Difference In Current Densities Of Two Pore Domain Potassium Channel Between Ventricular And Ventricular Outflow Tract Cardiomyocytes In Rabbit Heart

Objective: Idiopathic ventricular tachycardia mainly originates fromright ventricular outflow tract.(RVOT). The ionic channel mechanism ofidiopathic ventricular tachycardia arising from right ventricular outflowtract(RVOT-VT) has been seldom reported experimentally， for thetechnical difficulties. The aim of the experiment was to explore thedifference of IK2pbetween the myocardial cells in RVOT and free rightventricular wall (RV) in rabbit heart and the mechanism of the ventriculartachycardia genesis from RVOT.Methods: The ionic currents of rabbit cardiomyocytes in RVOT andin RV were recorded with the whole-cell patch-clamp technique. Theeffect of Chloroform, a specific activator of TREK-1, and high pH, anactivator of TASK-1, on the currents were tested respectively. TREK-1and TASK-1are subtypes of K2p.Results:The steady-state current in RVOT cardiomyocytes was lessthan that in RV. The further observation on the steady-state currentshowed that K2pcurrents existed in rabbit RVOT and RV myocardial cells，displaying that K2pcurrent in RVOT was less than that in RV.Application of Chloroform produced a strong increase of the steady-statecurrent in RVOT and RV myocytes. The augmentation of PH to8.3byapplying NaOH to the bath solution also generated a similar effect inRV myocytes.Conclusion: It was the first time on the electrophysiological levelverified the existence of the K2pcurrent in rabbit RVOT and RVmyocytes and further confirmed the subtypes were TREK-1and TASK-1.The low K2pcurrent density in some RVOT myocytes led to lowersteady-state outward current and prolonged APD in RVOT myocytes.These might induce EAD and resulted to genesis of RVOT-VT.