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作 者:马瑞彦[1] 杨宗英[1] 钟前进[1] 陈林[1] 王学锋[1] 肖颖彬[1]
机构地区:[1]第三军医大学新桥医院全军心血管外科中心,重庆400037
出 处:《中华心血管病杂志》2007年第12期1111-1115,共5页Chinese Journal of Cardiology
基 金:国家自然科学基金(30370583)
摘 要:目的建立家兔快速心房起搏模型,探讨快速心房起搏早期心房超微结构变化和相关离子通道基因和蛋白表达的改变。方法 36只家兔给予600次/min 的频率进行心房起搏,按起搏时间分成6组,透射电镜观察心房肌超微结构变化,用反转录聚合酶链反应进行检测 L 型钙通道α1c、β1、α2亚单位和钾通道 Kv4.3的 mRNA 表达,Western bolt 检测 L 型钙通道α1c、钾通道 Kv4.3的蛋白表达。结果心房肌细胞超微结构的改变在起搏3 h 后出现,随着起搏时间的延长,出现线粒体空泡化、肌丝溶解和糖原聚集。L 型钙通道的α1c、β1的 mRNA 表达下调出现在起搏6 h 后;在24 h后并没有随着起搏时间的延长而进一步下降,钾通道 Kv4.3的 mRNA 表达在起搏24 h 后开始明显下降,α2亚单位的表达水平在起搏后没有改变。L 型钙通道的α1c、钾通道 Kv4.3的蛋白表达水平改变与相应的 mRNA 表达改变相平行。结论在快速起搏早期,L 型钙通道和钾通道 Kv4.3的基因和蛋白表达水平下降,心房肌细胞超微结构改变早于离子通道表达水平发生变化,主要的机制可能是与快速起搏引起的钙超载导致离子通道转录水平的下降有关。Objective To investigate rapid atrial pacing (RAP) induced atrial uhrastructural changes and mRNA and protein expression changes of L-type calcium channel subunits and potassium channel Kv4. 3 in a rabbit model. Methods Thirty-six rabbits were electrically paced at a frequency of 600 beats/min for durations ranging from 0 - 48 h via bipolar endocardial leads through surgical techniques. Ultrastructural changes of the atrium were observed through a transmission electron microscope (TEM), L- type calcium channel subunits and potassium channel Kv4. 3 expressions at mRNA and protein levels were analyzed by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot. Results Atrial ultrastructure changes characterized by mitochondrial vacuolization, myofilament lysis, and glucogen accumulation were detected obvious at 3 h post pacing. Down-regulated mRNA expression of Ca^2+ channel β1 and α1 subunits was observed 6 h post pacing, Kvg. 3 mRNA down-regulation occurred 24 h post pacing, auxiliary subunit α2 was not affected by pacing. Protein expression of α1c subunit and potassium channel Kv4. 3 paralleled their mRNA expression changes. Conclusion RAP induced uhrastructural changes of the atrium and down-regulated mRNA and protein expressions of L-type calcium channel subunits and potassium channel Kv4. 3 occurred thereafter in response to intracellular calcium overload induced by RAP.
分 类 号:R541.75[医药卫生—心血管疾病]
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