ABSTRACT
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.