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A Murine Model of Subarachnoid Hemorrhage
Published on: November 21, 2013
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サバラクノイド下出血後の急性神経心臓学的損傷
Nader M Banki1, Alexander Kopelnik, Michael W Dae
1Division of Cardiology, Department of Radiology, UCSF Medical Center, San Francisco, California, USA.
Circulation
|November 16, 2005
まとめ
サバラクノイド出血 (SAH) の後の左心室機能不全は,心臓への血流の減少ではなく,異常な交感神経の活動に関連しています. これは,神経損傷がSAH患者で心筋の問題を引き起こす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
- 神経科学は神経科学である.
- メディカルイマージング (医学イメージング)
背景:
- 左心室 (LV) 収縮機能不全は,ヒト亜arachnoid出血 (SAH) 患者の既知の合併症です.
- この機能不全の正確な原因は議論されており,心筋不全や過剰なカテキオラミン放出を含む理論があります.
研究 の 目的:
- SAH患者におけるLVシストリック機能不全の根本的な病理生理学を調査する.
- 心筋 perfusion と 交感内膜の異常を区別するために.
主な方法:
- エコーカルディオグラフィーとミオカルディアスシンチグラフィー (MIBIとMIBG) は,38ヶ月間にわたって42人のSAH患者で使用されました.
- 心臓トロポニンI (cTI) レベルは,筋細胞死滅を評価するために測定されました.
- LVエジェクション分数と壁運動スコアは,盲目の観察者によって計算されました.
主要な成果:
- 解釈可能なスキャンを受けたすべての患者 (N=41) は正常な心筋 perfusion (MIBI 吸収) を示した.
- 12人の患者は異常な交感性内置 (MIBG吸収の欠如) を示した.
- デナーベーションを有する患者は,LV壁運動異常 (92%対52%,P=0.030) と高度のcTI (58%対21%,P=0.029) を持つ可能性がより高かった.
結論:
- SAHにおけるLVシストリック機能不全は,正常な心筋 perfusion と関連しているが,異常な交感性内置と関連している.
- 研究結果は,心臓の交感神経からの過剰なノレピネフリン放出は,筋細胞と神経末端の損傷を引き起こす可能性があることを示唆しています.
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