暫定性イシュケミア中の心筋カテキオラミン放出の時間経過とメカニズム in vivo
T W Lameris1, S de Zeeuw, G Alberts
1Department of Internal Medicine I, Cardiovascular Research Institute COEUR, Erasmus University Rotterdam, Rotterdam, The Netherlands. TWL@mediaport.org
Circulation
|June 7, 2000
まとめ
筋動脈不全は,筋動脈間流体 (MIF) のカテキオラミンを著しく上昇させ,部分的に神経の再吸収の逆転によって引き起こされます. これは,機能的な交感性神経末端が,心臓発作後でも持続することを示唆しています.
科学分野:
- 心臓病学 心臓病学
- 神経科学は神経科学である.
- 生理学 生理学とは
背景:
- 高濃度のノレピネフリン (NE) は,缺血性心筋で観察される.
- 缺血および再注射中の心筋間流体 (MIF) のカテキオラミン放出メカニズムを調査することは極めて重要です.
研究 の 目的:
- 筋動脈不全と再注射の間にMIFでカテキオラミン放出の大きさとメカニズムを決定する.
- 心臓イシュケミア中のカテキオラミン放出におけるニューロン再吸収の役割を明らかにする.
主な方法:
- 麻酔した豚の微細透析を用いて,腸内カテキオラミン濃度を測定した.
- 左側前側下垂動脈 (LAD) を60分間遮断し,その後150分間再注射することで誘発された地域性心筋不全症.
- 閉塞の最後の30分間にチラミンを投与し,神経細胞の解放能力を評価する.
主要な成果:
- MIF ノルエピネフリン,ドーパミン,エピネフリンの濃度は,閉塞中の缺血領域で有意に増加した.
- 局所吸収-1ブロックは,カテキオラミンの放出を50%以上減少させた.
- MIF カテコラミン濃度は再注射中にベースラインに戻り,ティラミン誘発によるNE放出は,心臓発作組織に無傷のまま残りました.
結論:
- 筋動脈不全は,部分的には神経の再吸収の逆転による,MIFカテキオラミンの大幅な増加を引き起こします.
- MIFエピネフリンの増加は,心臓神経源を示唆しています.
- ティラミンに対するカテキオラミン反応の保存は,発血後心筋梗塞における機能的な交感性神経末端を示している.
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