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Is visceral sympathoexcitation to heat stress dependent on activation of ionotropic excitatory amino acid receptors in the rostral ventrolateral medulla?内脏交感兴奋对热应激的反应是否依赖于延髓腹外侧头端兴奋性氨基酸离子型受体的激活?
Am J Physiol Regul Integr Comp Physiol. 2011 Aug;301(2):R548-57. doi: 10.1152/ajpregu.00113.2011. Epub 2011 Jun 1.
2
AT1 receptors in the paraventricular nucleus mediate the hyperthermia-induced reflex reduction of renal blood flow in rats.室旁核内的 AT1 受体介导发热引起的大鼠肾血流反射性减少。
Am J Physiol Regul Integr Comp Physiol. 2011 Feb;300(2):R479-85. doi: 10.1152/ajpregu.00604.2010. Epub 2010 Dec 1.
3
Influence of endogenous angiotensin II on control of sympathetic nerve activity in human dehydration.内源性血管紧张素 II 对人体脱水时交感神经活性控制的影响。
J Physiol. 2009 Nov 15;587(Pt 22):5441-9. doi: 10.1113/jphysiol.2009.176693. Epub 2009 Oct 5.
4
Neural control and mechanisms of eccrine sweating during heat stress and exercise.热应激和运动期间的神经控制及汗腺分泌机制
J Appl Physiol (1985). 2006 May;100(5):1692-701. doi: 10.1152/japplphysiol.01124.2005.
5
Heat stress enhances arterial baroreflex control of muscle sympathetic nerve activity via increased sensitivity of burst gating, not burst area, in humans.在人类中,热应激通过增加爆发门控而非爆发面积的敏感性来增强动脉压力反射对肌肉交感神经活动的控制。
J Physiol. 2006 Jun 1;573(Pt 2):445-51. doi: 10.1113/jphysiol.2006.108662. Epub 2006 Mar 31.
6
Components and mechanisms of thermal hyperpnea.热呼吸急促的组成部分和机制。
J Appl Physiol (1985). 2006 Aug;101(2):655-63. doi: 10.1152/japplphysiol.00210.2006. Epub 2006 Mar 24.
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Spectral characteristics of skin sympathetic nerve activity in heat-stressed humans.热应激状态下人体皮肤交感神经活动的频谱特征
Am J Physiol Heart Circ Physiol. 2006 Apr;290(4):H1601-9. doi: 10.1152/ajpheart.00025.2005. Epub 2005 Nov 23.
8
Orthostatic challenge does not alter skin sympathetic nerve activity in heat-stressed humans.直立位应激不会改变热应激状态下人体的皮肤交感神经活动。
Auton Neurosci. 2004 Nov 30;116(1-2):54-61. doi: 10.1016/j.autneu.2004.08.009.
9
Muscle sympathetic nerve activity during lower body negative pressure is accentuated in heat-stressed humans.热应激状态下的人体在下肢负压期间,肌肉交感神经活动会增强。
J Appl Physiol (1985). 2004 Jun;96(6):2103-8. doi: 10.1152/japplphysiol.00717.2003. Epub 2004 Feb 20.
10
Forebrain and brain stem neural circuits contribute to altered sympathetic responses to heating in senescent rats.前脑和脑干神经回路导致衰老大鼠对热刺激的交感反应改变。
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人体的交感神经活动和全身热应激。

Sympathetic nerve activity and whole body heat stress in humans.

机构信息

Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital Dallas, Dallas, TX 75231, USA.

出版信息

J Appl Physiol (1985). 2011 Nov;111(5):1329-34. doi: 10.1152/japplphysiol.00498.2011. Epub 2011 Aug 25.

DOI:10.1152/japplphysiol.00498.2011
PMID:21868685
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3220304/
Abstract

We and others have shown that moderate passive whole body heating (i.e., increased internal temperature ∼0.7°C) increases muscle (MSNA) and skin sympathetic nerve activity (SSNA). It is unknown, however, if MSNA and/or SSNA continue to increase with more severe passive whole body heating or whether these responses plateau following moderate heating. The aim of this investigation was to test the hypothesis that MSNA and SSNA continue to increase from a moderate to a more severe heat stress. Thirteen subjects, dressed in a water-perfused suit, underwent at least one passive heat stress that increased internal temperature ∼1.3°C, while either MSNA (n = 8) or SSNA (n = 8) was continuously recorded. Heat stress significantly increased mean skin temperature (Δ∼5°C, P < 0.001), internal temperature (Δ∼1.3°C, P < 0.001), mean body temperature (Δ∼2.0°C, P < 0.001), heart rate (Δ∼40 beats/min, P < 0.001), and cutaneous vascular conductance [Δ∼1.1 arbitrary units (AU)/mmHg, P < 0.001]. Mean arterial blood pressure was well maintained (P = 0.52). Relative to baseline, MSNA increased midway through heat stress (Δ core temperature 0.63 ± 0.01°C) when expressed as burst frequency (26 ± 14 to 45 ± 16 bursts/min, P = 0.001), burst incidence (39 ± 13 to 48 ± 14 bursts/100 cardiac cyles, P = 0.03), or total activity (317 ± 170 to 489 ± 150 units/min, P = 0.02) and continued to increase until the end of heat stress (burst frequency: 61 ± 15 bursts/min, P = 0.01; burst incidence: 56 ± 11 bursts/100 cardiac cyles, P = 0.04; total activity: 648 ± 158 units/min, P = 0.01) relative to the mid-heating stage. Similarly, SSNA (total activity) increased midway through the heat stress (normothermia; 1,486 ± 472 to mid heat stress 6,467 ± 5,256 units/min, P = 0.03) and continued to increase until the end of heat stress (11,217 ± 6,684 units/min, P = 0.002 vs. mid-heat stress). These results indicate that both MSNA and SSNA continue to increase as internal temperature is elevated above previously reported values.

摘要

我们和其他人已经表明,适度的被动全身加热(即内部温度升高约 0.7°C)会增加肌肉(MSNA)和皮肤交感神经活动(SSNA)。然而,尚不清楚 MSNA 和/或 SSNA 是否会随着更严重的被动全身加热而继续增加,或者在中度加热后这些反应是否会达到平台期。本研究的目的是检验以下假设,即 MSNA 和 SSNA 会从中度到更严重的热应激持续增加。13 名受试者穿着水灌注服,至少经历了一次被动热应激,使内部温度升高约 1.3°C,同时连续记录 MSNA(n=8)或 SSNA(n=8)。热应激显著增加平均皮肤温度(Δ约 5°C,P < 0.001)、内部温度(Δ约 1.3°C,P < 0.001)、平均体温(Δ约 2.0°C,P < 0.001)、心率(Δ约 40 次/分钟,P < 0.001)和皮肤血管传导率[Δ约 1.1 任意单位(AU)/mmHg,P < 0.001]。平均动脉血压保持良好(P=0.52)。与基线相比,当以爆发频率(26 ± 14 至 45 ± 16 次/分钟,P = 0.001)、爆发发生率(39 ± 13 至 48 ± 14 次/100 次心跳,P = 0.03)或总活动量(317 ± 170 至 489 ± 150 单位/分钟,P = 0.02)表示时,MSNA 在热应激中期增加(爆发频率:26 ± 14 次/分钟,P = 0.001),并且一直持续到热应激结束(爆发频率:61 ± 15 次/分钟,P = 0.01;爆发发生率:56 ± 11 次/100 次心跳,P = 0.04;总活动量:648 ± 158 单位/分钟,P = 0.01)与中期加热阶段相比。同样,SSNA(总活动量)在热应激中期(正常体温;1,486 ± 472 至中期热应激 6,467 ± 5,256 单位/分钟,P = 0.03)增加,并一直持续到热应激结束(11,217 ± 6,684 单位/分钟,P = 0.002 与中期热应激相比)。这些结果表明,随着内部温度升高到先前报道的值以上,MSNA 和 SSNA 都会继续增加。