在高工作状态下的心脏中,肌动脉氧化在心脏中具有心脏病发作后重塑
1Departments of Medicine, Biochemistry, and Radiology and the Center for Magnetic Resonance Research, University of Minnesota, Minneapolis, MN, USA.
Circulation
|February 23, 1999
概括
心脏病发作后的左心室重塑 (LVR) 会导致高能酸盐 (HEP) 的减少. 这项研究发现,心力衰竭中低HEP水平并不是由于氧气供应不足,即使心脏工作量增加时也是如此.
科学领域:
- 心脏病学 心脏病学
- 心血管生理学心血管生理学
- 生物化学 生物化学
背景情况:
- 心脏病发作后的左心室重塑 (LVR) 与心肌高能酸盐 (HEP) 水平的降低有关.
- 在患有充血性心力衰竭 (CHF) 的动物中,这些HEP减少更为严重.
- 心脏工作量增加加剧了HEP损失,这表明需求诱导的缺血症.
研究的目的:
- 测试假设,肌细胞氧气供应不足是发心后LVR和CHF中HEP异常的基础.
- 在基底和刺激条件下,研究心肌氧供应和HEP水平之间的关系.
主要方法:
- 在猪中通过冠状动脉绑定诱导的心肌梗塞.
- 组包括正常,补偿LVR和CHF动物.
- 用31P核磁共振测量脂蛋白/ATP (PCr/ATP);用1H核磁共振测量脱氧球蛋白 (Mb-delta) 在远程心肌中.
主要成果:
- 基础PCr/ATP在心脏病发作后心脏中降低,在CHF中显著降低.
- 多布胺在正常心脏和LVR心脏中增加了速率-压力产物,导致可比的PCr/ATP下降,没有可检测的Mb-delta.
- 在CHF中,多布他胺反应减弱,与Mb-delta无关.
结论:
- 多布胺诱导的PCr/ATP降低并不是由于氧气供应不足.
- 低基底PCr/ATP和减弱的dobutamine响应在CHF发生在没有心肌缺氧.
- 在CHF中,HEP和收缩异常不是由于氧气供应不足造成的.
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