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人体运动期间皮肤主动血管收缩与主动血管舒张之间的竞争。

Competition between cutaneous active vasoconstriction and active vasodilation during exercise in humans.

作者信息

Kellogg D L, Johnson J M, Kosiba W A

机构信息

Department of Physiology, University of Texas Health Science Center, San Antonio 78284-7756.

出版信息

Am J Physiol. 1991 Oct;261(4 Pt 2):H1184-9. doi: 10.1152/ajpheart.1991.261.4.H1184.

DOI:10.1152/ajpheart.1991.261.4.H1184
PMID:1928401
Abstract

Cutaneous vasoconstriction occurs in response to the initiation of dynamic exercise in hyperthermia. To find whether this response was due to increased vasoconstrictor activity or to withdrawal of active vasodilator activity, blood flow monitoring with laser-Doppler flowmetry (LDF) was combined with the local iontophoresis of bretylium. Each of six male subjects had two forearm sites treated with bretylium for selective local blockade of noradrenergic vasoconstrictor nerves in skin. LDF was monitored at those sites and at two adjacent untreated sites. Mean arterial pressure (MAP) was measured, and cutaneous vascular conductance (CVC) was calculated as LDF/MAP. After iontophoresis, subjects underwent 3 min of cold stress (water-perfused suits) to verify vasoconstrictor blockade. CVC at untreated sites fell by 35.9 +/- 3.1% (P less than 0.01) and at bretylium-treated sites was not significantly changed (P greater than 0.10). During strenuous exercise in normothermia, CVC at untreated sites fell by 16.1 +/- 4.1% (P less than 0.05) and was unchanged at bretylium-treated sites (+12.7 +/- 6.6%, P greater than 0.05). Whole body heat stress was then applied. When exercise was repeated in hyperthermia, CVC at untreated sites fell by 11.6 +/- 3.8% (P less than 0.05) but was not significantly changed at bretylium-treated sites (+3.6 +/- 3.0%, P greater than 0.30). Following return to normothermia, cold stress verified the persistence of the blockade. We conclude that exercise initiation causes a cutaneous vasoconstriction largely or entirely due to enhanced active vasoconstrictor tone in both normothermia and hyperthermia. Little or no role in this response can be ascribed to reduced active vasodilator activity.

摘要

在高温环境下进行动态运动时,皮肤血管会发生收缩。为了确定这种反应是由于血管收缩活性增加还是由于活性血管舒张活性的减弱,采用激光多普勒血流仪(LDF)监测血流,并结合溴苄铵的局部离子导入。6名男性受试者的每只前臂有两个部位接受溴苄铵治疗,以选择性地局部阻断皮肤中去甲肾上腺素能血管收缩神经。在这些部位以及两个相邻的未治疗部位监测LDF。测量平均动脉压(MAP),并将皮肤血管传导率(CVC)计算为LDF/MAP。离子导入后,受试者接受3分钟的冷应激(水灌注服)以验证血管收缩阻断情况。未治疗部位的CVC下降了35.9±3.1%(P<0.01),而溴苄铵治疗部位的CVC没有显著变化(P>0.10)。在正常体温下进行剧烈运动时,未治疗部位的CVC下降了16.1±4.1%(P<0.05),而溴苄铵治疗部位的CVC没有变化(+12.7±6.6%,P>0.05)。然后施加全身热应激。当在高温环境下重复运动时,未治疗部位的CVC下降了11.6±3.8%(P<0.05),而溴苄铵治疗部位的CVC没有显著变化(+3.6±3.0%,P>0.30)。恢复到正常体温后,冷应激证实了阻断的持续性。我们得出结论,运动开始引起的皮肤血管收缩在很大程度上或完全是由于正常体温和高温环境下活性血管收缩张力增强所致。这种反应中活性血管舒张活性降低的作用很小或没有作用。

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