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慢性心不全患者の内皮機能に対するエンドセリン受容体阻害の効果
R Berger1, B Stanek, M Hülsmann
1Department of Cardiology, University of Vienna, Austria.
Circulation
|February 22, 2001
まとめ
エンドセリンA受容体阻害は,慢性心不全患者の内皮依存性血管拡張を改善しました. この治療はフロー・メディエイト・ディラテーション (FMD) を強化し,CHFにおける血管機能に対する潜在的な治療効果を示唆した.
科学分野:
- 心血管医学は,心臓血管医学である.
- 薬理学 薬理学とは
背景:
- 慢性心不全 (CHF) は,内皮に依存した血管拡張の障害と,内皮リン-1濃度の上昇と関連しています.
- CHFにおける基礎血管トーンの増加は,内皮機能不全に寄与する.
研究 の 目的:
- エンドセリンA受容体を阻害することで,心筋梗塞の患者における内皮に依存した,フローメディエートされた血管拡張 (FMD) を改善できるかどうかを調査する.
- 血管トーン低下に対するエンドセリンA受容体阻害の効果を評価する.
主な方法:
- 21人のCHF患者と11人の対照群を対象としたランダム化研究.
- 患者は3週間,エンドセリンA受容体ブロッカーLU 135252 (30 mg/dまたは300 mg/d) またはプラセボを投与されました.
- 高解像度の超音波を用いて,口炎とニトログリセリンによる腕動脈の拡張を測定した.
主要な成果:
- ベースライン FMDは,対照群 (3.2%対9.7%) に比べて,CHF患者で著しく低下しました.
- LU135252による治療は,心筋梗塞患者の口腔炎を有意に改善した (3.0%から4.9%),而プラセボは変化を示さなかった.
- 低用量LU135252 (30mg/日) は口腔炎を有意に増加させた (2.4%から5.5%),高用量では有意な増加は示されなかった.
結論:
- エンドセリンA受容体阻害は,慢性心不全の患者の口腔炎を改善する可能性があることを示しています.
- この発見は,標的型受容体ブロックを介して,CHFにおける血管機能の強化のための治療的道を示唆しています.
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