Effects of Oxygen Free Radical on Action Potential in Mouse Atrial Myocardium

BACKGROUND AND OBJECTIVES: 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. SUBJECTS AND METHODS: 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). RESULTS: 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. CONCLUSION: 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.

A study on determinants of the inducibility and maintenance of atrial fibrillation / 대한내과학회지

BACKGROUND: Atrial fibrillation (AF) is thought to beget AF by shortening atrial refractoriness and reversal of rate adaptation of atrial refractoriness. This phenomenon of electrophysiologic remodeling of the atria during AF has been reported to play a major role in inducibility and stability of AF. METHODS: Thirty-one patients with induced AF lasting >1 second during electrophysiologic study for documented or suspected supraventricular or ventricular tachycardia were included in this study. All the patients had no structural heart disease and history of AF. High right atrium (HRA) burst pacing or extra-stimulation was applied to induce AF. Eleven patients with AF sustained >or=3 min was grouped into Group I and 20 patients with AF <3 min into Group II. P wave duration and amplitude, left atrial (LA) size, atrial refractory period (ARP), intraatrial conduction time (IACT) from HRA electrode catheter to His bundle electrode catheter and characteristics of atrial activities during induced AF were compared between 2 groups. RESULTS: There was no difference in the distribution of underlying cardiac arrhythmias. P wave durations and amplitudes and echocardiographic LA sizes were similar between 2 groups. ARPs and IACTs in group I and II were similar (198.0 +/- 23.9 ms vs. 200.8 +/- 23.0 ms; 38.7 +/- 8.5 ms vs. 38.6 +/- 9.5 ms, respectively). During AF, mean interval of atrial activities in group I was significantly shorter than group II (156.6 +/- 24.2 ms vs. 187.6 +/- 28.0 ms, p<0.01). The degree of irregularity of atrial activities during AF was significantly higher in group I than group II (16.9 +/- 8.7 vs. 9.8 +/- 5.0, p<0.05). The duration of the atrial activities was wider in group I than group II (81.4 +/- 17.5 ms vs. 53.9 +/- 12.4 ms, p<0.001) and the amplitude was lower in group I than group II (56.1 +/- 36.0% vs. 109.0 +/- 51.8%, p<0.05), and the degree of fractionation was greater in group I than group II (4.8 +/- 1.1 vs. 3.2 +/- 0.5, p<0.05). CONCLUSION: These results suggest that shortening of atrial refractoriness and lengthening of local conduction time at the time of or shortly after induction of AF may play a major role in the induction and stabilization of AF.