CAJ | 학술논문

目的：本研究在兔离体心脏模型上观察伊伐布雷定对心房和心室肌单相动作电位时程(MAPD)的影响及其在海葵毒素（ATX-Ⅱ）处理后的致心律失常作用。方法：雌性新西兰兔离体心脏采用Langendorff系统进行灌流，记录左心耳和左心室内外膜动作电位，观察在固定频率起搏刺激周长为350 ms（对应的心率为171次/min）时，伊伐布雷定单独作用以及ATX-Ⅱ（3 nmol/L）作用下伊伐布雷定对心房肌和心室肌复极90%的单相动作电位时程（MAPD90）的影响。此外，观察伊伐布雷定减慢心率至自主心率为（156±10）次/min时，伊伐布雷定单独和ATX-Ⅱ（3 nmol/L）作用下伊伐布雷定的致心律失常作用。结果：伊伐布雷定（3~10μmol/L）单独作用可显著延长心房肌、心室肌内膜和外膜的MAPD90，延长幅度分别为（15.9±2.0）ms、（31.5±4.0）ms和（23.9±3.0）ms（n=6，P<0.01）。ATX-Ⅱ（3 nmol/L）可显著延长心房肌和心室肌MAPD90，延长幅度在心房肌为（36.5±5.0）ms（n=6，P<0.01），而在心室肌内膜和外膜分别为（19.9±3.0）ms和（19.5±4.0）ms（n=6，P<0.01）。在ATX-Ⅱ处理后的心脏，伊伐布雷定（6~10μmol/L）可使心房肌MAPD90显著缩短（14.4±4.0）ms（n=6，P<0.01），且可诱发房性心律失常；但在心室肌伊伐布雷定（3~10μmol/L）显著延长心内膜和心外膜MAPD90，延长幅度分别为（36.2±7.0）ms和（27.5±5.0）ms（n=6，P<0.01）。无论是否经ATX-Ⅱ处理，伊伐布雷定均不增加心室肌MAPD90的逐搏变异性和跨壁离散度，且无室性心律失常发生。结论：伊伐布雷定可延长心房肌和心室肌MAPD。在晚钠电流增大后，伊伐布雷定可诱发房性心律失常，但不引起室性心律失常。
목적：본연구재토리체심장모형상관찰이벌포뢰정대심방화심실기단상동작전위시정(MAPD)적영향급기재해규독소（ATX-Ⅱ）처리후적치심률실상작용。방법：자성신서란토리체심장채용Langendorff계통진행관류，기록좌심이화좌심실내외막동작전위，관찰재고정빈솔기박자격주장위350 ms（대응적심솔위171차/min）시，이벌포뢰정단독작용이급ATX-Ⅱ（3 nmol/L）작용하이벌포뢰정대심방기화심실기복겁90%적단상동작전위시정（MAPD90）적영향。차외，관찰이벌포뢰정감만심솔지자주심솔위（156±10）차/min시，이벌포뢰정단독화ATX-Ⅱ（3 nmol/L）작용하이벌포뢰정적치심률실상작용。결과：이벌포뢰정（3~10μmol/L）단독작용가현저연장심방기、심실기내막화외막적MAPD90，연장폭도분별위（15.9±2.0）ms、（31.5±4.0）ms화（23.9±3.0）ms（n=6，P<0.01）。ATX-Ⅱ（3 nmol/L）가현저연장심방기화심실기MAPD90，연장폭도재심방기위（36.5±5.0）ms（n=6，P<0.01），이재심실기내막화외막분별위（19.9±3.0）ms화（19.5±4.0）ms（n=6，P<0.01）。재ATX-Ⅱ처리후적심장，이벌포뢰정（6~10μmol/L）가사심방기MAPD90현저축단（14.4±4.0）ms（n=6，P<0.01），차가유발방성심률실상；단재심실기이벌포뢰정（3~10μmol/L）현저연장심내막화심외막MAPD90，연장폭도분별위（36.2±7.0）ms화（27.5±5.0）ms（n=6，P<0.01）。무론시부경ATX-Ⅱ처리，이벌포뢰정균불증가심실기MAPD90적축박변이성화과벽리산도，차무실성심률실상발생。결론：이벌포뢰정가연장심방기화심실기MAPD。재만납전류증대후，이벌포뢰정가유발방성심률실상，단불인기실성심률실상。
Objective: To observe the effect of ivabradine (IVA) on atrial and ventricular monophasic action potential duration (MAPD) and its proarrhythmic action at presence of sea anemone toxin-II (ATX-II) in isolated rabbit heart modelin vitro. Methods: The perfusion of isolated heart from female New Zealand white rabbit was conducted by Langendorff method in vitro. Left atrial and left ventricular endo- , epi-cardial action potential were recorded when pacing with ifxed frequency of 350 ms (in correspondence with the heart rate of 171 times/min) to observe the effect of IVA alone and ATX-II (3 nmol/L) with IVA on MAPD90. In addition, to observe the action of IVA alone and ATX-II with IVA on proarrhythmia when IVA reducing the heart rate to autonomous cardiac rhythm as (156±10) times/min. Results: IVA at (3-10) μmol/L prolonged atrial and ventricular endo- , epi-cardial MAPD90 by (15.9 ± 2.0) ms, (31.5 ± 4.0) ms and (23.9 ± 3.0) ms (n=6,P<0.01), respectively. ATX-II at 3 nmol/L prolonged atrial and ventricular MAPD90 by (36.5 ± 5.0)ms and (19.9 ± 3.0) ms, (19.5 ± 4.0) ms (n=6,P<0.01) respectively. With ATX-II treatment, IVA at (6-10) μmol/L decreased atrial MAPD90 by (14.4 ± 4.0) ms (n=6,P<0.01), it induced atrial arrhythmia. With 3 nmol/L of ATX-II treated ventricle, IVA at (3-10) μmol/L obviously prolonged endo- and epi-cardial MAPD90 by (36.2 ± 7.0) ms and (27.5 ± 5.0) ms(n=6,P<0.01), respectively. IVA didn’t increase ventricular beat-to-beat variability and transmural dispersion of MAPD90 no matter with or without ATX-II treatment, no ventricular arrhythmia occurred. Conclusion: IVA prolongs both atrial and ventricular MAPD, with increased late sodium current, IVA may induce atrial arrhythmia but not ventricular arrhythmia in experimental rabbits in vitro.