在缺血性心肌病的心脏血管氨基素-(1-7) 中
David B Averill1, Yuichiro Ishiyama, Mark C Chappell
1The Hypertension and Vascular Disease Center, Wake Forest University School of Medicine, Medical Center Blvd, Winston-Salem, NC 27157, USA. daverill@wfubmc.edu
Circulation
|October 1, 2003
概括
在心肌梗塞之后,大鼠心肌细胞中的 angiotensin-(1-7) (Ang-[1-7]) 表达增加. 这一发现表明Ang-(1-7) 在心力衰竭的心脏反应中起作用.
科学领域:
- 心血管生理学心血管生理学
- 腎臟系統和高血壓
- 分子心脏病学分子心脏病学
背景情况:
- ангиотензин-(1-7) (Ang-[1-7]) 抵消了 ангиотензин II 在心脏中的作用.
- 在心肌梗塞 (MI) 模型中研究Ang-(1-7) 表达是至关重要的.
研究的目的:
- 为了确定Ang-(1-7) 在老鼠心肌梗塞后心肌梗塞表达.
- 了解Ang-(1-7) 在心脏组织中的细胞局部.
主要方法:
- 在路易斯大鼠中,冠状动脉绑定引起的心肌梗塞.
- 血液动力学参数和心脏缩评估MI后4周.
- 针对心脏肌细胞,间歇细胞和血管局部化的Ang-(1-7) 的免疫活性.
主要成果:
- 肌痛性心脏病的老鼠表现出左心室末端压力升高和压缩性压力降低.
- 在MI大鼠中观察到显著的心脏缩.
- 在心脏病发作区域周围的腹腔组织中,Ang-(1-7) 免疫活性显著增加.
结论:
- 冠状动脉绑定后的心力衰竭增加Ang-(1-7) 表达.
- 增加的Ang-(1-7) 仅在心脏肌细胞内局部化.
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