性化学反射激活不会导致心力衰竭中肌肉交感神经活动升高
P van de Borne1, R Oren, E A Anderson
1Cardiovascular Center, University of Iowa, Iowa City 52242, USA.
Circulation
|September 15, 1996
概括
在心力衰竭患者中,交感神经活动的增加并不是由过度活跃的化学受体引起的. 呼吸纯氧并没有改变交感神经活动,反驳了化学反射假说.
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.
- 心脏衰竭研究研究
背景情况:
- 心力衰竭与交感神经系统活动增加有关.
- 这种同情激活可能源于大脑干信号的改变或化学受体敏感度的提高.
- 激发性化学受体对心力衰竭的同情驱动的作用尚不清楚.
研究的目的:
- 调查一种假设,即激发性化学受体附属体的强化激活有助于心力衰竭中同情活性升高.
- 为了确定通过呼吸100%的氧气来禁用化疗受体是否会影响心力衰竭患者的同情神经活动.
主要方法:
- 在12名慢性心力衰竭患者 (NYHA III类,LVEF 24±2%) 中,从经神经测量了交感神经活动.
- 在患者呼吸室内空气和100%氧气时进行测量,以禁用化疗受体.
- 在9个健康对照组中,也记录了休息时的交感神经活动.
主要成果:
- 与对照组相比,心力衰竭患者的静止交感神经活动 (59±5次/分钟) 与对照组 (36±4次/分钟) 相比显著增加.
- 呼吸100%氧气增加了氧和 (94%至99%),但没有显著改变肌肉交感神经活动 (798±122单位/分钟在室内空气上,而824±35单位/分钟在100%氧气上).
- 血压没有受到氧气给药的影响.
结论:
- 该研究得出的结论是,心力衰竭患者肌肉循环的efferent交感活动增加并不能通过激发性化学反射 afferents的强化激活来解释.
- 这些发现表明,其他机制负责心力衰竭中观察到的同情力驱动的增加.
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