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Propagation velocity profile in a cross-section of a cardiac muscle bundle from PSpice simulation
BACKGROUND: The effect of depth on propagation velocity within a bundle of cardiac muscle fibers is likely to be an important factor in the genesis of some heart arrhythmias. MODEL AND METHODS: The velocity profile of simulated action potentials propagated down a bundle of parallel cardiac muscle fi...
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Formato: | Texto |
Lenguaje: | English |
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BioMed Central
2006
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1578564/ https://www.ncbi.nlm.nih.gov/pubmed/16911777 http://dx.doi.org/10.1186/1742-4682-3-29 |
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author | Sperelakis, Nicholas Ramasamy, Lakshminarayanan |
author_facet | Sperelakis, Nicholas Ramasamy, Lakshminarayanan |
author_sort | Sperelakis, Nicholas |
collection | PubMed |
description | BACKGROUND: The effect of depth on propagation velocity within a bundle of cardiac muscle fibers is likely to be an important factor in the genesis of some heart arrhythmias. MODEL AND METHODS: The velocity profile of simulated action potentials propagated down a bundle of parallel cardiac muscle fibers was examined in a cross-section of the bundle using a PSpice model. The model (20 × 10) consisted of 20 chains in parallel, each chain being 10 cells in length. All 20 chains were stimulated simultaneously at the left end of the bundle using rectangular current pulses (0.25 nA, 0.25 ms duration) applied intracellularly. The simulated bundle was symmetrical at the top and bottom (including two grounds), and voltage markers were placed intracellularly only in cells 1, 5 and 10 of each chain to limit the total number of traces to 60. All electrical parameters were standard values; the variables were (1) the number of longitudinal gap-junction (G-j) channels (0, 1, 10, 100), (2) the longitudinal resistance between the parallel chains (R(ol2)) (reflecting the closeness of the packing of the chains), and (3) the bundle termination resistance at the two ends of the bundle (R(BT)). The standard values for R(ol2 )and R(BT )were 200 KΩ. RESULTS: The velocity profile was bell-shaped when there was 0 or only 1 gj-channel. With standard R(ol2 )and R(BT )values, the velocity at the surface of the bundle (θ(1 )and θ(20)) was more than double (2.15 ×) that at the core of the bundle (θ(10), θ(11)). This surface:core ratio of velocities was dependent on the values of R(ol2 )and R(BT). When R(ol2 )was lowered 10-fold, θ(1 )increased slightly and θ(2)decreased slightly. When there were 100 gj-channels, the velocity profile was flat, i.e. the velocity at the core was about the same as that at the surface. Both velocities were more than 10-fold higher than in the absence of gj-channels. Varying R(ol2 )and R(BT )had almost no effect. When there were 10 gj-channels, the cross-sectional velocity profile was bullet-shaped, but with a low surface/core ratio, with standard R(ol2 )and R(BT )values. CONCLUSION: When there were no or few gj-channels (0 or 1), the profile was bell-shaped with the core velocity less than half that at the surface. In contrast, when there were many gj-channels (100), the profile was flat. Therefore, when some gj-channels close under pathophysiological conditions, this marked velocity profile could contribute to the genesis of arrhythmias. |
format | Text |
id | pubmed-1578564 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2006 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-15785642006-10-02 Propagation velocity profile in a cross-section of a cardiac muscle bundle from PSpice simulation Sperelakis, Nicholas Ramasamy, Lakshminarayanan Theor Biol Med Model Research BACKGROUND: The effect of depth on propagation velocity within a bundle of cardiac muscle fibers is likely to be an important factor in the genesis of some heart arrhythmias. MODEL AND METHODS: The velocity profile of simulated action potentials propagated down a bundle of parallel cardiac muscle fibers was examined in a cross-section of the bundle using a PSpice model. The model (20 × 10) consisted of 20 chains in parallel, each chain being 10 cells in length. All 20 chains were stimulated simultaneously at the left end of the bundle using rectangular current pulses (0.25 nA, 0.25 ms duration) applied intracellularly. The simulated bundle was symmetrical at the top and bottom (including two grounds), and voltage markers were placed intracellularly only in cells 1, 5 and 10 of each chain to limit the total number of traces to 60. All electrical parameters were standard values; the variables were (1) the number of longitudinal gap-junction (G-j) channels (0, 1, 10, 100), (2) the longitudinal resistance between the parallel chains (R(ol2)) (reflecting the closeness of the packing of the chains), and (3) the bundle termination resistance at the two ends of the bundle (R(BT)). The standard values for R(ol2 )and R(BT )were 200 KΩ. RESULTS: The velocity profile was bell-shaped when there was 0 or only 1 gj-channel. With standard R(ol2 )and R(BT )values, the velocity at the surface of the bundle (θ(1 )and θ(20)) was more than double (2.15 ×) that at the core of the bundle (θ(10), θ(11)). This surface:core ratio of velocities was dependent on the values of R(ol2 )and R(BT). When R(ol2 )was lowered 10-fold, θ(1 )increased slightly and θ(2)decreased slightly. When there were 100 gj-channels, the velocity profile was flat, i.e. the velocity at the core was about the same as that at the surface. Both velocities were more than 10-fold higher than in the absence of gj-channels. Varying R(ol2 )and R(BT )had almost no effect. When there were 10 gj-channels, the cross-sectional velocity profile was bullet-shaped, but with a low surface/core ratio, with standard R(ol2 )and R(BT )values. CONCLUSION: When there were no or few gj-channels (0 or 1), the profile was bell-shaped with the core velocity less than half that at the surface. In contrast, when there were many gj-channels (100), the profile was flat. Therefore, when some gj-channels close under pathophysiological conditions, this marked velocity profile could contribute to the genesis of arrhythmias. BioMed Central 2006-08-15 /pmc/articles/PMC1578564/ /pubmed/16911777 http://dx.doi.org/10.1186/1742-4682-3-29 Text en Copyright © 2006 Sperelakis and Ramasamy; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 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. |
spellingShingle | Research Sperelakis, Nicholas Ramasamy, Lakshminarayanan Propagation velocity profile in a cross-section of a cardiac muscle bundle from PSpice simulation |
title | Propagation velocity profile in a cross-section of a cardiac muscle bundle from PSpice simulation |
title_full | Propagation velocity profile in a cross-section of a cardiac muscle bundle from PSpice simulation |
title_fullStr | Propagation velocity profile in a cross-section of a cardiac muscle bundle from PSpice simulation |
title_full_unstemmed | Propagation velocity profile in a cross-section of a cardiac muscle bundle from PSpice simulation |
title_short | Propagation velocity profile in a cross-section of a cardiac muscle bundle from PSpice simulation |
title_sort | propagation velocity profile in a cross-section of a cardiac muscle bundle from pspice simulation |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1578564/ https://www.ncbi.nlm.nih.gov/pubmed/16911777 http://dx.doi.org/10.1186/1742-4682-3-29 |
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