Mechanisms of the occurrence, maintenance and propagation of EADs in a human ventricular cell model

  • Enomoto Suzuka
    The Bioinformatics Department of Life Sciences, Ritsumeikan University, Shiga, Japan
  • Kiyokawa Shotaro
    The Bioinformatics Department of Life Sciences, Ritsumeikan University, Shiga, Japan
  • Himeno Yukiko
    The Bioinformatics Department of Life Sciences, Ritsumeikan University, Shiga, Japan
  • Noma Akinori
    The Bioinformatics Department of Life Sciences, Ritsumeikan University, Shiga, Japan
  • Amano Akira
    The Bioinformatics Department of Life Sciences, Ritsumeikan University, Shiga, Japan

Bibliographic Information

Other Title
  • ヒト心室筋細胞モデルにおけるEADの発生、持続、伝播メカニズム

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Description

<p>EAD is suggested as one of the causes of ventricular fibrillation. We examined the mechanisms of generation and propagation of EADs by using a one-dimensional unit model, which was composed of two types of human ventricular cell models; normal and EAD-prone cells. In the EAD-prone cells, EAD was evoked by retarding the slow inactivation of the slow component of the Na+ current. We found that EADs were evoked repetitively because of Ca2+-dependent activation of the Na+-Ca2+ exchangers and reduction of the Na+- K+ pump current and/or propagation of the excitations through gap junction channels to adjacent repolarized cells. By blocking the gap junction currents, it was revealed that each EAD-prone cell generates EADs independently. The boundary between EAD-prone cells and normal cells was one of the factors that evoked repetitive EAD discharges. In the present study, the comprehensive ionic mechanisms underlying the repetitive discharge and propagation of EADs were revealed.</p>

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Details 詳細情報について

  • CRID
    1390008290064135552
  • NII Article ID
    130008105518
  • DOI
    10.11239/jsmbe.annual59.513
  • ISSN
    18814379
    1347443X
  • Text Lang
    ja
  • Data Source
    • JaLC
    • CiNii Articles
  • Abstract License Flag
    Disallowed

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