Ischemia-Related Subcellular Redistribution of Sodium Channels Enhances the Proarrhythmic Effect of Class I Antiarrhythmic Drugs: A Simulation Study
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{"title"=>"Ischemia-Related Subcellular Redistribution of Sodium Channels Enhances the Proarrhythmic Effect of Class i Antiarrhythmic Drugs: A Simulation Study", "type"=>"journal", "authors"=>[{"first_name"=>"Kunichika", "last_name"=>"Tsumoto", "scopus_author_id"=>"56210378800"}, {"first_name"=>"Takashi", "last_name"=>"Ashihara", "scopus_author_id"=>"7005403360"}, {"first_name"=>"Ryo", "last_name"=>"Haraguchi", "scopus_author_id"=>"6603872547"}, {"first_name"=>"Kazuo", "last_name"=>"Nakazawa", "scopus_author_id"=>"55701780200"}, {"first_name"=>"Yoshihisa", "last_name"=>"Kurachi", "scopus_author_id"=>"7101623295"}], "year"=>2014, "source"=>"PLoS ONE", "identifiers"=>{"pui"=>"608759044", "sgr"=>"84942377560", "issn"=>"19326203", "pmid"=>"25279776", "scopus"=>"2-s2.0-84942377560", "doi"=>"10.1371/journal.pone.0109271"}, "id"=>"dd504d2e-3710-326c-8a7f-1d26d7272924", "abstract"=>"BACKGROUND: Cardiomyocytes located at the ischemic border zone of infarcted ventricle are accompanied by redistribution of gap junctions, which mediate electrical transmission between cardiomyocytes. This ischemic border zone provides an arrhythmogenic substrate. It was also shown that sodium (Na+) channels are redistributed within myocytes located in the ischemic border zone. However, the roles of the subcellular redistribution of Na+ channels in the arrhythmogenicity under ischemia remain unclear.\\n\\nMETHODS: Computer simulations of excitation conduction were performed in a myofiber model incorporating both subcellular Na+ channel redistribution and the electric field mechanism, taking into account the intercellular cleft potentials.\\n\\nRESULTS: We found in the myofiber model that the subcellular redistribution of the Na+ channels under myocardial ischemia, decreasing in Na+ channel expression of the lateral cell membrane of each myocyte, decreased the tissue excitability, resulting in conduction slowing even without any ischemia-related electrophysiological change. The conventional model (i.e., without the electric field mechanism) did not reproduce the conduction slowing caused by the subcellular Na+ channel redistribution. Furthermore, Na+ channel blockade with the coexistence of a non-ischemic zone with an ischemic border zone expanded the vulnerable period for reentrant tachyarrhythmias compared to the model without the ischemic border zone. Na+ channel blockade tended to cause unidirectional conduction block at sites near the ischemic border zone. Thus, such a unidirectional conduction block induced by a premature stimulus at sites near the ischemic border zone is associated with the initiation of reentrant tachyarrhythmias.\\n\\nCONCLUSIONS: Proarrhythmia of Na+ channel blockade in patients with old myocardial infarction might be partly attributable to the ischemia-related subcellular Na+ channel redistribution.", "link"=>"http://www.mendeley.com/research/ischemiarelated-subcellular-redistribution-sodium-channels-enhances-proarrhythmic-effect-class-i-ant", "reader_count"=>3, "reader_count_by_academic_status"=>{"Professor > Associate Professor"=>1, "Student > Ph. D. Student"=>1, "Student > Master"=>1}, "reader_count_by_user_role"=>{"Professor > Associate Professor"=>1, "Student > Ph. D. Student"=>1, "Student > Master"=>1}, "reader_count_by_subject_area"=>{"Agricultural and Biological Sciences"=>3}, "reader_count_by_subdiscipline"=>{"Agricultural and Biological Sciences"=>{"Agricultural and Biological Sciences"=>3}}, "group_count"=>0}

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Figshare

  • {"files"=>["https://ndownloader.figshare.com/files/1704523"], "description"=>"<p>(A) and (B), Relative ratios of CV (%CV) normalized by CV in the myocardial fiber with 50%<i>g</i><sub>Na,JM</sub> and 50%<i>g</i><sub>Na,LM</sub> as a function of %<i>g</i><sub>Na,JM</sub> or %<i>g</i><sub>Na,LM</sub> in the cleft (A) and non-cleft (B) models. (C), Peak values of post-junctional <i>I</i><sub>Na</sub> (post-<i>I</i><sub>Na,JM</sub>), pre-junctional <i>I</i><sub>Na</sub> (pre-<i>I</i><sub>Na,JM</sub>), and lateral <i>I</i><sub>Na</sub> (<i>I</i><sub>Na,LM</sub>) in a myocyte in the cleft model in which the Na<sup>+</sup> channels are fixed at 50%<i>g</i><sub>Na,JM</sub> with 50%<i>g</i><sub>Na,LM</sub>, 30%<i>g</i><sub>Na,LM</sub>, or 10%<i>g</i><sub>Na,LM</sub> (<i>left</i>) and at 50%<i>g</i><sub>Na,LM</sub> with 50%<i>g</i><sub>Na,JM</sub>, 30%<i>g</i><sub>Na,JM</sub>, or 10%<i>g</i><sub>Na,JM</sub> (<i>right</i>). (D), Peak values of post-<i>I</i><sub>Na,JM</sub>, pre-<i>I</i><sub>Na,JM</sub>, and <i>I</i><sub>Na,LM</sub> in a myocyte in the non-cleft model with 50%<i>g</i><sub>Na,JM</sub> and 50%<i>g</i><sub>Na,LM</sub>, 30%<i>g</i><sub>Na,LM</sub>, or 10%<i>g</i><sub>Na,LM</sub> (<i>left</i>), and 50%<i>g</i><sub>Na,LM</sub> with 50%<i>g</i><sub>Na,JM</sub>, 30%<i>g</i><sub>Na,JM</sub>, or 10%<i>g</i><sub>Na,JM</sub> (<i>right</i>). The peak values of <i>I</i><sub>Na</sub> in each membrane segment were measured in the middle of the myofiber.</p>", "links"=>[], "tags"=>["subcellular Na", "field mechanism", "intercellular cleft potentials.ResultsWe", "channel redistribution", "Sodium Channels Enhances", "myofiber model", "ischemic border zone", "subcellular redistribution", "channel blockade", "conduction block", "Simulation Study BackgroundCardiomyocytes"], "article_id"=>1193421, "categories"=>["Biological Sciences"], "users"=>["Kunichika Tsumoto", "Takashi Ashihara", "Ryo Haraguchi", "Kazuo Nakazawa", "Yoshihisa Kurachi"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0109271.g002", "stats"=>{"downloads"=>0, "page_views"=>23, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Conduction_velocities_and_changes_in_regional_I_Na_in_cardiomyocytes_in_each_myofiber_model_/1193421", "title"=>"Conduction velocities and changes in regional <i>I</i><sub>Na</sub> in cardiomyocytes in each myofiber model.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-10-03 02:54:28"}
  • {"files"=>["https://ndownloader.figshare.com/files/1704533"], "description"=>"<p>(A), Conduction velocity (CV) as a function of %<i>G</i><sub>Na</sub> block. Open circles with the dashed lines denote CV under AP alternans. The relationship between the excitation conduction mode and %<i>G</i><sub>Na</sub> block is represented by the bottom bars. SC, stable conduction; UC, unstable conduction (e.g., AP alternans, or 2∶1 or 3∶1 conduction); CB, complete conduction block. (B), Examples of AP propagation observed in NZ (i) and IBZ (ii) myofibers. (C)–(E), Examples of 2∶1 conduction by 55%<i>G</i><sub>Na</sub> block (C), 3∶1 conduction by 56% <i>G</i><sub>Na</sub> block (D), and complete conduction block by 60% <i>G</i><sub>Na</sub> block (E) in the IBZ.</p>", "links"=>[], "tags"=>["subcellular Na", "field mechanism", "intercellular cleft potentials.ResultsWe", "channel redistribution", "Sodium Channels Enhances", "myofiber model", "ischemic border zone", "subcellular redistribution", "channel blockade", "conduction block", "Simulation Study BackgroundCardiomyocytes"], "article_id"=>1193428, "categories"=>["Biological Sciences"], "users"=>["Kunichika Tsumoto", "Takashi Ashihara", "Ryo Haraguchi", "Kazuo Nakazawa", "Yoshihisa Kurachi"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0109271.g003", "stats"=>{"downloads"=>0, "page_views"=>13, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Destabilization_of_action_potential_propagation_by_Na_channel_blockade_/1193428", "title"=>"Destabilization of action potential propagation by Na<sup>+</sup> channel blockade.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-10-03 02:54:28"}
  • {"files"=>["https://ndownloader.figshare.com/files/1704521"], "description"=>"<p>(A), Schematic representation of a myocardial fiber comprising cylindrical 300 cells. (B) and (C), Schematic representations of the intercellular junction in the cleft (B) and non-cleft (C) models. (D), The AP of each membrane segment is represented by the modified Luo–Rudy dynamic (mLRd) ventricular myocyte model <a href=\"http://www.plosone.org/article/info:doi/10.1371/journal.pone.0109271#pone.0109271-Faber1\" target=\"_blank\">[24]</a>, <a href=\"http://www.plosone.org/article/info:doi/10.1371/journal.pone.0109271#pone.0109271-Suzuki1\" target=\"_blank\">[25]</a>. (E), Schematic representation of the myocardial ring comprising 900 cells (a), and the pacing protocol (b). <i>G</i><sub>g</sub>, gap junctional conductance; <i>G</i><sub>j</sub>, radial cleft conductance; <i>G</i><sub>d</sub>, axial cleft conductance.</p>", "links"=>[], "tags"=>["subcellular Na", "field mechanism", "intercellular cleft potentials.ResultsWe", "channel redistribution", "Sodium Channels Enhances", "myofiber model", "ischemic border zone", "subcellular redistribution", "channel blockade", "conduction block", "Simulation Study BackgroundCardiomyocytes"], "article_id"=>1193419, "categories"=>["Biological Sciences"], "users"=>["Kunichika Tsumoto", "Takashi Ashihara", "Ryo Haraguchi", "Kazuo Nakazawa", "Yoshihisa Kurachi"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0109271.g001", "stats"=>{"downloads"=>0, "page_views"=>14, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Cleft_and_non_cleft_models_of_myocardial_fibers_and_rings_/1193419", "title"=>"Cleft and non-cleft models of myocardial fibers and rings.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-10-03 02:54:28"}
  • {"files"=>["https://ndownloader.figshare.com/files/1704537"], "description"=>"<p>(A), Phase diagram of %<i>G</i><sub>Na</sub> block vs. S1–S2 interval showing proarrhythmic events under Na<sup>+</sup> channel blockade in the myocardial ring model. Right bar (control): responses to S2 stimulus in the myocardial ring constructed of only NZ myocytes under 50%<i>G</i><sub>Na</sub> block. (B), Examples of AP propagation in response to S1–S2 interval. Arrows and black short bars indicate the directions of AP propagation and entrance block, respectively.</p>", "links"=>[], "tags"=>["subcellular Na", "field mechanism", "intercellular cleft potentials.ResultsWe", "channel redistribution", "Sodium Channels Enhances", "myofiber model", "ischemic border zone", "subcellular redistribution", "channel blockade", "conduction block", "Simulation Study BackgroundCardiomyocytes"], "article_id"=>1193432, "categories"=>["Biological Sciences"], "users"=>["Kunichika Tsumoto", "Takashi Ashihara", "Ryo Haraguchi", "Kazuo Nakazawa", "Yoshihisa Kurachi"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0109271.g005", "stats"=>{"downloads"=>1, "page_views"=>24, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Reentry_induction_by_Na_channel_blockade_in_myocardial_ring_models_/1193432", "title"=>"Reentry induction by Na<sup>+</sup> channel blockade in myocardial ring models.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-10-03 02:54:28"}
  • {"files"=>["https://ndownloader.figshare.com/files/1704550", "https://ndownloader.figshare.com/files/1704551", "https://ndownloader.figshare.com/files/1704552", "https://ndownloader.figshare.com/files/1704554", "https://ndownloader.figshare.com/files/1704555"], "description"=>"<div><p>Background</p><p>Cardiomyocytes located at the ischemic border zone of infarcted ventricle are accompanied by redistribution of gap junctions, which mediate electrical transmission between cardiomyocytes. This ischemic border zone provides an arrhythmogenic substrate. It was also shown that sodium (Na<sup>+</sup>) channels are redistributed within myocytes located in the ischemic border zone. However, the roles of the subcellular redistribution of Na<sup>+</sup> channels in the arrhythmogenicity under ischemia remain unclear.</p><p>Methods</p><p>Computer simulations of excitation conduction were performed in a myofiber model incorporating both subcellular Na<sup>+</sup> channel redistribution and the electric field mechanism, taking into account the intercellular cleft potentials.</p><p>Results</p><p>We found in the myofiber model that the subcellular redistribution of the Na<sup>+</sup> channels under myocardial ischemia, decreasing in Na<sup>+</sup> channel expression of the lateral cell membrane of each myocyte, decreased the tissue excitability, resulting in conduction slowing even without any ischemia-related electrophysiological change. The conventional model (i.e., without the electric field mechanism) did not reproduce the conduction slowing caused by the subcellular Na<sup>+</sup> channel redistribution. Furthermore, Na<sup>+</sup> channel blockade with the coexistence of a non-ischemic zone with an ischemic border zone expanded the vulnerable period for reentrant tachyarrhythmias compared to the model without the ischemic border zone. Na<sup>+</sup> channel blockade tended to cause unidirectional conduction block at sites near the ischemic border zone. Thus, such a unidirectional conduction block induced by a premature stimulus at sites near the ischemic border zone is associated with the initiation of reentrant tachyarrhythmias.</p><p>Conclusions</p><p>Proarrhythmia of Na<sup>+</sup> channel blockade in patients with old myocardial infarction might be partly attributable to the ischemia-related subcellular Na<sup>+</sup> channel redistribution.</p></div>", "links"=>[], "tags"=>["subcellular Na", "field mechanism", "intercellular cleft potentials.ResultsWe", "channel redistribution", "Sodium Channels Enhances", "myofiber model", "ischemic border zone", "subcellular redistribution", "channel blockade", "conduction block", "Simulation Study BackgroundCardiomyocytes"], "article_id"=>1193445, "categories"=>["Biological Sciences"], "users"=>["Kunichika Tsumoto", "Takashi Ashihara", "Ryo Haraguchi", "Kazuo Nakazawa", "Yoshihisa Kurachi"], "doi"=>["https://dx.doi.org/10.1371/journal.pone.0109271.s001", "https://dx.doi.org/10.1371/journal.pone.0109271.s002", "https://dx.doi.org/10.1371/journal.pone.0109271.s003", "https://dx.doi.org/10.1371/journal.pone.0109271.s004", "https://dx.doi.org/10.1371/journal.pone.0109271.s005"], "stats"=>{"downloads"=>3, "page_views"=>17, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Ischemia_Related_Subcellular_Redistribution_of_Sodium_Channels_Enhances_the_Proarrhythmic_Effect_of_Class_I_Antiarrhythmic_Drugs_A_Simulation_Study_/1193445", "title"=>"Ischemia-Related Subcellular Redistribution of Sodium Channels Enhances the Proarrhythmic Effect of Class I Antiarrhythmic Drugs: A Simulation Study", "pos_in_sequence"=>0, "defined_type"=>4, "published_date"=>"2014-10-03 02:54:28"}
  • {"files"=>["https://ndownloader.figshare.com/files/1704535"], "description"=>"<p>Conduction velocity (CV) restitution curves in the NZ (A) and IBZ (B) myofiber models as a function of S1–S2 interval. Ten S1 stimuli of basic cycle length (400 ms) were applied transmembranously followed by an S2 stimulus with various coupling intervals.</p>", "links"=>[], "tags"=>["subcellular Na", "field mechanism", "intercellular cleft potentials.ResultsWe", "channel redistribution", "Sodium Channels Enhances", "myofiber model", "ischemic border zone", "subcellular redistribution", "channel blockade", "conduction block", "Simulation Study BackgroundCardiomyocytes"], "article_id"=>1193430, "categories"=>["Biological Sciences"], "users"=>["Kunichika Tsumoto", "Takashi Ashihara", "Ryo Haraguchi", "Kazuo Nakazawa", "Yoshihisa Kurachi"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0109271.g004", "stats"=>{"downloads"=>0, "page_views"=>32, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Conduction_velocity_restitution_properties_/1193430", "title"=>"Conduction velocity restitution properties.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-10-03 02:54:28"}

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