Li Xi, Wang Tingzhong, Han Ke, Zhuo Xiaozhen, Lu Qun, Ma Aiqun
Department of Cardiovascular Medicine, the First Affiliated Hospital of Medical School, Xi'an Jiaotong University, Xi'an, Shaanxi 710061, China.
J Biomed Res. 2011 Jul;25(4):274-9. doi: 10.1016/S1674-8301(11)60037-7.
Remodeling of ion channels is an important mechanism of arrhythmia induced by heart failure (HF). We investigated the expression of potassium channel encoding genes in the ventricles of rabbit established by volume-overload operation followed with pressure-overload. The reversible effect of these changes with bisoprolol was also evaluated. The HF group exhibited left ventricular enlargement, systolic dysfunction, prolongation of corrected QT interval (QTc), and increased plasma brain natriuretic peptide levels in the HF rabbits. Several potassium channel subunit encoding genes were consistently down-regulated in the HF rabbits. After bisoprolol treatment, heart function was improved significantly and QTc was shortened. Additionally, the mRNA expression of potassium channel subunit genes could be partially reversed. The down-regulated expression of potassium channel subunits Kv4.3, Kv1.4, KvLQT1, minK and Kir 2.1 may contribute to the prolongation of action potential duration in the heart of rabbits induced by volume combined with pressure overload HF. Bisoprolol could partially reverse these down-regulations and improve heart function.
离子通道重塑是心力衰竭（HF）诱发心律失常的重要机制。我们研究了通过容量超负荷手术继以压力超负荷建立的兔心室中钾通道编码基因的表达情况。还评估了比索洛尔对这些变化的可逆作用。HF组兔表现出左心室扩大、收缩功能障碍、校正QT间期（QTc）延长以及血浆脑钠肽水平升高。在HF兔中，多个钾通道亚基编码基因持续下调。比索洛尔治疗后，心脏功能显著改善，QTc缩短。此外，钾通道亚基基因的mRNA表达可部分逆转。钾通道亚基Kv4.3、Kv1.4、KvLQT1、minK和Kir 2.1的下调表达可能导致容量联合压力超负荷HF诱导的兔心脏动作电位时程延长。比索洛尔可部分逆转这些下调并改善心脏功能。
