Shih-Yu Huang1, Yen-Yu Lu2, Yao-Chang Chen3, Wei-Ta Chen4, Yung-Kuo Lin5, Shih-Ann Chen6, Yi-Jen Chen5. 1. Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei; ; Fu Jen Catholic University, School of Medicine; ; Division of Cardiology, Sijhih Cathay General Hospital, New Taipei City; 2. Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei; ; Division of Cardiology, Sijhih Cathay General Hospital, New Taipei City; 3. Department of Biomedical Engineering, National Defense Medical Center; 4. Division of Cardiovascular Medicine, Department of Internal Medicine, Wan Fang Hospital, Taipei Medical University; 5. Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei; ; Division of Cardiovascular Medicine, Department of Internal Medicine, Wan Fang Hospital, Taipei Medical University; 6. National Yang-Ming University, School of Medicine; ; Division of Cardiology and Cardiovascular Research Center, Taipei Veterans General Hospital, Taipei, Taiwan.
Abstract
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 H2O2 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 (IK1), and sodium-calcium exchanger (NCX) before and after H2O2 (100 μM) in isolated rabbit LA myocytes. RESULTS: H2O2 (100 μM) shortened by 50% (from 40 ± 7 to 21 ± 5 ms) 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 AP morphology and ionic currents in LA myocytes, which may contribute to the genesis of AF in oxidative stress. KEY WORDS: Action potential; Ionic current; Oxidative stress.
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 H2O2 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 (IK1), and sodium-calcium exchanger (NCX) before and after H2O2 (100 μM) in isolated rabbit LA myocytes. RESULTS:H2O2 (100 μM) shortened by 50% (from 40 ± 7 to 21 ± 5 ms) 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 AP morphology and ionic currents in LA myocytes, which may contribute to the genesis of AF in oxidative stress. KEY WORDS: Action potential; Ionic current; Oxidative stress.
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