- 作者: Yung-Kuo Lin; Yen-Yu Lu; Yao-Chang Chen; Yi-Jen Chen; Shih-Ann Chen
- 作者服務機構: Taipei Medical University, Graduate Institute of Clinical Medicine, Taipei, Taiwan, R.O.C.
- 中文摘要: --
- 英文摘要:
Background: Pulmonary veins (PVs) are the most important sources of ectopic beats
with the initiation of paroxysmal atrial fibrillation, or the foci of ectopic atrial
tachycardia and focal atrial fibrillation. Elimination of nitric oxide (NO) enhances
cardiac triggered activity, and NO can decrease PV arrhythmogensis through
mechano-electrical feedback. However, it is not clear whether NO may have direct
electrophysiological effects on PV cardiomyocytes. This study is aimed to study the
effects of nitroprusside (NO donor), on the ionic currents and arrhythmogenic activity
of single cardiomyocytes from the PVs.
Methods: Single PV cardiomyocytes were isolated from the canine PVs. The action
potential and ionic currents were investigated in isolated single canine PV
cardiomyocytes before and after sodium nitroprusside (80 μM,) using the whole-cell
patch clamp technique.
Results: Nitroprusside decreased PV cardiomyocytes spontaneous beating rates from
1.7±0.3 Hz to 0.5±0.4 Hz in 9 cells (P<0.05); suppressed delayed afterdepolarization
in 4 (80%) of 5 PV cardiomyocytes. Nitroprusside inhibited L-type calcium currents,
transient outward currents and transient inward current, but increased delayed
rectified potassium currents.
Conclusion: Nitroprusside regulates the electrical activity of PV cardiomyocytes,
which suggests that NO may play a role in PV arrhythmogenesis. - 中文關鍵字: --
- 英文關鍵字: --