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心脏特异性增加的阿尔多斯特的生产诱导冠状动脉功能障碍在阿尔多斯特合成酶转基因小鼠
Anne Garnier1, Jennifer K Bendall, Sebastien Fuchs
1INSERM U572, Université Paris 7, France.
Circulation
|September 15, 2004
概括
雄性小鼠心脏中阿尔多素的产量增加导致冠状动脉功能障碍,但不影响心脏结构或功能. 这可能会影响心脏适应血流需求增加的能力.
科学领域:
- 心血管生理学心血管生理学
- 内分泌学 在内分泌学.
- 分子心脏病学分子心脏病学
背景情况:
- 过高的阿尔多素与心血管功能障碍有关.
- 阿尔多激素对手可以改善心力衰竭和心肌梗塞的结果.
- 心脏中的局部阿尔多素合成表明病理作用.
研究的目的:
- 为了研究心脏阿尔多激素产量增加对心脏结构和功能的影响.
- 阐明阿尔多斯特诱导的心脏病理背后的机制.
主要方法:
- 生成的转基因小鼠在心脏中过度表达阿尔多合成酶 (AS).
- 在心脏组织中测量AS mRNA和阿尔多斯特的度.
- 评估心脏结构,功能和冠状动脉流动,使用心声学和隔离心脏输液.
主要成果:
- 转基因小鼠的AS mRNA增加了100倍,心脏阿尔多斯特增加了1.7倍.
- 没有观察到心脏结构,心室质量或心肌功能的显著变化.
- 冠状动脉功能受损,基本流量减少和血管扩张减弱,独立于氧化的产生.
结论:
- 在雄性小鼠中,心脏阿尔多斯特的增加会导致显著的冠状动脉内皮独立功能障碍.
- 这种功能障碍发生在心脏结构或整体功能没有检测到的改变的情况下.
- 冠状动脉功能障碍可能会损害心脏对血流需求增加的适应性反应.
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