Elucidating mechanisms of attenuated skin vasodilation during passive heat stress in persons with spinal cord injury.
Elucidating mechanisms of attenuated skin vasodilation during passive heat stress in persons with spinal cord injury.
复制标题
阐明脊髓损伤患者被动热应激期间皮肤血管舒张减弱的机制。
DOI：
10.1080/10790268.2023.2203535
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发表时间：
2023
期刊：
影响因子：
--
通讯作者：
Kellogg,Dean
中科院分区：
文献类型：
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作者：
Trbovich,Michelle;Wu,Yubo;Koek,Wouker;Wecht,Jill;Kellogg,Dean
目的脊髓损伤（SCI）患者在全身被动热应激（PHS）过程中不能像正常人那样通过热调节血管舒张有效地散热。皮肤血流（SkBF）由两个交感血管运动系统控制：去肾上腺素能血管收缩（VC）神经和胆碱能血管舒张（VD）神经。因此，血管舒张受损可能是由于去肾上腺素能性VC张力的不适当增加与胆碱能性血管舒张或胆碱能张力的降低相竞争。为了解决这个问题，我们使用溴代溴胺（BR）选择性地阻断神经释放去甲肾上腺素，从而降低去甲肾上腺素能的VC张力。如果小灵通期间的血管舒张受损是由于VC张力的不适当增加，BR治疗将改善小灵通期间的SkBF反应。前瞻性介入试验，设置实验室。参与者为脊髓损伤退伍军人22人。干预：先前定义的热调节性血管舒张功能完好与受损的皮肤表面区域采用溴离子导入治疗，附近未治疗的部位作为对照/CON。参与者接受小灵通治疗，直到核心温度上升1°C。结果测量：激光多普勒流量计测量了热调节性血管舒张受损和完整区域BR和CON部位的SkBF。计算所有部位的皮肤血管传导（CVC）。将峰值- phs CVC归一化为基线（BL）：（CVC峰值- phs /CVC BL）以量化SkBF变化。结果热调节性血管舒张功能完好区（P= 0.03）和受损区（P= 0.04） BR部位scvc升高明显低于CON部位。结论皮肤阻断去甲肾上腺素能神经递质的神经释放影响血管收缩，并不能增强脊髓损伤患者PHS期的热调性血管舒张；相反，BR减弱了反应。皮肤阻断影响血管收缩的去甲肾上腺素能神经递质的神经释放并不能恢复脊髓损伤患者PHS期间皮肤的血管活性扩张。
ObjectivePersons with spinal cord injury (SCI) are unable to efficiently dissipate heat via thermoregulatory vasodilation as efficiently as able-bodied persons during whole body passive heat stress (PHS). Skin blood flow (SkBF) is controlled by dual sympathetic vasomotor systems: noradrenergic vasoconstrictor (VC) nerves and cholinergic vasodilator (VD) nerves. Thus, impaired vasodilation could result from inappropriate increases in noradrenergic VC tone that compete with cholinergic vasodilation or diminished cholinergic tone. To address this issue, we used bretylium (BR) which selectively blocks neural release of norepinephrine, thereby reducing noradrenergic VC tone. If impaired vasodilation during PHS is due to inappropriate increase in VC tone, BR treatment will improve SkBF responses during PHS.DesignProspective interventional trial.Settinglaboratory.Participants22 veterans with SCI.InterventionsSkin surface areas with previously defined intact vs. impaired thermoregulatory vasodilation were treated with BR iontophoresis with a nearby untreated site serving as control/CON. Participants underwent PHS until core temperature rose 1°C.Outcome MeasuresLaser doppler flowmeters measured SkBF over BR and CON sites in areas with impaired and intact thermoregulatory vasodilation. Cutaneous vascular conductance (CVC) was calculated for all sites. Peak-PHS CVC was normalized to baseline (BL): (CVC peak-PHS/CVC BL) to quantify SkBF change.ResultsCVC rise in BR sites was significantly less than CON sites in areas with intact (P= 0.03) and impaired (P= 0.04) thermoregulatory vasodilation.ConclusionCutaneous blockade of neural release of noradrenergic neurotransmitters affecting vasoconstriction did not enhance thermoregulatory vasodilation during PHS in persons with SCI; rather BR attenuated the response. Cutaneous blockade of neural release of noradrenergic neurotransmitters affecting vasoconstriction did not restore cutaneous active vasodilation during PHS in persons with SCI.