酸化窒素は,心不全の心臓における心筋の酸素消費を調節する
YingJie Chen1, Jay H Traverse, Ruisheng Du
1Department of Medicine, Division of Cardiology, University of Minnesota Medical School, Minneapolis 55455, USA.
Circulation
|July 10, 2002
まとめ
閉塞性心不全では,誘導性酸化窒素合成酵素 (iNOS) を阻害すると,心筋の酸素消費量 (MVO2) が増加する. これは,INOSが心不全におけるMVO2の調節に重要な役割を果たしていることを示唆しています.
科学分野:
- 心血管生理学 心血管の生理学
- 酸化窒素の生物学 酸化窒素の生物学
背景:
- 固有の酸化窒素 (NO) は通常,心筋の酸素消費 (MVO2) を抑制する.
- 非選択的酸化窒素合成酵素 (NOS) 阻害は,健康な心臓ではMVO2を増加させます.
- 閉塞性心不全 (CHF) では内皮NOSが低下しますが,誘導性NOS (iNOS) が存在する可能性があります.
研究 の 目的:
- NOSの阻害が心不全患者のMVO2を増加させるかどうかをテストする.
- CHFにおけるMVO2調節におけるiNOSの役割を調査する.
主な方法:
- 犬の急性心室ペースで誘発された心不全 (CHF).
- S-メチルイソチオureaを使用した選択的なiNOS阻害.
- MVO2の測定,冠動脈の血流量,左心房圧,および休息および運動中のdP/dt.
主要な成果:
- CHFの犬は,休息時の冠動脈血流とMVO2が低下し,運動反応が鈍化した.
- 選択的なiNOS阻害は,CHFの犬の休息状態および運動中にMVO2を増加させた.
- iNOS阻害は,非選択的なNOS阻害とは異なり,正常な犬のMVO2に効果がなかった.
結論:
- 内生的なNOは,心不全でMVO2を調節する.
- iNOSはCHF心筋梗塞におけるNO生成に寄与する.
- NOを調節するMVO2の源は,正常な心臓と衰弱している心臓の間で異なります.
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