Reactive oxygen species are known to be produced when atrial fibrillation develops. This study was performed to investigate the effects of hydrogen peroxide (H₂O₂) on the action potential parameters of the mouse atrium.

Mouse (ICR) atrial fibers were excised and immersed in cold bicarbonate-containing Tyrode's solution. The preparations were then perfused with oxygenated (95% O₂, 5% CO₂) Tyrode's solution and driven by an electrical stimuli 1 ms in duration at a frequency of 1 Hz. The transmembrane potentials were recorded at 0, 2.5, 5, 10, 20 and 30 minute, and compared between groups I (control), II (H₂O₂ 0.1 mM), III (H₂O₂ 0.5 mM) and IV (H₂O₂ 1 mM).

In group I, the maximal diastolic potential (MDP), action potential amplitude (APA), maximal slope at phase 0 depolarization (Vmax), action potential duration until 50% and 90% of repolarization (APD₅₀, APD₉₀) were unchanged with increasing time. In group II, the MDP and APA were unchanged, but the Vmax was decreased, and the APD₅₀ and APD₉₀ prolonged. In group III, the MDP was increased and the Vmax decreased; the APD₅₀ and APD₉₀ were prolonged, but the APA unchanged. In group IV, the MDP was increased, the Vmax and APA decreased And the APD₅₀ and APD₉₀ prolonged. After-depolarization was observed in 40% (8/20) and 54.5% (12/22) of groups III and IV, respectively, and asystole occurred in 18.2% (4/22) of group IV.

Hydrogen peroxide changed the action potential parameters in both time and dose dependent manner, and also elicited after-depolarization at higher concentrations. These results suggest reactive oxygen species are involved in the electrical remodeling and arrhythmogenesis in atrial myocardium.