摘要
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 calcium channel gene mRNA expression effects in atrial fibrillation mecha nisms. Method:Fifteen dogs were randomly individed into three groups-atrial fibrillation group (n= 5), atrial fibrillation and mibefradil group (n=5) and control group (without pacemaker implantation) (n=5). Atrial fibril lation dogs underwent continuous rapid atrial pacing (520 bpm) for twenty-four weeks to create persistent atrial fibrillation. L-type calcium channel α1 subunit, T-type calcium channel α1H subunit, Na+/Ca2+ exchanger and Kv4.3 mRNA were analysed by reverse transcription and polymerase chain reaction (RT PCR). Result:In the atrial fibrillation group, Ltype calcium channel α1 subunit mRNA slightly decreased (P〉0.05), T-type calcium channel α1H subunit mRNA remarkably increased (P〈0.05), Na+/Ca2+ exchanger mRNA did not change signifi cantly (P〉0.05), and Kv4.3 mRNA significantly decreased (P〈0.05), compared with in the control group. Conelusion:T type calcium channel α1H subunit mRNA significantly increased and Kv4.3 mRNA significantly de creased, which may be a major cause of calcium overload in persistent atrial fibrillation for six months. L-type calcium channel α1 subunit and Na+/Ca2+ exchanger mRNA did not change remarkably, suggesting that they did not play an important role in atrial fibrillation mechanisms.
出处
《临床心血管病杂志》
CAS
CSCD
北大核心
2009年第3期170-173,共4页
Journal of Clinical Cardiology
基金
国家自然科学基金资助(No:30271431)
北京大学985项目
北京市自然科学基金资助(No:7032030)
首都医学发展科研基金资助(No:20023036)
关键词
心房颤动
钙通道
基因
atrial fibrillation
calcium channel
gene