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肥満や睡眠時無呼吸症候群における血管炎症
Sanja Jelic1, David J Lederer, Tessa Adams
1Columbia University College of Physicians and Surgeons, Division of Pulmonary, Allergy, and Critical Care Medicine, PH8 Center, Room 101, 630 W 168th St, New York, NY 10032, USA. sj366@columbia.edu
Circulation
|February 18, 2010
まとめ
肥満ではなく,阻害性睡眠時無呼吸症 (OSA) は,血管内皮機能不全と炎症を大きく引き起こします. OSAを継続的な陽性空気圧で治療すると,内皮機能が改善され,酸化ストレスが軽減されます.
科学分野:
- 心血管科学 心血管科学
- スリープ・メディシン (睡眠医学)
- 血管生物学 血管生物学
背景:
- 阻害性睡眠時無呼吸症 (OSA) は,肥満で一般的であり,心血管疾患のリスクと関連しています.
- 肥満とOSAの両方が,血管内皮炎に寄与する.
- この研究は,OSAの内皮効果と肥満を区別することを目的とした.
研究 の 目的:
- 肥満に起因する内皮の変異が実際にOSAによって引き起こされているかどうかを調査する.
- 血管炎症,酸化ストレス,内皮機能に対するOSAの影響を評価する.
- OSA患者における内皮機能不全に対する継続的な陽性気道圧 (CPAP) 治療の効果を評価する.
主な方法:
- 71人の被験者 (正常体重から肥満者) がポリソムノグラフィーを受けた.
- 炎症と酸化ストレスに対する内皮細胞における核因子-kappaBとニトロチロシン発現の定量化.
- 測定された内皮酸化窒素合成酵素 (eNOS),リン酸化eNOS,および内皮機能のための腕動脈の流れ媒介の拡張.
- OSA患者におけるCPAP治療の4週間後に評価された変化.
主要な成果:
- OSAの患者は,OSAのない被験者と比較して,より低いENOSおよびリン酸化ENOS発現と,流動媒介の膨張の障害を示した.
- ニトロチロシン発現は,OSA患者で有意に高かった.
- CPAP治療は,OSA患者で,フローメディエーションによる膨張とeNOS発現を改善し,同時にニトロチロシンと核因子-kappaBを減少させた.
結論:
- 未治療のOSAは,肥満患者の血管内皮機能不全,炎症,酸化ストレスの主な要因です.
- 肥満自体は,OSAと比較して,内皮機能にそれほど大きな影響を与えない.
- CPAP療法は,OSAに関連した内皮機能不全と炎症を効果的に逆転させます.
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