骨肌中的对素敏感的 afferent神经元在心力衰竭中异常
Scott A Smith1, Maurice A Williams, Jere H Mitchell
1Department of Internal Medicine, Harry S. Moss Heart Center, University of Texas Southwestern Medical Center, Dallas, TX 75390-9174, USA.
Circulation
|April 27, 2005
概括
心力衰竭加剧了运动压力反射 (EPR) 由于改变了IV组 afferent神经元. 这些神经元在扩张性心肌病症中表现出反应迟,导致EPR功能障碍和运动能力下降.
科学领域:
- 心血管生理学心血管生理学
- 神经科学是一个神经科学.
- 运动生理学 运动生理学
背景情况:
- 运动压力反射 (EPR) 在心力衰竭中被夸大.
- 由肌肉代谢物刺激的IV组 afferent神经元是EPR的关键贡献者.
- 这些神经元的变化可能是心力衰竭中EPR功能障碍的基础.
研究的目的:
- 为了研究IV组 afferent神经元在心力衰竭中观察到的夸张EPR中的作用.
- 在心力衰竭模型中,确定第四组神经元中的功能和分子变化是否有助于EPR功能障碍.
主要方法:
- 在新生小鼠中,IV组的 afferent 纤维使用素被切除.
- 在成年大鼠中,EPR通过电气诱导的静态肌肉收缩来激活.
- 评估了对动脉内素和TRPv1mRNA表达的压力反应.
主要成果:
- 新生儿素治疗模仿了扩张心肌病 (DCM) 的老鼠所观察到的过度心率和血压反应.
- 接受素治疗的老鼠和DCM老鼠都对后肢素给药的压力反应有所降低.
- 在DCM大鼠中,TRPv1 mRNA表达,IV组纤维的标志物,被下调.
结论:
- 心力衰竭中的EPR功能障碍涉及第四组 afferent纤维的功能和分子变化.
- 这些代谢敏感神经元的反应能力在DCM中变得模糊,尽管整体EPR夸大了.
- 了解这些机制对于开发改善心力衰竭运动能力的疗法至关重要.
相关概念视频
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