マトリックスメタルプロテインアース阻害が,体積過負荷による心室改造に及ぼす影響
Amanda L Chancey1, Gregory L Brower, J Thomas Peterson
1Department of Anatomy, Physiology, and Pharmacology, Auburn University, Auburn, Ala 36849, USA.
Circulation
|May 9, 2002
まとめ
マトリックスメタルプロテインアース (MMP) 阻害療法により,心不全のラットモデルにおける左心室 (LV) のリモデリングと高縮が著しく減少しました. この治療は,慢性的な体積過負荷時に心室の膨張を弱め,心臓機能を保ちました.
科学分野:
- 心臓病学 心臓病学
- 薬理学 薬理学とは
- バイオメディカルエンジニアリング
背景:
- 左心室 (LV) の膨張と膨張は,慢性的な体積過負荷に対する補償反応である.
- 心筋の再編成は適応不良になり,心不全につながる可能性があります.
- マトリックスメタルプロテインアース (MMP) の活性の増加は,体積過負荷モデルにおけるLVの膨張と関連しています.
研究 の 目的:
- LVのサイズと機能に対するMMP阻害療法の効果を調査する.
- 量過負荷による心不全のラットモデルでPD 166793 (1 mg x kg ((-1) x d ((-1)) を評価する.
主な方法:
- ネズミは,赤下腹部アオルトカバルフィスチュラ (体積過負荷) または偽手術を受けた.
- グループには,治療されたフィスチュラと未治療のフィスチュラ,治療されたフィスチュラと未治療のフェイクコントロールが含まれていました.
- PD 166793は,MMP阻害療法を評価するために投与されました.
主要な成果:
- 両方のフィスチュラ群では,対照群と比較して,LV重量が増加しました.
- 治療を受けたフィスチュラ群は,未治療のフィスチュラ群 (P<0.012) と比較して8週間でより低いLV体重を示しました.
- 治療を受けたフィスチュラ群では,心室の膨張が著しく減少した.
結論:
- MMP阻害療法は,慢性的な体積過負荷における心筋リモデリングを著しく弱める.
- この治療は,LVの膨張を予防し,LVの縮を著しく減少させました.
- MMP阻害で治療されたラットでは,心室機能が保たれた.
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