慢性的なβ-アドレノ受容体阻害は,犬における実験的な右側閉塞性心不全におけるβ-アドレノ受容体の過敏性の発症を防ぐ
C S Liang1, R P Frantz, M Suematsu
1Department of Medicine, University of Rochester Medical Center, N.Y. 14642.
Circulation
|July 1, 1991
まとめ
ナドロールによるベータ受容体阻害は,右心不全の犬において,心筋筋ベータ受容体密度および心筋ベータアドレナージ感度の低下を予防した. これは,過剰な交感性刺激が心不全における受容体変化に寄与することを示唆しています.
科学分野:
- 心臓病学 心臓病学
- 薬理学 薬理学とは
- 生理学 生理学とは
背景:
- 閉塞性心不全は,過剰な交感性刺激による心筋のβ-アドレネルゲン受容体密度と応答性の低下を伴う.
- 心不全の病理生理学における交感性過活性の役割を理解することは極めて重要です.
研究 の 目的:
- ベータ受容体阻害が,右心不全における過剰な交感性刺激に関連した心筋の変化を予防できるかどうかを調査する.
主な方法:
- 犬で実験的に右心不全を誘発し,ベータ受容体ブロッカーナドロール (40 mg/日) を5週間投与した.
- コントロールグループには,シャム手術を受けた犬と,ナドロールを投与していない右心不全の動物が含まれていました.
- 血液動力学的パラメータ,血のノルエピネフリン,心筋ベータ受容体およびアデニラートサイクラースの活性が評価されました.
主要な成果:
- ナドロール治療は,心不全における右心室縮または血ノルエピネフリン値上昇を予防しませんでした.
- しかし,ナドロールは,心筋ベータ受容体密度の低下を防止し,心筋ベータアドレナジック感受性の低下を弱めた.
- ナドロール治療後の偽手術を受けた犬では,心筋ベータ受容体またはアデニラートサイクラースの活性に重大な変化は見られなかった.
結論:
- 過剰な交感刺激は,ベータ受容体のダウンレギュレーションと右心不全における過敏性の発達に重要な役割を果たします.
- ベータ受容体阻害は,心不全における受容体機能を保存するための治療戦略を提供することができる.
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