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目的:探讨钙离子通道基因mRNA表达在心房颤动(房颤)发生机制中的作用。方法:杂种犬15只,随机分为3组,分别为正常对照组、单纯房颤组和房颤加mibefradil组。房颤组置入埋藏式高频率心脏起搏器,起搏频率520次/min。正常对照组不置入起搏器。术后观测24周。采用RT-PCR扩增心房肌组织的L型钙通道α1亚单位、T型钙通道α1H亚单位、钠/钙交换体和Kv4.3基因的mRNA。结果:单纯房颤组与正常对照组相比较,L型钙钙通道α1亚单位的mRNA有轻微下调(P>0.05),T型钙通道α1H亚单位的mRNA明显上调(P<0.05),钠/钙交换体的mRNA下调13%(P>0.05),Kv4.3基因的mRNA明显下调(P<0.05)。房颤加mibefradil组与单纯房颤组相比较,钠/钙交换体的mRNA上调10%(P>0.05),Kv4.3基因的mRNA上调(P<0.05)。结论:持续性房颤6个月时T型钙通道α1H亚单位mRNA的表达显著增加而Kv4.3mRNA的表达显著下调,可能是持续性房颤钙超载的主要原因。而L型钙通道α1亚单位和钠/钙交换体mRNA的表达无明显改变,提示它们可能在房颤的发生机制中不起重要作用。
Objective: To investigate the role of calcium channel mRNA expression in the pathogenesis of atrial fibrillation (AF). Methods: Fifteen hybrid dogs were randomly divided into 3 groups: normal control group, atrial fibrillation group and mibefradil group. Atrial fibrillation group embedded buried high-frequency pacemaker, pacing frequency of 520 beats / min. The normal control group did not put pacemaker. After 24 weeks of observation. The mRNAs of L-type calcium channel α1 subunit, T-type calcium channel α1H subunit, sodium / calcium exchanger and Kv4.3 gene in atrial myocardium were amplified by RT-PCR. Results: Compared with the normal control group, mRNA of L-type calcium-calcium channel α1 subunit was slightly downregulated (P> 0.05), T-type calcium channel α1H subunit mRNA was significantly up-regulated / Calcium exchanger was down-regulated by 13% (P> 0.05), Kv4.3 mRNA was significantly down-regulated (P <0.05). Atrial fibrillation plus mibefradil group compared with the atrial fibrillation group, the sodium / calcium exchanger mRNA up 10% (P> 0.05), Kv4.3 mRNA (P <0.05). CONCLUSION: The expression of α1H subunit mRNA of T-type calcium channel is significantly increased and the expression of Kv4.3 mRNA is significantly down-regulated at 6 months of persistent atrial fibrillation, which may be the main reason of persistent calcium overload in atrial fibrillation. There was no significant change in the expression of L-type calcium channel α1 subunit and sodium / calcium exchanger mRNA, suggesting that they may play an important role in the pathogenesis of atrial fibrillation.