Electrophysiological Properties of Pulmonary Vein Cardiomyocytes with Early

Afterdepolarization Induced by β–Adrenoceptor Agonist


Yao-Chang Chen, Yi-Jen Chen, Shih-Ann Chen and Cheng-I Lin

Departments of Biomedical Engineering and Pharmacology, National Defense Medical Center, Neihu 114, Taipei, Division of Cardiology, Veterans General Hospital-Taipei, and Taipei Medical University Wan-Fang Hospital, Taipei, Taiwan, R.O.C.               


Pulmonary veins (PVs) are important foci of ectopic beats to initiate paroxysmal atrial fibrillation. Previous study has shown that early afterdepolarization (EAD) may play a role in the arrhythmogenic activity of PVs. This study investigated the electrophysiological characteristics of PVs cardiomyocytes with EAD induced by a β–adrenoceptor agonist isoproterenol. Single rabbit PVs cardiomyocytes were isolated from retrograde perfusion with Ca2+-free Tyrode solution containing digestive enzyme. The action potentials (APs) and ionic currents were investigated in isolated single PVs cardiomyocytes using the whole-cell clamp technique before and after the infusion of 0.1 to 10 nM isoproterenol. Results show that EAD was induced in 10 (26%) of 38 PVs cardiomyocytes. Before isoproterenol infusion, the action potential duration (APD), slow inward, transient inward and delayed rectified currents were similar between the cardiomyocytes with or without EAD. However, after isoproterenol infusion, the cardiomyocytes with EAD had longer APD or greater increase of APD than the cardiomyocytes without EAD. Furthermore, cardiomyocytes with EAD had greater increase of slow-inward currents (ICa) than cardiomyocytes without EAD. However, increase of delayed rectified currents (IK) was similar between the cardiomyocytes with and without EAD. It is concluded that there were different electrophysiological effects of β-adrenergic stimulation on PVs cardiomyocytes, which may underlie the mechanism of isoproterenol-induced EAD in PVs cardiomyocytes.