意識のある羊の左心室圧圧過負荷過剰症候群の発達中に,補償性高縮から内在性心筋機能不全への移行. シストリック機能不全は,ダイアストリック機能不全に先行する
T Aoyagi1, A M Fujii, M F Flanagan
1Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115.
Circulation
|November 1, 1993
まとめ
動脈筋機能不全は,左心室縮が進行するにつれて,継続的な余分な負荷にもかかわらず,大動脈収縮の羊に発症します. シストリック機能障害は,この圧力過負荷モデルにおいて,ダイアストリック機能障害の前に現れる.
科学分野:
- 心血管生理学 心血管の生理学
- 心臓のリモデリング
- 心不全 病理生理学 心不全 病理生理学
背景:
- 大動脈狭窄は,補償された左心室高症につながる可能性があり,潜在的に心不全に進行します.
- 以前の研究では,軽度の短期的な圧力過負荷と重度の過負荷の機能不全との正常な収縮性が示されました.
- 大人の大型動物の補償性高縮から機能不全への移行は十分に実証されていません.
研究 の 目的:
- 成人羊における補償された左心室縮症から心筋機能不全への移行を実験的に実証する.
- 左心室機能不全が後負荷の不一致または内在的な心筋の問題によるかどうかを調査する.
- 圧力の過負荷で静脈動力障害が静脈動力障害に先行するかどうかを判断する.
主な方法:
- 左心室高縮症は,上昇性大動脈の水圧圧縮器を使用して,羊に誘発されました.
- 6週間にわたって左心室圧力が増加した一方で,アフターロードは一定に維持されました.
- ベータブロックとメトキサミン注入を含む連続血液動力学的研究は,マッチした負荷条件下で心筋収縮性を評価した.
主要な成果:
- 左心室高縮症は41%増加しました (左心室と体重の比率).
- 心筋機能障害は,中壁の縮小と縮小率の減少によって示され,第4週から第6週の間に発症した.
- 負荷独立の収縮性指数は,6週目に心筋収縮性の低下を確認し,下痢性パラメータは変化しませんでした.
結論:
- この研究では,正常から機能不全の心筋収縮性への移行が示されました.
- この移行は,進行性高縮の進行中の継続的な後負荷上昇にもかかわらず発生しました.
- この圧力過負荷モデルでは,シストリック機能不全がダイアストリック機能不全に先行することが観察されました.
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