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低酸素誘発性肺高血圧後の血管内血栓症:サイクロオキシゲネーゼ-2による調節

Graham P Pidgeon¹, Rasa Tamosiuniene, Gang Chen

¹Department of Clinical Pharmacology, Royal College of Surgeons Ireland, 123 St. Stephens Green, Dublin 2, Ireland. gpidgeon@rcsi.ie

|October 20, 2004

まとめ

サイクロオキシゲネーゼ-2 (COX-2) 抑制は,血中毒が誘発した肺高血圧を悪化させ,血栓素A2と血小板活性化を増加させます. COX-2は,この状態における血管反応と血栓形成の調節に重要な役割を果たします.

科学分野:

心血管科学の研究について
肺内医学肺内医学肺内医学
炎症と免疫学について

背景:

慢性的な低酸素症は,肺動脈壁の厚み,血管抵抗の増大,右心不全によって特徴づけられる肺高血圧につながる.
プラスタサイクリン類は,肺圧縮の低下に有効性を示しており,肺血管の低酸素反応におけるサイクロオキシゲナーゼ-2 (COX-2) の役割を示唆しています.

研究の目的:

低酸素誘発性肺高血圧の発生と進行におけるサイクロオキシゲナーゼ-2 (COX-2) の役割を調査する.
このモデルでは,COX-2抑制が肺動脈圧,血小板活動,血栓形成に影響するかどうかを判断する.

主な方法:

肺高血圧は,スプラグ・ダウリー・ラットで14日間,ヒポバリック・ヒポキシーを介して誘発された.
動物は選択性COX-2阻害剤 (SC236) または媒介剤で治療され,同時に肺動脈平均圧 (mPAP) の評価が行われました.
トロンボキサンB2 (TXB2) と6-ケトプロスタグランジンF1αのレベルは,小便で測定され,同時に,血小板活性化マーカーとCOX-2ノックアウトマウスにおける遺伝子発現分析も行われました.

主要な成果:

低酸素症はmPAP,肺動脈壁の厚さ,COX-2発現,およびプロスタサイクリン形成を増加させた.
選択的なCOX-2阻害はmPAPの増加を著しく悪化させ,これはトロンボキサンA2受容体対抗剤によって減弱された効果である.
COX-2の阻害は,尿中のTXB2を増加させ,プロスタサイクリン代謝産物分泌を減少させ,血小板活性化を高め,肺動脈における血小板収縮を促進した.

結論:

COX-2発現は,低酸素誘発性肺高血圧において上調される.
COX-2は,この状態における血小板活動と血管内血栓の調節に重要な役割を果たします.
COX-2を標的にすると,肺高血圧が悪化し,この疾患におけるプロスタグランディンの複雑な役割が強調される可能性があります.

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