Muscle metaboreflex activation speeds the recovery of arterial blood pressure following acute hypotension in humans

Muscle metaboreflex activation speeds the recovery of arterial blood pressure following acute hypotension in humans
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肌肉代谢反射激活可加速人类急性低血压后动脉血压的恢复

DOI:
10.1152/ajpheart.00833.2012
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发表时间:
2013
影响因子:
4.8
通讯作者:
Narihiko Kondo and Takeshi Nishiyasu
Narihiko Kondo and Takeshi Nishiyasu
中科院分区:
医学2区
文献类型:
--
作者:
Masashi Ichinose;Kazuhito Watanabe、 Naoto Fujii;Narihiko Kondo and Takeshi Nishiyasu

文献摘要

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已经表明,动脉压力反射和肌肉代谢反射在剧烈运动期间都被激活,并且它们相互作用以调节初级心血管反射反应。然而,这种拟议的相互作用及其后果尚未完全理解。本研究的目的是验证我们的假设,即动态动脉压力反射介导的心血管反应,急性全身性低血压在人类增强时,肌肉代谢反射是活跃的,这会导致动脉血压更快的恢复。在12名健康受试者中,通过在9分钟的超收缩静息缺血后释放双侧大腿袖带,在50%最大自主收缩的等长握力运动1分钟后,通过运动后肌肉缺血(PEMI)激活和不激活肌肉代谢反射,非稳态地诱导急性低血压。在控制条件下和PEMI期间,大腿袖带释放引起平均动脉压(MAP)迅速降低,心率、心输出量(多普勒)和总血管传导性(TVC)增加。与对照组相比,PEMI期间MAP较基线的降低幅度更大,TVC的增加幅度更小。此外,动脉压力感受性反射介导的外周血管收缩在PEMI期间增强,MAP和TVC的恢复率几乎加倍。这些结果表明,当肌肉代谢反射在人体中被激活时,响应于急性低血压引起的动脉压力反射介导的外周血管收缩增强,这使MAP恢复所需的时间减半。压力反射功能的这种调节对于在肌肉代谢反射的激活期间维持升高的动脉血压将是有利的。
It has been suggested that the arterial baroreflex and muscle metaboreflex are both activated during heavy exercise and that they interact to modulate primary cardiovascular reflex responses. This proposed interaction and its consequences are not fully understood, however. The purpose of present study was to test our hypothesis that dynamic arterial baroreflex-mediated cardiovascular responses to acute systemic hypotension in humans are augmented when the muscle metaboreflex is active and that this results in a faster recovery of arterial blood pressure. Acute hypotension was induced nonpharmacologically in 12 healthy subjects by releasing bilateral thigh cuffs after 9 min of suprasystolic resting ischemia, with and without muscle metaboreflex activation via postexercise muscle ischemia (PEMI) after 1 min of isometric handgrip exercise at 50% maximum voluntary contraction. The thigh-cuff release evoked rapid reductions in mean arterial pressure (MAP) and increases in heart rate, cardiac output (Doppler), and total vascular conductance (TVC) under control conditions and during PEMI. The reductions in MAP from baseline were greater and the increases in TVC were smaller during PEMI than control. In addition, arterial baroreflex-mediated peripheral vasoconstriction was augmented during PEMI, as evidenced by a near doubling of the rate of recovery of MAP and TVC. These results show that when the muscle metaboreflex is activated in humans, arterial baroreflex-mediated peripheral vasoconstriction elicited in response to acute hypotension is augmented, which halves the time needed for MAP recovery. Such modulation of baroreflex function would be advantageous for maintaining an elevated arterial blood pressure during activation of the muscle metaboreflex.