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ヒトの心室性心筋細胞における新しい,超遅い非活性化ナトリウム電流

V A Maltsev¹, H N Sabbah, R S Higgins

¹Department of Medicine, Division of Cardiovascular Medicine, Henry Ford Heart and Vascular Institute, Detroit, MI, USA.

|December 8, 1998

まとめ

後期ナトリウム流 (INaL) は,ヒトの心不全の心筋細胞に存在します. この発見は,心臓機能不全 (HF) 治療の新たなターゲットとなり,心臓の再構築におけるナトリウムチャネルの役割を理解する.

科学分野:

心血管生理学心血管の生理学
心臓電気生理学心臓電気生理学
イオンチャンネル研究イオンチャンネル研究

背景:

心不全 (HF) はアクションポテンシャルの改造を伴うもので,しばしばK+チャネル変化に起因する.
犬での以前の研究では,HFに関連する改造において,遅いナトリウム電流 (INaL) の役割が示されました.

研究の目的:

INaLの存在と特性について,正常な心臓と心不全の心臓の両方のヒト心筋細胞で調査する.

主な方法:

全細胞パッチ・クランプ技術が,心筋細胞に適用され,ヒトの心臓を抽出した (10末期HF,3正常).
INaLの活性化,安定状態の可用性,電圧依存性,およびNa+チャネルブロッカー (テトロドトキシン,サキシトキシン) によるブロックの分析.

主要な成果:

INaLは,正常な心臓と衰弱した心臓の両方の心筋細胞に検出されました.
INaLは,超遅い,電圧独立の不活性化と再活性化 (tau ≈ 0.6秒) を示した.
電流は,テトロドトキシンとサキシトキシンによって,投与量に依存した方法で有意に遮断されました.

結論:

人間の心筋細胞は,健康状態と障害状態の両方で,INaLを発現します.
INaLの特徴的な超遅い無活性化および再活性化特性は,心不全における心臓の電気再構成への潜在的貢献を示唆しています.

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