Background and Objective: Reactive oxygen species (ROS) are produced when atrial fibrillation develops because consumption of oxygen is rapidly increased. ROS can damage myocardium resulting in structural and electrical remodeling. The aim of this study was to investigate the effects of hydrogen peroxide (H2O2) on various action potential parameters of mouse atrium. Subjects and Methods: Mouse (ICR) atrial tissues were excised, 0.5-1 mm in diameter and 3-5 mm long, and immediately immersed in cold bicarbonate-containing Tyrode solution. The preparations were then perfused with oxygenated (95% O2, 5% CO2) Tyrode solution and were driven by electrical stimuli of 1-ms duration at a frequency of 1 Hz. Transmembrane potentials were recorded using traditional glass microelectrodes filled with 3 M KCl at the time of 0, 2.5, 5, 10, 20, and 30 minute. The results were compared among group I (control), group II (H2O2 0.1 mM) and group III (H2O2 0.5 mM) and group IV (H2O2 1 mM). Results: Maximal diastolic potential (MDP), action potential amplitude (APA), maximal slope at phase 0 depolarization (V max), action potential duration until 50%, 90% of repolarization (APD50, APD90) in group I did not change with the pass of time. MDP and APA were not changed but Vmax decreased (baseline 199짹51 V/sec, 30 min 166짹88 V/sec). APD50 (baseline 104짹16 ms, 30 min 134짹43 ms) and APD90 (baseline 187짹29 ms, 30 min 241짹78 ms) in group II were progressively prolonged with the pass of time. In group III, MDP was increased (baseline -78짹4 mV, 30 min -69짹3 mV) and Vmax decreased (baseline 198짹42 ms, 30 min 89짹38 V/sec). APD50 (baseline 105짹17 ms, 30 min 287짹86 ms) and APD90 (baseline 181짹31 ms, 30 min 516짹56 ms) were prolonged. APA was decreased but that was not statistiscally significant. Early after-depolarization was observed in 40% (8/20)of group III, 54.5% (12/22) of group IV and asystole occurred in 18.2% (4/22) of group IV. Conclusion: Hydrogen peroxide reduced the Vmax and prolonged action potential duration in time and dose-dependent manner. These results suggest reactive oxygen species involve in the arrhythmogenesis and electrical remodeling in atrial myocardium.