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隔離された低密度高密度リポプロテインを有する被験者における高密度リポプロテインを増やすことにより,内皮機能の回復

Radjesh J Bisoendial¹, G Kees Hovingh, Johannes H M Levels

¹Department of Vascular Medicine, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, Netherlands.

|May 29, 2003

まとめ

ATP結合カセット (ABCA) -1の変異による家族性低アルファリポプロテイン血症は,低HDLを引き起こし,内皮機能不全を引き起こす. アポリポプロテインA-I/フォスファティディルコリン (apoA-I/PC) の注入により,円盤の血管機能が急速に回復し,HDLが顕著になりました.

科学分野:

心血管生物学心血管生物学
脂質代謝についてです.
血管生理学血管生理学

背景:

家族性低アルファリポプロテイン血症 (低HDL) は,ATP結合カセット (ABCA) -1遺伝子における機能喪失変異によって引き起こされます.
これは,孤立した低高密度リポプロテイン (HDL) コレステロールを研究するためのモデルを提供します.

研究の目的:

孤立した低HDLが内皮機能に与える影響を評価する.
HDLの急激な増加による血管効果を評価する.

主な方法:

血管機能は,静脈閉塞プレチスモグラフィーを用いて,9人のABCA1ヘテロジゴトと9人の対照群で測定されました.
血管拡張剤 (セロトニン) と酸化窒素合成酵素抑制剤 (L-NMMA) に対する前腕の血流反応を評価した.
アポリポプロテインA-I/フォスファティディルコリン (apoA-I/PC) ディスクを静脈注入した後,反応を再評価した.

主要な成果:

ABCA1ヘテロジゴト群は,対照群と比較して,HDLレベルが著しく低下し,前腕の血流反応がセロトニンとL-NMMAに鈍化した.
apoA-I/PCディスクの注入により,ABCA1ヘテロジゴトのHDLレベルが正常化しました.
輸液後,セロトニンとL-NMMAの両方に対する血管運動反応は,ABCA1ヘテロジゴトで完全に回復しました.

結論:

ABCA1ヘテロジゴトにおける単離された低HDLは,内皮機能不全と窒素酸化物の生物活性低下に関連しています.
apoA-I/PCの単発注入により,内皮機能が迅速かつ完全に回復しました.
HDLは,逆コレステロール輸送における役割を超えて,動脈壁に直接的な有益な影響を及ぼします.

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