Electrical remodeling of pulmonary vein cardiomyocytes during atrial overload

2015 Fiscal Year Final Research Report

• Project/Area Number: 25460281
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: General physiology
• Research Institution: Akita University
• Principal Investigator: ONO Kyoichi 秋田大学, 医学(系)研究科(研究院), 教授 (70185635)
• Co-Investigator(Kenkyū-buntansha): OHBA Takayoshi 秋田大学, 大学院医学系研究科, 助教 (80431625) ; SHIBATA Shigehiro 秋田大学, 大学院医学系研究科, 講師 (10326671)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 心房細動 / 肺静脈 / 自動能 / 不整脈 / イオンチャネル / Clチャネル

Outline of Final Research Achievements

Extensions of striated myocardium from the left atrium into the pulmonary veins (PVs) are termed myocardial sleeves. Ectopic activity of cardiomyocytes in the sleeves is thought to be responsible for initiation and maintenance of atrial fibrillation, the most frequent sustained arrhythmia encountered in clinical practice. We have reported that PV cardiomyocytes have the potential to generate spontaneous activity. In this study, we found a novel hyperpolarizing-activated Cl- current in PV cardiomyocytes, not in atrial and ventricular myocytes. We also showed that the norepinephrine-induced automaticity could be stopped by Cl- channel blocker, indicating that IClh may play a functional role in the NE-induced automaticity. Furthermore, a computer simulation model was constructed to reconstruct electrical activity of PV cardiomyocytes, and electrical remodeling of rat atrial myocytes using rapid atrial pacing were analyzed.

Free Research Field

心臓循環生理学、電気生理学