Referenced in: none

Automatically associated channels: Kv1.4 , Kv3.1 , Kv4.2

Title: Electrical remodeling of the ventricular myocardium in myocarditis: studies of rat experimental autoimmune myocarditis.

Authors: Junko Saito, Shinichi Niwano, Hiroe Niwano, Takayuki Inomata, Yoshihiro Yumoto, Kazuko Ikeda, Kimiatsu Inuo, Jisho Kojima, Minoru Horie, Tohru Izumi

Journal, date & volume: Circ. J., 2002 Jan , 66, 97-103

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/11999674

Abstract
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.