腕動脈の血管拡張機能と,フレミングハムの子孫研究における全身性炎症
Joseph A Vita1, John F Keaney, Martin G Larson
1Evans Memorial Department of Medicine, Boston University School of Medicine, Boston, Mass, USA. jvita@bu.edu
Circulation
|December 1, 2004
まとめ
炎症は,血管内皮機能,特に前腕の微小血管を損なう,従来の危険因子を考慮した後でも. これは,全身の炎症が血管運動機能不全に作用することを示唆しています.
科学分野:
- 心血管科学 心血管科学
- 血管生物学 血管生物学
- 炎症の研究 炎症の研究
背景:
- 伝統的な危険因子と炎症は,血管内皮の機能を破壊し,動脈硬化を促進します.
- 内皮機能不全は白血球の粘着が増加し,酸化窒素の生物利用性が低下する.
- 危険因子,炎症,酸化窒素との相互作用は不明である.
研究 の 目的:
- 炎症がヒト内皮機能を損なうという仮説を検証する.
- 炎症マーカーと内皮機能の測定値との関係を評価する.
主な方法:
- 評価したフレミングハム研究参加者2701人 (平均年齢61歳).
- 腕動脈の流動媒介の膨張と反応性高血圧の測定.
- C反応性タンパク質 (CRP),インタールイキン-6 (IL-6),溶性細胞間粘着分子-1 (sICAM-1),および単細胞化学反応性タンパク質-1 (MCP-1) の血清濃度を評価した.
主要な成果:
- フローメディエイトの膨張は,CRP,IL-6,sICAM-1との逆相関を示し,リスク要因を調整した後に無意味となった.
- 反応性高血症は,炎症マーカーと逆相関を示し,リスク因子調整によって弱まった.
- CRP,IL-6,sICAM-1と反応性高血症の部分的な相関は依然として有意であった.
結論:
- 発見は,リスク要因が炎症を誘発し,血管機能を損なうという仮説を支持しています.
- 炎症は,従来の危険因子を超えて,フローメディエートされた膨張に追加的な効果を示さなかった.
- CRP,IL-6,sICAM-1で示される全身性炎症は,前腕の微小血管の血管運動機能の障害に寄与する可能性があります.
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