CAJ | 학술논문

目的：研究硫化氢（H2 S）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 H2 S 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（H2 S 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）pA/ pF 分别至（-10.7±1.4）pA/ pF（n =6，P <0.05）、（-7.4±2.5）pA/ pF（P <0.01）和（-5.3±1.1）pA/ pF（P <0.01），H2 S 使稳态激活曲线右移，而不影响稳态失活曲线。结论 H2 S 通过对 L 型钙通道的抑制而发挥抗心律失常作用。
목적：연구류화경（H2 S）대왜파인유발적촉발성심률실상급 L 형개통도적작용，탐토류화경항심률실상적궤제。방법운용전세포막편겸기술，기록 L 형개통도전류，관찰류화경대단개심실기세포 L 형개통도각삼수적영향。결과 H2 S 억제왜파인유발적지후거겁화（DAD）급촉발활동（TA），50，100화200μmol/ L 류경화납（H2 S 적공체）사 ICa - L적봉치강저，농도의뢰성적사 I - V 곡선상이，봉치유（-13.9±1.4）pA/ pF 분별지（-10.7±1.4）pA/ pF（n =6，P <0.05）、（-7.4±2.5）pA/ pF（P <0.01）화（-5.3±1.1）pA/ pF（P <0.01），H2 S 사은태격활곡선우이，이불영향은태실활곡선。결론 H2 S 통과대 L 형개통도적억제이발휘항심률실상작용。
Objective:To investigate effects of hydrogen sulfide(H2 S)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 L-type calcium channel and observe the effects on arrhythmias induced by ouabain and L-type calcium channel of single ar-rhythmic 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 - L was decreased from( - 13. 9 ± 1. 4)pA/ pF to( -10. 7 ± 1. 4)pA/ pF(n = 5,P < 0. 05),( - 7. 4 ± 2. 5)pA/ pF(P < 0. 01)and( - 5. 3 ± 1. 1)pA/ pF(P < 0. 01)by 50, 100,200μmol sodium hydrosulfide(H2 S donor)respectively,and I - V curve was shifted upward in a concentration-de-pendent 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.