急性心筋不全後の冠動脈血管の反応性

D D Ku

Science (New York, N.Y.)

|November 5, 1982

まとめ

トロンビンは血管を広げて狭める原因となります. 損傷した冠動脈は,トロンビンに対する拡大反応を失い,冠動脈血管に潜在的に寄与します.

科学分野:

心血管生理学心血管の生理学
内皮機能の機能について
トロンボシス研究研究

背景:

トロンビンは,血液凝固における重要な酵素です.
血管を覆う内皮細胞は,血管トーンを調節する上で重要な役割を果たします.
血管の反応の変化は,血管などの心血管疾患に関与しています.

研究の目的:

犬冠動脈に対する外因性トロンビンの影響を調査する.
トロンビン誘発の血管反応における内皮細胞の役割を決定する.
異動性トロンビン反応が,不血症や血管縮に及ぼす影響を調査する.

主な方法:

犬の冠動脈に外因性トロンビンを投与する.
血管応答の評価 (血管拡張と血管収縮).
阻害剤 (ヘパリン,プロプラノロール,アトロピン,インドメタシン) の効果と内皮剥離の評価.

主要な成果:

外因性トロンビンは二相反応を誘発した:投与量による血管拡張に続いて非血栓性動脈の血管収縮.
血管拡張はヘパリンまたは内皮脱皮によって阻害されたが,プロプラノロール,アトロピン,またはインドメタシンによって阻害されなかった.
発血性動脈では,トロンビン誘発の血管拡張が失われ,血管収縮が強化された.

結論:

内皮細胞は,冠動脈におけるトロンビン媒介の血管拡張に不可欠です.
損傷した内皮は,トロンビンに対する反応を変化させ,潜在的に血管収縮につながります.
損傷した冠動脈におけるトロンビン反応の変化は,冠動脈血管の病原化に寄与する可能性があります.

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