Background: Oxidative stress plays an important role in the pathophysiology of atrial fibrillation (AF). The hydrogen peroxide (H2O2) mainly underlies the cellular oxidative stress and free radicals. Left atrium (LA) is the most important AF substrate. However, the effects of H 2O2 on the action potential (AP) and ionic currents in LA myocytes have not been fully elucidated. Methods: The whole-cell patch clamp was used to investigate the APs and ionic currents of L-type calcium current (ICa-L), transient outward currents (Ito), ultra-rapid delayed rectifier potassium current (IKur), delayed rectifier potassium currents (IK), inward rectifier potassium current (I K1), and sodium-calcium exchanger (NCX) before and after H 2O2 (100 μM) in isolated rabbit LA myocytes. Results: H2O2 (100 μM) shortened by 50% (from40 ± 7 to 21 ± 5ms) and 90% the AP duration (from 95 ± 12 to 74 ± 11 ms) in LA myocytes (n = 9), but did not change the resting membrane potentials. The H2O2 (100 μM) decreased Ito, but increased IKur and IK. H2O2 (100 μM) also reduced the ICa-L and the reverse mode NCX. However, H2O2 (100 μM) did not change IK1. Conclusions: H2O2 directly modulated the APmorphology and ionic currents in LAmyocytes, which may contribute to the genesis of AF in oxidative stress.
|頁（從 - 到）||38-45|
|期刊||Acta Cardiologica Sinica|
|出版狀態||已發佈 - 2014|
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine