Electrolyte disturbances differentially regulate sinoatrial node and pulmonary vein electrical activity: A contribution to hypokalemia- or hyponatremia-induced atrial fibrillation

Yen Yu Lu, Chen Chuan Cheng, Yao Chang Chen, Yung-Kuo Lin, Shih Ann Chen, Yi-Jen Chen

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23 引文 斯高帕斯(Scopus)

摘要

Background Hypokalemia and hyponatremia increase the occurrence of atrial fibrillation. Sinoatrial nodes (SANs) and pulmonary veins (PVs) play a critical role in the pathophysiology of atrial fibrillation. Objective The purpose of this study was to evaluate whether electrolyte disturbances with low concentrations of potassium ([K+]) or sodium ([Na+]) modulate SAN and PV electrical activity and arrhythmogenesis, and to investigate potential underlying mechanisms. Methods Conventional microelectrodes were used to record electrical activity in rabbit SAN and PV tissue preparations before and after perfusion with different low [K+] or [Na+], interacting with the Na+-Ca2+ exchanger inhibitor KB-R7943 (10 μΜ). Results Low [K+] (3.5, 3, 2.5, and 2 mM) decreased beating rates in PV cardiomyocytes with genesis of delayed afterdepolarizations (DADs), burst firing, and increased diastolic tension. Low [K+] (3.5, 3, 2.5, and 2 mM) also decreased SAN beating rates, with genesis of DADs. Low [Na+] increased PV diastolic tension, DADs, and burst firing, which was attenuated in the co-superfusion with low [K+] (2 mM). In contrast, low [Na+] had little effect on SAN electrical activities. KB-R7943 (10 μΜ) reduced the occurrences of low [K+] (2 mM)- or low [Na+] (110 mM)-induced DAD and burst firing in both PVs and SANs. Conclusion Low [K+] and low [Na+] differentially modulate SAN and PV electrical properties. Low [K+]- or low [Na+]-induced slowing of SAN beating rate and genesis of PV burst firing may contribute to the high occurrence of atrial fibrillation during hypokalemia or hyponatremia.
原文英語
頁(從 - 到)781-788
期刊Heart Rhythm
DOIs
出版狀態已發佈 - 2016

ASJC Scopus subject areas

  • 心臟病學與心血管醫學
  • 生理學(醫學)

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