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Research
Nitroprusside modulates pulmonary vein arrhythmogenic activity
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* Corresponding author: Yao-Chang Chen bme02@mail.ndmctsgh.edu.tw
1 Taipei Medical University, Graduate Institute of Clinical Medicine, Taipei, Taiwan
2 Division of Cardiovascular Medicine, Taipei Medical University, Wan Fang Hospital, Taipei, Taiwan
3 Department of Biomedical Engineering, National Defense Medical Center, Taipei, Taiwan
4 National Yang-Ming University, School of Medicine, Division of Cardiology and Cardiovascular Research Center, Veterans General Hospital, Taipei, Taiwan
5 Division of Cardiology, Sijhih Cathay General Hospital, Sijhih, Taiwan
Journal of Biomedical Science 2010, 17:20 doi:10.1186/1423-0127-17-20
Published: 20 March 2010Abstract
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.