心力衰竭中的收缩功能障碍的起源:循环与肌纤维相比
N G Pérez1, K Hashimoto, S McCune
1Section of Molecular and Cellular Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Md, USA.
Circulation
|March 2, 1999
概括
心力衰竭涉及严重的肌纤维激活. 变化的细胞内 (Ca2+) 动力学补偿了这种收缩机械功能障碍,挑战了当前的心力衰竭病理生理学概念.
科学领域:
- 心脏病学 心脏病学
- 生理学 生理学 生理学
背景情况:
- 慢性心力衰竭是一种致命的心脏收缩性障碍,病理生理学不清楚.
- 目前的重点是异常的 (Ca2+) 循环,尽管有证据表明肌纤维功能受损.
研究的目的:
- 调查肌纤维功能和Ca2+循环在心力衰竭中的作用.
- 为了比较失败和健康的心脏肌肉中的Ca2+处理和收缩力.
主要方法:
- 测量了自发高血压心力衰竭 (SHHF) 的腹腔肌中的细胞内Ca2+度 ([Ca2+]i) 和收缩力.
- 利用相平面分析来评估Ca2+循环和肌纤维激活动态.
主要成果:
- 与对照组相比,SHHF大鼠肌肉表现出延迟的[Ca2+]i峰值和较慢的抽力发展.
- 在SHHF肌肉中,最大的Ca2+激活力被显著抑制 (53%).
- 在衰弱的肌肉中改变了Ca2+循环动力学,部分补偿了肌纤维功能障碍.
结论:
- 肌纤维激活在心力衰竭中严重受损.
- [Ca2+]i动态的变化起到了补偿机制的作用,最大限度地减少了收缩性抑郁.
- 肌纤维是心力衰竭病理生理学的核心,Ca2+循环变化是适应性的,而不是因果性的.
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