高密度リポプロテインは,体内において心筋 perfusion を刺激する
Bodo Levkau1, Sven Hermann, Gregor Theilmeier
1Institute of Pathophysiology, Center of Internal Medicine, University Hospital Essen, Hufelandstrasse 55, 45122 Essen, Germany. levkau@uni-essen.de
Circulation
|November 17, 2004
まとめ
高密度脂質タンパク質 (HDL) は,生体内で酸化窒素 (NO) を通して心筋 perfusion を強化する. しかし,HDL内のスフィンゴシン1-リン酸 (S1P) は,S1P3受容体を通じた perfusion を阻害し,HDL を示唆しています.
科学分野:
- 心血管科学の研究について
- 内分泌学 エンドックリノロジー
- 薬理学 薬理学とは
背景:
- HDLコレステロールは,内皮に依存した血管拡張に関連しています.
- HDLは,動脈中の酸化窒素 (NO) の放出を通じて血管拡張を媒介する.
- HDL投与は,高コレステロール血症患者の内皮機能を改善します.
研究 の 目的:
- 心筋パルフュージョンに対するHDLの効果を in vivoで調査する.
- 冠動脈循環に対するHDLの影響の背後にあるメカニズムを解明する.
- 心筋 perfusion での HDL とその成分 S1P の役割を区分する.
主な方法:
- マウスにヒトHDLを投与し,99mTc-MIBIを用いて心筋 perfusion を測定した.
- 内皮 NO合成酵素 (eNOS) とS1P受容体3 (S1P3) が不足しているマウスを利用した.
- 直接S1Pを投与し,心筋 perfusionに対する効果を評価した.
主要な成果:
- HDL投与は,体内では心筋 perfusion を ~18% 増加させた.
- このHDL誘発の増加は,eNOS欠乏したマウスでは廃止された.
- S1Pの投与は心筋 perfusion を ~25% 減少させ,S1P3-/-マウスには効果がなかった.
- 心筋 perfusion に HDL の刺激効果は,S1P3-/- マウスで維持されました.
結論:
- HDLは,NOに依存するメカニズムを通じて心筋の perfusion を強化する.
- S1P3はS1P3受容体を通して心筋膜の輸血を抑制する.
- HDLは,冠動脈循環における直接的なNO媒介の血管拡張によって冠動脈のリスクを軽減する可能性があります.
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