氧化调节了心脏衰竭的人类线粒体呼吸
K E Loke1, S K Laycock, S Mital
1Department of Physiology, New York Medical College, Valhalla, NY, USA.
Circulation
|September 24, 1999
概括
氧化 (NO) 影响人类心脏衰竭的组织呼吸. 内源性和外源性NO都调节氧气消耗,突出显示NO.
科学领域:
- 心血管生理学心血管生理学
- 线粒体呼吸 线粒体呼吸
- 氧化信号传输 氧化信号传输
背景情况:
- 失败的人类心肌表现出改变的代谢功能.
- 氧化 (NO) 在心力衰竭中调节组织呼吸的作用尚未完全理解.
研究的目的:
- 为了研究通过氧化 (NO) 在人类心肌衰竭中调节组织呼吸.
- 为了确定内源和外源NO对心力衰竭中氧气消耗的影响.
主要方法:
- 他们使用了从心脏中抽取的人类心肌组织样本.
- 用克拉克型氧气电极测量组织的氧气消耗.
- 在NO合成酶阻断之前和之后,评估了布拉迪基宁,阿姆洛迪平,拉米普利拉特,硫和NO释放化合物的作用.
主要成果:
- 布拉迪基宁,阿姆洛迪平,拉米普利拉特和尔方降低了心肌氧耗氧.
- 这些减少被NO合成酶抑制显著减弱,表明NO的参与.
- 外源的NO释放化合物也减少了氧气消耗,独立于NO合成酶阻断.
结论:
- 通过NO调节氧气消耗,在失败的人类心肌中保持不变.
- 抑制氨酸降解对于调节心力衰竭中的线粒体呼吸至关重要.
- 内源和外源的NO都在心肌组织呼吸中发挥作用.
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