デフィブリレーションの代謝的決定因子. アデノシンの役割
1Department of Medicine, New York Hospital-Cornell Medical Center, New York 10021.
Circulation
|February 1, 1995
まとめ
アデノシンは,A1受容体経由でカテキオラミンの効果を阻害することによって,除細動値 (DFT) を上昇させます. これは,心房細動 (VF) 中のアデノシン放出が,除細動の成功を損なう可能性があることを示唆しています.
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:
- 静脈細動 (VF) の持続時間は,除細動値 (DFT) に与える影響のために,心停止の結果にとって非常に重要です.
- 低酸素症,酸性症,またはアルカリ症は,DFTに悪影響を与えない.
- カテコラミンとアデノシン濃度が低酸素時に上昇し,アデノシンはカテコラミンが心室筋に及ぼす効果を阻害する.
研究 の 目的:
- 長期VF中のアデノシン放出が,抗アドレナジックメカニズムを通じてDFTに悪影響を及ぼすという仮説を検証する.
主な方法:
- アデノシンとディピリダモールは,VFの5分後に観察されたアデノシンレベルを模倣するために犬に注入されました.
- トランストラシックとトランスミオカルディアのDFTを測定した.
- 実験は,A1アデノシン受容体を8-cyclopentyltheophylline (CPT) でブロックした後に,そして無神経状態で繰り返されました.
主要な成果:
- アデノシンは,トランストラシック (49%) とトランスミオカルディア (103%) DFTの両方を有意に増加させた.
- A1アデノシン受容体アンタゴニストであるCPTは,DFTに対するアデノシンの効果を完全に阻害した.
- アデノシンは,無神経状態ではDFTに影響を与えず,抗アドレナージックメカニズムを示唆しました.
結論:
- アデノシンは,抗アドレナジックメカニズムを通じて,A1心筋受容体を通してDFTを増加させます.
- VF中にアデノシンが上昇すると,デフィブリレーションが損なわれる可能性があります.
- A1アデノシンアンタゴニストは,DFTを低下させることで,VF中の除細動を促進する可能性があります.
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