Abstract
BackgroundPulmonary 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.MethodsSingle 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.ResultsNitroprusside 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.ConclusionNitroprusside regulates the electrical activity of PV cardiomyocytes, which suggests that NO may play a role in PV arrhythmogenesis.
Highlights
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
In canine PVs, we demonstrated that PVs have arrhythmogenic activity through the enhancement of spontaneous activities or high frequency irregular rhythms [10,11]
After the dogs were anesthetized with sodium pentobarbital (30 mg/kg, i.v.), the hearts were rapidly removed through a thoracotomy and dissected at room temperature in normal Tyrode solution with the composition of 137 NaCl; 4 KCl; 15 NaHCO3; 0.5 NaH2PO4; 0.5 MgCl2; 2.7 CaCl2, and 11 dextrose
Summary
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. It is not clear whether NO may have direct electrophysiological effects on PV cardiomyocytes. In canine PVs, we demonstrated that PVs have arrhythmogenic activity through the enhancement of spontaneous activities or high frequency irregular rhythms [10,11]. These findings confirmed the previous observation in embryological heart, whereas PVs were suggested to work as a subsidiary pacemaker [12]. Enhancement of automaticity and triggered activity in PV cardiomyocytes with pacemaker
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