Roles of T tubular distribution in genesis of atrial fibrillation

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K08407
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Experimental pathology
• Research Institution: Kyoto Prefectural University of Medicine
• Principal Investigator: TANAKA Hideo 京都府立医科大学, 医学研究科, 教授 (60236619)
• Co-Investigator(Kenkyū-buntansha): 山岡 禎久 佐賀大学, 工学(系)研究科(研究院), 准教授 (80405274)
• Co-Investigator(Renkei-kenkyūsha): MATSUYAMA Takaaki 昭和大学, 医学部・法医学講座, 准教授 (40349113)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: 横行小管 / カルシウム / 心房筋 / 心房細動 / 不整脈 / プルキンエ線維 / 心筋梗塞 / 共焦点顕微鏡

Outline of Final Research Achievements

We address the possibility that altered distribution of transverse (T) tubules contributes to genesis of cardiac arrhythmias by confocal microscopy. Compared with ventricular myocytes, atrial cells, which barely show T tubules, exhibited spatiotemporally non-uniform Ca2+ dynamics, whereas ventricular myocytes showing fine, regular distribution of the tubules had uniform Ca2+ transients. The inhomogeneous Ca2+ dynamics in the atrial cells were more evident at higher frequency of excitation. However, no definitive relevance was obtained between the T tubule distribution and arrhythmogenesis. Besides, we obtained exact relevance of inhomogeneity of Ca2+ dynamics to T-tubule distribution in Purkinje fibers in mouse infarct border zone. Together, inhomogeneous Ca2+ dynamics owing to the paucity of T tubular distribution does not directly evoke arrhythmias; however, such inhomogeneity may contribute to depressed conductivity and mechanical performances, which may lead to arrhythmogenesis.

Free Research Field

実験病理学、心臓病理学、不整脈