摘要
目的研究硫化氢(H2S)对哇巴因诱发的触发性心律失常及L型钙通道的作用,探讨硫化氢抗心律失常的机制。方法运用全细胞膜片钳技术,记录L型钙通道电流,观察硫化氢对单个心室肌细胞L型钙通道各参数的影响。结果 H2S抑制哇巴因诱发的迟后去极化(DAD)及触发活动(TA),50,100和200μmol/L硫氢化钠(H2S的供体)使ICa-L的峰值降低,浓度依赖性的使I-V曲线上移,峰值由(-13.9±1.4)p A/p F分别至(-10.7±1.4)p A/p F(n=6,P<0.05)、(-7.4±2.5)p A/p F(P<0.01)和(-5.3±1.1)p A/p F(P<0.01),H2S使稳态激活曲线右移,而不影响稳态失活曲线。结论 H2S通过对L型钙通道的抑制而发挥抗心律失常作用。
Objective： To investigate effects of hydrogen sulfide（ H2S） on arrhythmias induced by ouabain and L-type calcium channel of myocardial cell. Methods： The whole-cell patch clamp technique was applied to record the current of Ltype calcium channel and observe the effects on arrhythmias induced by ouabain and L-type calcium channel of single arrhythmic ventricular cell. Results： H2 S showed protective function of inhibiting the delayed afterdepolarization（ DAD） and triggerd activity（ TA） induced by ouabain. The peak current of Ica- Lwas decreased from（- 13. 9 ± 1. 4） p A / p F to（-10. 7 ± 1. 4） p A / p F（ n = 5,P〈 0. 05）,（- 7. 4 ± 2. 5） p A / p F（ P〈 0. 01） and（- 5. 3 ± 1. 1） p A / p F（ P〈 0. 01） by 50,100,200μmol sodium hydrosulfide（ H2 S donor） respectively,and I- V curve was shifted upward in a concentration-dependent manner. The steady state activation curve was shifted to the right by H2 S while no effect on inactivation curve was shown. Conclusion： H2 S shows anti-arrhythmic function through its effects on L-type calcium channel.
出处
《泰山医学院学报》
CAS
2015年第11期1201-1204,共4页
Journal of Taishan Medical College
基金
山东省高校科技计划资助项目(J12LE08)
