Electrical Remodeling of the Ventricular Myocardium in Myocarditis

• Saito Junko

  Department of Internal Medicine, Kitasato University School of Medicine

• Niwano Shinichi

  Department of Internal Medicine, Kitasato University School of Medicine

• Niwano Hiroe

  Department of Internal Medicine, Kitasato University School of Medicine

• Inomata Takayuki

  Department of Internal Medicine, Kitasato University School of Medicine

• Yumoto Yoshihiro

  Department of Internal Medicine, Kitasato University School of Medicine

• Ikeda Kazuko

  Department of Internal Medicine, Kitasato University School of Medicine

• Inuo Kimiatsu

  Department of Internal Medicine, Kitasato University School of Medicine

• Kojima Jisho

  Department of Internal Medicine, Kitasato University School of Medicine

• Horie Minoru

  Department of Cardiovascular Medicine, Kyoto University

• Izumi Tohru

  Department of Internal Medicine, Kitasato University School of Medicine

書誌事項

タイトル別名

• Studies of Rat Experimental Autoimmune Myocarditis

抄録

The purpose of this study was to evaluate the electrical remodeling of the ventricular myocardium in the experimental autoimmune myocarditis (EAM) model in Lewis rats. EAM was induced by immunization with cardiac myosin. During the active myocarditis phase, the effective refractory period (ERP), the duration of the monophasic action potential (MAPD) was extracted from the left ventricular free wall, and the mRNA levels of Kv1.4, 4.2, 4.3 and L type Ca²⁺ channel were determined by RNase protection assays. The inducibility of ventricular arrhythmia was higher in EAM rats than in the control rat, and the direct relationship between the coupling intervals of the premature stimulus and the ventricular arrhythmia in EAM rats. The ERP was prolonged in EAM rats compared with the control group. The MAPDs determined as 20% and 90% repolarization time, were both longer in EAM rats than in the controls. The level of expression of Kv4.2 mRNA was reduced in EAM rats in comparison with the controls, whereas those of Kv1.4, 4.3 and the L type Ca²⁺ channel were unchanged. Ventricular vulnerability was higher in EAM rats than in the control rats, and some of the ventricular arrhythmias observed in the EAM group seemed to be based on triggered activity. The level of expression of Kv4.2 mRNA was significantly reduced, and this change was compatible with prolongation of the action potential duration. (Circ J 2002; 66: 97 - 103)<br>

収録刊行物

• Circulation Journal

  Circulation Journal 66 (1), 97-103, 2002

  一般社団法人 日本循環器学会

キーワード

• Cardiac ion channel
• Electrical remodeling
• Experimental autoimmune myocarditis (EAM)
• Myocarditis
• Ventricular arrhythmias

詳細情報

• CRID: 1390001205105257216
• NII論文ID: 110002625741
• NII書誌ID: AA11591968
• DOI: 10.1253/circj.66.97
• COI: 1:STN:280:DC%2BD383lvFOiuw%3D%3D
• ISSN: 13474820
• ISSN: 13469843
• PubMed: 11999674
• Web Site: http://www.jstage.jst.go.jp/article/circj/66/1/66_1_97/_pdf
• Web Site: https://search.jamas.or.jp/link/ui/2002153809
• 本文言語コード: en
• データソース種別:
  • JaLC
  • Crossref
  • PubMed
  • CiNii Articles
• 抄録ライセンスフラグ: 使用不可