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心筋梗塞の拡張とマトリックスメタルプロテインアースの阻害

Rupak Mukherjee¹, Theresa A Brinsa, Kathryn B Dowdy

¹Division of Cardiothoracic Surgery, Medical University of South Carolina, Charleston, SC 29425, USA.

|February 5, 2003

まとめ

マトリックスメタルプロテインアース阻害 (MMPi) は,心筋梗塞 (MI) の後の左心室 (LV) の膨張と心臓発作の拡大を減少させた. また,MMPiは,MMPとMMPの組織阻害剤 (TIMP) の特定のレベルを,心臓の影響を受けた領域で調節した.

科学分野:

心血管科学の研究について
心臓のリモデリング
薬理学的介入薬理学的介入

背景:

心筋梗塞 (MI) の後の左心室 (LV) の改造には,マトリックスメタルプロテインアース (MMP) の活性化が含まれることがあります.
MMP阻害 (MMPi) を調査することは,潜在的な治療戦略を提供します.

研究の目的:

発心筋梗塞の後の地域的なLV幾何学に対するMMP阻害の影響を評価する.
MMPとMMPiのMI後のMMPとMMPの組織阻害剤 (TIMP) レベルの変化を評価する.

主な方法:

放射性オパックマーカーを装着した豚を用いて,MIを誘発した後の心筋膜の地域幾何学を測定した.
MMPi (PD166793) またはプラセボをMI後の豚に投与し,2週と8週間にわたって評価した結果.
測定された LV 寸法,心臓発作のサイズ,MMP 活動,TIMP-1 レベル.

主要な成果:

MMPiは,MIのみのグループと比較して,MI後8週間で,LVのエンド・ダイアストリック次元を著しく弱め,地域性心臓発作領域を減少させた.
MMPiによって,ex vivo MMPのプロテオリチス活性が低下した.
MMPiは,膜型のMMPレベルを正常化し,MI領域のTIMP-1レベルを上昇させた.

結論:

MMPの阻害は,MIの治癒の遅い段階で,LVの拡張と心臓発作の拡大を効果的に弱めた.
外源的なMMPiは,MMPsとTIMPsの地域特有の調節を示した.

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