Abstract: AIM:To study the transmural dispersion of repolarization (TDR) and electrophysiological characteristics in left ventricle of rabbits during acute ischemia and to explore the mechanism of the antiarrhythmic effect of amiodarone. METHODS: The effects of amiodarone in acute nonflow cardiac ischemia on action potential duration (APD) of epi- and endomyocardial cells, TDR and arrhythmia were observed using floating glass microelectrode and recording electrocardiogram. RESULTS: 1) After 5, 10, and 15 min of acute ischemia, in rabbit left ventricular wedge preparation, amiodarone produced a greater prolongation of APD in cardiac cells of the endo- and epicardium ［(228±19) msec and (203±15) msec］ respectively, compared with control group ［(212±6) msec and (180±5) msec］ respectively, especially in epicardium. 2) During acute ischemia, two-layer cells APD shortened and the shortening in epicardium was greater than that of the endocardium, thus leading to increased TDR. TDR in amiodarone group was significantly lower than control group. CONCLUSION: Amiodarone causes a prolongation in APD and a decrease in TDR in arterially perfused rabbit left ventricular wedge preparation in acute cardiac ischemia. This may be an important cellular electrophysiological foundation of anti-arrhythmia mechanism.