Propagated repolarization of simulated action potentials in cardiac muscle and smooth muscle
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Propagated repolarization of simulated action potentials in cardiac muscle and smooth muscle Nicholas Sperelakis*1, Lakshminarayanan Ramasamy2 and Bijoy Kalloor2 Address: 1Dept. of Molecular & Cellular Physiology University of Cincinnati College of Medicine Cincinnati, OH 45267-0576 USA and 2Dept. of Electrical Computer Engineering and Computer Science University of Cincinnati College of Engineering Cincinnati, OH 45219 USA Email: Nicholas Sperelakis* - [email protected]; Lakshminarayanan Ramasamy - [email protected]; Bijoy Kalloor - [email protected] * Corresponding author
Published: 14 February 2005 Theoretical Biology and Medical Modelling 2005, 2:5
doi:10.1186/1742-4682-2-5
Received: 30 November 2004 Accepted: 14 February 2005
This article is available from: http://www.tbiomed.com/content/2/1/5 © 2005 Sperelakis et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Propagated RepolarizationSimulated Action PotentialsPSpice simulationsElectric Field mechanismCardiac electrophysiology
Abstract Background: Propagation of repolarization is a phenomenon that occurs in cardiac muscle. We wanted to test whether this phenomenon would also occur in our model of simulated action potentials (APs) of cardiac muscle (CM) and smooth muscle (SM) generated with the PSpice program. Methods: A linear chain of 5 cells was used, with intracellular stimulation of cell #1 for the antegrade propagation and of cell #5 for the retrograde propagation. The hyperpolarizing stimulus parameters applied for termination of the AP in cell #5 were varied over a wide range in order to generate strength / duration (S/D) curves. Because it was not possible to insert a second "black box" (voltage-controlled current source) into the basic units representing segments of excitable membrane that would allow the cells to respond to small hyperpolarizing voltages, gap-junction (g.j.) channels had to be inserted between the cells, represented by inserting a resistor (Rgj) across the four cell junctions. Results: Application of sufficient hyperpolarizing current to cell #5 to bring its membrane potential (Vm) to within the range of the sigmoidal curve of the Na+ conductance (CM) or Ca++ conductance (SM) terminated the AP in cell #5 in an all-or-none fashion. If there were no g.j. channels (Rgj = ∞), then only cell #5 repolarized to its stable resting potential (RP; -80 mV for CM and -55 mV for SM). The positive junctional cleft potential (VJC) produced only a small hyperpolarization of cell #4. However, if many g.j. channels were inserted, more hyperpolarizing current was required (for a constant duration) to repolarize cell #5, but repolarization then propagated into cells 4, 3, 2, and 1. When duration of the pulses was varied, a typical S/D curve, ch
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