Roles of subcellular sodium channel redistribution in the generation of lethal arrhythmia: in silico study

2014 Fiscal Year Final Research Report

• Project/Area Number: 24790214
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: General physiology
• Research Institution: Osaka University
• Principal Investigator: TSUMOTO Kunichika 大阪大学, 医学(系)研究科(研究院), 助教 (70353331)
• Research Collaborator: KURACHI Yoshihisa 大阪大学, 大学院医学系研究科, 教授 (30142011) ; ASHIHARA Takashi 滋賀医科大学, 循環器内科, 講師 (80396259) ; HARAGUCHI Ryo (00393215) ; NAKAZAWA Kazuo (50198058)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: ナトリウムチャネル / 心筋細胞モデル / 興奮伝播 / コンピュータシミュレーション / リエントリー性頻拍 / Phase-2 リエントリー

Outline of Final Research Achievements

The contractile function in the heart results from the accurate propagation of action potentials in cardiomyocytes. The voltage-gated sodium (Na) channels, playing key roles in the action potential initiation and the propagation, alters the distribution within a myocyte in congenital and acquired disorder. We considered effects of changes in subcellular Na channel distribution on the occurrence of lethal arrhythmia. Using computer simulation, we showed that the conduction disorder and the initiation of reentrant tachyarrhythmia may be partly attributable to the subcellular Na channel distribution. These results suggest that not only the function of ion channels but also the subcellular distribution may be partly responsible for the occurrence of lethal arrhythmia.

Free Research Field

計算生理学