ブラジキニニンによって引き起こされる冠動脈血管拡張のメカニズム
L R Pelc1, G J Gross, D C Warltier
1Department of Anesthesiology, Medical College of Wisconsin, Milwaukee 53226.
Circulation
|June 1, 1991
まとめ
ブラディキニンは,B2受容体を活性化させ,内皮由来のリラックス因子を放出することにより,心臓の下腸内臓への血流を増大させ,冠動脈循環の研究の重要な発見である.
科学分野:
- 心血管生理学 心血管の生理学
- 血管生物学 血管生物学
- 薬理学 薬理学とは
背景:
- ブラディキニンは,脳循環における血管拡張剤として知られています.
- 犬の冠動脈循環における地域性輸血に対するその影響は,以前は研究されていなかった.
研究 の 目的:
- ブラジキニンが誘発する冠動脈血管拡張のメカニズムを調査する.
- サイクロオキシゲナーゼ,ブラジキニンB2受容体,および内皮由来のリラックス因子 (EDRF) の役割を決定する.
主な方法:
- 麻酔を受けた犬に冠動脈内ブラジキニンを注入し,冠動脈の流れに影響を隔離する.
- 放射性微小球を用いて,地域の血流量を測定する.
- 薬理学的介入:インドメタシン,B2受容体抗体,EDRF阻害剤 (キナクリン,L-アルギニン).
主要な成果:
- ブラジキニンは,優遇的に心下下臓の血流を増加させた.
- B2受容体阻害は,ブラジキニンの流れと分布への影響を弱めた.
- EDRFの阻害により,全血流が低下し,下腸内循環の再分配が阻害されました.
結論:
- 冠内ブラジキニンは,下腸内循環の perfusion を強化する.
- この効果はB2受容体の刺激とEDRFの放出,おそらく酸化窒素によって媒介されます.
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