局灶性心肌炎心室肌细胞钙电流与钙通道基因改变的研究

Replicating rat ventricular myocyte model infected by coxsackievirus B3 and recording ventricular myocyte action potential and L-type calcium current（Ica-L） by whole-cell patch clamp technique,we found ventricular myocyte average current density of Ica-L increasing significantly（8.66±0.31 pA/pF vs 6.97±0.05 pA/pF） and current peak of I-V curve increasing significantly（P<0.01）. According to rat cardiomyocyte calcium channel subunits primers（α1、α2/δ、β） and CVB3 primer performing RT-PCR and electrophoresis, we foundα1（4.00±0.07 vs 2.21±0.41，p<0.01）， β2c（2.06±0.06 vs 1.22±0.30，p<0.05）subunits mRNA abundance increasing in CVB3 infected groups compared with normal controls and α2/δ(4.12±0.19 vs 4.13±0.27，P>0.05) subunit have no significant increase. The main finding of this project is CVB3 infected ventricular myocyte membrane Ica-L average current density increasing and the increasing is related with L-type calcium channel α1，β2c subunits mRNA abundance increase, and then providing cell and molecular theory basis for ventricular myocytes electrophysiological dysfounction after CVB3 infected.

复制局灶性CVB3病毒心肌炎小鼠模型，应用组织薄片膜片钳技术，在心室肌薄片上记录细胞动作电位和钙电流，提取病变心肌细胞内容物和心肌组织RNA，借助钙通道各亚单位引物和《疽铮卸縍T-PCR、钙通道基因克隆和测序，观察心肌细胞膜钙电流变化与通道基蚪峁购?或表达变异的关系，阐明心肌炎室性心律失常发生的细胞电生理和分子机制。