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Ferric Chloride-induced Murine Thrombosis Models
Published on: September 5, 2016
組織型プラズミノゲン活性化剤による冠動脈血栓溶解中の血小板および血管機能
D M Kerins1, L Roy, G A FitzGerald
1Division of Clinical Pharmacology, Vanderbilt University, Nashville, Tennessee 37232.
Circulation
|December 1, 1989
まとめ
血小板活性化は,組織型プラズミノゲン活性化剤 (t-PA) による冠動脈血栓溶解中に増加します. アスピリンはこれを阻害し,再注入された患者のプロスタサイクリン (PGI2) の減少は血管損傷の兆候となる可能性があります.
科学分野:
- 心血管医学 心血管医学
- 血液学 ヘマトロジ
- 薬理学 薬理学とは
背景:
- 血小板の活性化は,血栓形成の重要な要因であり,血栓駆除薬療法の効果を阻害する可能性があります.
- 組織型プラズミノゲン活性化剤 (t-PA) は急性心筋梗塞の重要な治療法ですが,その有効性は血小板の反応によって影響を受けることがあります.
研究 の 目的:
- 急性心筋梗塞を経験している患者の静脈内t-PAによる冠動脈血栓溶解中の血小板活性化を調査する.
- 血小板活性化および再注血のマーカーとして,トロンボキサンA2およびプロスタサイクリン (PGI2) バイオシンセシスを評価する.
主な方法:
- t-PA治療を受けている患者の尿中の2,3-ディノール-トロンボキサンB2および2,3-ディノール-6-ケト-PGF1アルファ分泌の測定.
- アスピリンを事前投与した患者と,アスピリンを投与しなかった患者の代謝産物濃度の比較.
- リパルフュージョン状態に関連したメタボライト濃度の分析.
主要な成果:
- 静脈内でのt-PA投与は,尿中の2,3-ディノール-トロンボキサンB2濃度が48時間上昇することで示される,トロンボキサンA2バイオシンセシスを有意に増加させた.
- アスピリンの前治療は,t-PAが誘発したトロンボキサンA2バイオシンセシスの増加を廃止しました.
- プラスタサイクリン (PGI2) バイオシンセシスはt-PA後も増加しましたが,この増加は,再注射を達成した患者では,そうでない患者と比較して著しく低下しました.
結論:
- これらの発見は,t-PA媒介冠動脈血栓解離の間に有意な血小板活性化の証拠を提供します.
- 成功的に再注射された患者のPGI2バイオシンセシスの減少は,血管再注射損傷のマーカーとして機能する可能性があります.
- 増幅された血小板活性化は,再注射損傷の結果であり,治療結果に潜在的に影響を与える可能性があります.
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