机械反射调解了心力衰竭中夸张的运动压力反射
Scott A Smith1, Jere H Mitchell, R Haris Naseem
1Department of Internal Medicine, Harry S. Moss Heart Center, University of Texas Southwestern Medical Center, Dallas, TX 75390-9174, USA.
Circulation
|October 12, 2005
概括
在心力衰竭中,肌肉机械反射,而不是第四组附属神经元,驱动了过度的运动压力反射反应. 这表明,准机械反射可以治疗心力衰竭中的异常运动反应.
科学领域:
- 心血管生理学心血管生理学
- 运动生理学 运动生理学
- 心脏衰竭研究研究
背景情况:
- 心力衰竭的特点是运动期间平均动脉压 (MAP) 和心率 (HR) 的过度增加.
- 这种过度的心血管反应是由过度活跃的运动压力反射 (EPR) 介导的.
- 虽然IV组 afferent神经元启动了夸张的EPR,但它们并不介导增强的循环反应.
研究的目的:
- 调查假设,EPR的机械敏感元件,主要涉及III组 afferent纤维,调解心力衰竭中增强的EPR.
主要方法:
- 使用了患有扩张性心肌病 (DCM) 的老鼠模型和对照 (假) 组.
- 在新生儿素治疗 (NNCAP) 动物中切除了IV组 afferent纤维.
- 通过电气诱导的静态肌肉收缩来激活EPR,有或没有加多 (一种机械受体阻断剂).
主要成果:
- 与假老鼠相比,DCM和NNCAP老鼠在EPR激活期间在MAP和HR中表现出更大的增加.
- 在所有组中,加多的使用减弱了MAP和HR对收缩的反应.
- 在DCM和NNCAP大鼠中,应答的减少显着更大,表明对机械受体的依赖程度更大.
结论:
- 肌肉机械反射是心力衰竭中夸张的运动压力反射的主要媒介.
- 机械反射过度活跃可能是改变IV组纤维功能的补偿机制.
- 肌肉机械反射为管理心力衰竭中异常运动诱导的循环反应提供了一个潜在的新型治疗点.
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