マウスハートのバンドル・ブランチの伝導機能障害は,ギャップ・ジャンクション・プロテイン・コネクシン4040が欠けています

H V van Rijen¹, T A van Veen, M J van Kempen

¹Department of Medical Physiology, Utrecht, The Netherlands. H.V.M.vanRijen@med.uu.nl

Circulation

|March 21, 2001

まとめ

マウスにおけるコネキシン (Cx) 40の欠乏は,右束の枝を遮断し,左束の枝の伝導を損なう. この研究は,共通の束と隔膜の間の心筋の連続性を明らかにし,心臓の電気的活動に影響を与えます.

科学分野:

心血管の生理学心血管の生理学
分子心臓病学分子心臓病学
電気生理学電気生理学

背景:

コネクシン (Cx) 40とCx45は,哺乳類の心臓伝導における重要なギャップジャンクションタンパク質です.
心臓の電気活動におけるCx40の特定の役割を理解することは極めて重要です.

研究の目的:

心臓の電気伝導におけるCx40の役割を調査する.
Cx40欠乏マウスにおけるコネキシンの分布と心臓活性化パターンを相関させるため.

主な方法:

ランゲンドルフが浸透したマウスハートにマルチ電極配列を用いた電気生理学的記録.
コネキシンの分布と筋動脈の構造を分析するための免疫ヒスト化学とヒストロジー.
野生型とCx40欠乏マウスハートの比較.

主要な成果:

エピカルディアとセプトの活性化パターンは,野生型のマウスとCx40欠乏マウスの間で類似していました.
筋細胞の連続性は,共通の束から断面筋心臓まで観察されました.
Cx40欠乏症は右束枝ブロックと左束枝伝導の障害と相関しており,Cx45は近接束枝における唯一のコネクシンである.

結論:

マウスでは,共通の束と心室隔膜の間に直接的な連続性が存在します.
Cx40の欠乏は,右バンドル-ブランチブロックと左バンドル-ブランチ伝導の障害を含む,重要な伝導異常につながる.

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