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在人类持续的压力感受器刺激过程中,精神压力会增加交感神经活动。

Mental stress increases sympathetic nerve activity during sustained baroreceptor stimulation in humans.

作者信息

Anderson E A, Sinkey C A, Mark A L

机构信息

Department of Anesthesia, University of Iowa College of Medicine, Iowa City 52242.

出版信息

Hypertension. 1991 Apr;17(4 Suppl):III43-9. doi: 10.1161/01.hyp.17.4_suppl.iii43.

DOI:10.1161/01.hyp.17.4_suppl.iii43
PMID:2013492
Abstract

Muscle sympathetic nerve activity (MSNA) in humans is regulated in part by arterial baroreceptors. However, although mental stress increases blood pressure, it also increases MSNA. This suggests that baroreceptor control of MSNA is altered during mental stress. In nine healthy men (age range, 20-26 years), we recorded heart rate, blood pressure, and efferent MSNA (peroneal nerve, microneurography) during a 4-minute mental arithmetic task performed both before and during infusion of phenylephrine sufficient to markedly suppress resting MSNA. Before phenylephrine, mental stress significantly increased mean blood pressure (p less than 0.01), heart rate (p less than 0.01), and MSNA (from 18.5 +/- 3.2 to 24.8 +/- 3.5 bursts/min, p less than 0.001). Phenylephrine infusion increased resting mean blood pressure (from 84.0 +/- 2.6 to 90.0 +/- 2.7 mm Hg, p less than 0.01) and decreased resting heart rate (from 65.6 +/- 1.7 to 55.6 +/- 2.0 beats/min, p less than 0.01). Resting MSNA decreased dramatically during phenylephrine (from 18.5 +/- 3.2 to 3.3 +/- 1.3 bursts/min, p less than 0.01). During phenylephrine, mental stress again significantly (p less than 0.01) increased mean blood pressure, heart rate, and MSNA (from 3.1 +/- 1.4 to 10.9 +/- 1.8 bursts/min). The magnitude of stress-induced increases in MSNA and heart rate were comparable before and during phenylephrine infusion despite the greater elevation in diastolic pressure during stress plus phenylephrine. The present study demonstrates that mental stress produces sympathoexcitatory and pressor responses even during sustained stimulation of arterial baroreceptors.

摘要

人类的肌肉交感神经活动(MSNA)部分受动脉压力感受器调节。然而,尽管精神压力会升高血压,但它也会增加MSNA。这表明在精神压力期间,压力感受器对MSNA的控制发生了改变。在9名健康男性(年龄范围为20 - 26岁)中,我们在静注去氧肾上腺素足以显著抑制静息MSNA之前和期间,记录了他们在4分钟心算任务期间的心率、血压和传出MSNA(腓总神经,微神经ography)。在使用去氧肾上腺素之前,精神压力显著升高了平均血压(p < 0.01)、心率(p < 0.01)和MSNA(从18.5 ± 3.2次/分钟增加到24.8 ± 3.5次/分钟,p < 0.001)。静注去氧肾上腺素升高了静息平均血压(从84.0 ± 2.6毫米汞柱升高到90.0 ± 2.7毫米汞柱,p < 0.01)并降低了静息心率(从65.6 ± 1.7次/分钟降低到55.6 ± 2.0次/分钟,p < 0.01)。在使用去氧肾上腺素期间,静息MSNA显著降低(从18.5 ± 3.2次/分钟降低到3.3 ± 1.3次/分钟,p < 0.01)。在使用去氧肾上腺素期间,精神压力再次显著(p < 0.01)升高了平均血压、心率和MSNA(从3.1 ± 1.4次/分钟增加到10.9 ± 1.8次/分钟)。尽管在压力加去氧肾上腺素期间舒张压升高幅度更大,但在静注去氧肾上腺素之前和期间,压力诱导的MSNA和心率增加幅度相当。本研究表明,即使在持续刺激动脉压力感受器期间,精神压力也会产生交感兴奋和升压反应。

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