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机构地区:[1]华中科技大学同济医学院附属协和医院心内科华中科技大学同济医学院附属协和医院心血管病研究所,湖北武汉430022 [2]内蒙古医学院第三附属医院心内科,内蒙古包头014010
出 处:《中国心脏起搏与心电生理杂志》2008年第6期534-538,共5页Chinese Journal of Cardiac Pacing and Electrophysiology
基 金:湖北省重大科技攻关项目"恶性心律失常早期预测与防治研究"资助(项目编号:2006AA301A04)
摘 要:目的探讨阿魏酸钠对家兔心室肌细胞膜L型钙通道电流(ICa-L)的影响。方法酶解法急性分离兔单个心室肌细胞,以经典的Ⅲ类抗心律失常药物胺碘酮为对照,应用膜片钳全细胞记录技术观察3,10,30,100μmol/L的阿魏酸钠对心室肌细胞膜ICa-L的作用。结果阿魏酸钠及胺碘酮均呈浓度依赖性抑制L型钙电流。3,10,30,100μmol/L的阿魏酸钠对ICa-L的抑制率分别为11.1%±2.4%,26.9%±6.2%,40.5%±5.0%,61.9%±5.5%(P<0.05);1,3,10,30μmol/L的胺碘酮对ICa-L的抑制率分别为21.1%±3.8%,32.6%±2.6%,52.6%±4.6%,71.4%±7%(P<0.05);半数抑制浓度分别为32.6及9.5μmol/L,阿魏酸钠的抑制作用弱于胺碘酮(P<0.05)。阿魏酸钠及胺碘酮均能使ICa-L电流-电压曲线上移,稳态激活曲线右移,失活曲线左移,并可减慢钙通道灭活后的恢复过程。结论阿魏酸钠对ICa-L具有浓度依赖性阻滞作用,使ICa-L的激活减慢,失活加快,并且失活后的恢复时间延长,可能是其抗心律失常作用的电生理机制之一。Objective To study the effect of sodium ferulate on L-type calcium current ( ICa-L ) in isolated rabbit ventrieular myoeytes. Methods Compared with amiodarone, the single ventrieular myoeytes of rabbits were isolated enzymatieally and whole-cell patch clamp recording technique was used to record the changes of ICa-L following the administration of sodium ferulate at 3, 10, 30 and 100 μmol/L. Results Both sodium ferulate and amiodarone could block the ICa-L which had concentration dependence, however, sodium ferulate was inferior to amiodarone ( P 〈 0.05 ). Peak ICa- L was reduced 21.1% ± 3.8% ,32.6% ±2.6% ,52.6% ±4.6% and 71.4% -± 7% ( P 〈 0.05 ) respectively at amiodarone 1, 3, 10 and 30 μmol/L. In contrast , Peak ICa.L was reduced 11.1% ± 2.4% ,26.9% ± 6.2% ,40.5% ±5.0% and 61.9% ± 5.5% (P 〈 0.05 ) respectively at sodium ferulate 3, 10, 30 and 100 μmol/L. The concentration for haft - maximal block was 32.6 μmol/L and 9.5 μmol/L. The current-voltage curve moved upward, steadstate activation curve moved right and stead-state deactivation curve moved left, furthermore, they delayed the recovery time course of ICa-L from inactive state. Conclusion Sodium ferulate blocks L-type calcium channel, slows down it's activation, speeds up its inactivation and delays the recovery time. These may be the related mechanisms of the antiarrhythmic effects.
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