB effectively mimicked deactivation of the Na + channel conductance. We have now been able to repolarize the AP by inserting a second BB into the Na + leg of the basic units.
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