Background: Aging and pulmonary veins (PVs) play critical roles in the pathophysiology of atrial fibrillation. Aging increases oxidative stress, which may induce atrial fibrillation. Since oxidative stress can increase PV arrhythmogenesis, the purpose of this study was to investigate whether aging may modulate the electrophysiological effects of oxidative stress on PVs. Methods and Results: Conventional microelectrodes were used to record the action potentials (APs) and contractility in isolated aged (age, 3 years) rabbit PV specimens before and after H2O2 administration. H 2O2 (0.02 and 0.2 mM) increased the aged PV spontaneous activity rates from 96 ± 12 to 108 ± 12 and 102 ± 12 beats/min (n = 9, p <0.05), respectively. In contrast, H2O 2 (2 mM) decreased aged PV spontaneous activity rates from 96 ± 12 to 72 ± 12 beats/min. H2O2 (0.02, 0.2 and 2 mM) induced PV burst firing (33%, 33%, and 67%) and early afterdepolarizations (11%, 33%, and 44%) in aged PVs with spontaneous activity (n = 6). In the aged PVs without spontaneous activity, H2O 2 (0.02, 0.2 and 2 mM) shortened the 90% of AP duration. H 2O2 at 2 mM, but not 0.02 or 0.2 mM, increased the contractile force. Conclusion: H2O2 modulates aged PV arrhythmogenesis, which may play a role in the genesis of atrial fibrillation.
|頁（從 - 到）||109-114|
|期刊||Acta Cardiologica Sinica|
|出版狀態||已發佈 - 六月 2011|
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine