左心室高縮の電気生理学的影響. カルシウムとカリウムチャネル封鎖の効果
P R Kowey1, T D Friechling, J Sewter
1Cardiovascular Research Laboratory, Medical College of Pennsylvania, Philadelphia.
Circulation
|June 1, 1991
まとめ
左心室縮症 (LVH) は,電気回復を変化させることにより,心室細動に対する脆弱性を高めます. カリウムチャネルを遮断するが,カルシウムチャネルを遮断しないことで,この心律失調から身を守ることができる.
科学分野:
- 心臓病学 心臓病学
- 電気生理学 電気生理学
- 薬理学 薬理学とは
背景:
- 左心室多動症 (LVH) は心律不整に繋がる可能性があります.
- LVHの arritmogenic 効果は,詳細な電気生理学的調査を必要とします.
研究 の 目的:
- 無傷の心臓モデルでLVHのリズム異常効果を定義する.
- LVH誘発性不律症に対するカルシウムとカリウムチャネル阻害の影響を評価する.
主な方法:
- LVHの猫主動動脈帯バンドモデルにおける電気生理学的評価.
- 伝導時間,興奮性,屈折性,およびアクションポテンシャルの持続時間の測定.
- 室細動 (VF) の脆弱性および値の評価.
主要な成果:
- LVHの猫は,対照群と比較して,VF,自発的なVF,およびVFの低い値に対する脆弱性が高かった.
- LVHは,有効な耐火期とアクションポテンシャル持続時間の分散を大きくした.
- リソチリド (カリウムチャネルブロッカー) は分散と心室の脆弱性を低下させ,ベラパミル (カルシウムチャネルブロッカー) は有意な効果を示さなかった.
結論:
- LVHは,屈折性の分散と再極化を促進することによって,心房の繊細化に対する脆弱性を大幅に増加させます.
- 電圧依存のカリウムチャネル遮断は,LVH誘発性 arritmogenesisを緩和する.
- ゆっくりと内側へ向かうカルシウムチャネルの遮断は,LVHに関連する心房細動から保護しません.
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