Neurally mediated vasoconstriction is capable of decreasing skin blood flow during orthostasis in the heat-stressed human.
Neurally mediated vasoconstriction is capable of decreasing skin blood flow during orthostasis in the heat-stressed human.
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神经介导的血管收缩能够减少热应激人体直立期间的皮肤血流量。
DOI：
10.1113/jphysiol.2006.112649
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发表时间：
2006
期刊：
影响因子：
--
通讯作者：
Crandall,CraigG
中科院分区：
文献类型：
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作者：
Shibasaki,Manabu;Davis,ScottL;Cui,Jian;Low,DavidA;Keller,DavidM;Durand,Sylvain;Crandall,CraigG
考虑到全身热应激时皮肤血管传导（CVC）的大量增加，这种血管床在直立应激时的血压调节中很重要。在这种热状态下，CVC的变化据报道是由于主动血管扩张剂活性的退出。与目前的思路相反，本研究的目的是确定在热应激个体直立挑战期间，皮肤血管收缩神经活动是否增强并能够促进CVC的降低。健康血压正常的受试者皮下注射肉毒毒素A (BTX‐A)，以抑制皮肤活性血管舒张神经释放神经递质。在实验当天，微透析探针被放置在BTX - A处理过的部位和相邻的未处理过的部位。在方案1中，将体内温度升高~ 0.7°C，然后施加下体负压（LBNP;−30 mmHg）。LBNP降低了BTX‐A处理位点的CVC （Δ4.2±2.9%max）和对照位点（Δ9.8±4.1%max）。在方案2中，在确认BTX‐A治疗部位在全身加热过程中没有皮肤血管扩张后，通过在LBNP之前皮内给药异丙肾上腺素，该部位的CVC相对于对照部位升高到相似的水平（分别为55.4±13.4%和60.7±10.4%）。同样，当流量在位点之间匹配时，LBNP降低了BTX‐A处理位点（Δ15.3±4.6%max）和对照位点（Δ8.8±5.6%max）的CVC。这些数据表明，在热应激个体的直立挑战中，皮肤血管收缩系统参与并能够降低CVC。
Given the large increase in cutaneous vascular conductance (CVC) during whole‐body heat stress, this vascular bed is important in the regulation of blood pressure during orthostatic stress. In this thermal state, changes in CVC are reported to be due to withdrawal of active vasodilator activity. The purpose of this study was to identify, contrary to the current line of thinking, whether cutaneous vasoconstrictor neural activity is enhanced and capable of contributing to reductions in CVC during an orthostatic challenge of heat‐stressed individuals. Healthy normotensive subjects were pretreated, subcutaneously, with botulinum toxin A (BTX‐A) to inhibit the release of neurotransmitters from cutaneous active vasodilator nerves. On the experimental day, microdialysis probes were placed in the BTX‐A‐treated site and in an adjacent untreated site. In protocol 1, internal temperature was elevated ∼0.7°C, followed by the application of lower body negative pressure (LBNP; −30 mmHg). LBNP reduced CVC at the BTX‐A‐treated sites (Δ4.2 ± 2.9%max), as well as at the control site (Δ9.8 ± 4.1%max). In protocol 2, after confirming the absence of cutaneous vasodilatation at the BTX‐A‐treated site during whole‐body heating, CVC at this site was elevated to a similar level relative to the control site (55.4 ± 13.4versus60.7 ± 10.4%max, respectively) via intradermal administration of isoproterenol prior to LBNP. Similarly, when flow was matched between sites, LBNP reduced CVC at both the BTX‐A‐treated (Δ15.3 ± 4.6%max) and the control sites (Δ8.8 ± 5.6%max). These data suggest that the cutaneous vasoconstrictor system is engaged and is capable of decreasing CVC during an orthostatic challenge in heat‐stressed individuals.