相关实验视频
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Analytical Techniques for Assaying Nitric Oxide Bioactivity
Published on: June 18, 2012
阻断氧化的合成减少了心肌的氧气消耗 in vivo
A J Sherman1, C A Davis, F J Klocke
1Feinberg Cardiovascular Research Institute, Department of Medicine, Northwestern University Medical School, Chicago, III 60611-3008, USA.
Circulation
|March 4, 1997
概括
阻断氧化 (NO) 合成会减少心肌的氧气消耗,并在体内缩短部分. 这种效应涉及NO的直接心肌作用,独立于β阻塞.
科学领域:
- 心血管生理学心血管生理学
- 氧化生物学 氧化生物学
背景情况:
- 心脏肌细胞和冠状动脉血管内皮产生氧化 (NO).
- 内源性NO对心肌氧耗氧和收缩功能的体内影响尚未完全理解.
研究的目的:
- 调查氧化合成酶 (NOS) 阻断对心肌氧消耗和收缩性能的体内影响.
主要方法:
- 在完整的狗中,对NOS抑制剂 (L-NAME或N-nitro-L-arginine) 进行全身治疗.
- 测量心肌氧耗量和区域段缩短.
- 在开放胸部和慢性仪器动物模型中进行评估,有和没有β-上腺素阻塞.
主要成果:
- 在各种血液动力学需求中,NOS封锁显著降低了心肌氧消耗.
- 氧气消耗的减少平均为23-34%与L-NAME的管理.
- 冠心内L-NAME减少了心肌的氧气消耗和段缩短,独立于系统血压变化.
结论:
- 内生氧化的合成对于维持心肌的氧气消耗在体内至关重要.
- NO阻塞导致心肌氧消耗和收缩功能减少.
- 观察到的效应是通过NO对心肌的直接作用来介导的,而心肌不受β-上腺体阻塞的影响.
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