Elucidating mechanisms of attenuated skin vasodilation during passive heat stress in persons with spinal cord injury.

IF 1.8 4区 医学 Q3 CLINICAL NEUROLOGY
Journal of Spinal Cord Medicine Pub Date : 2024-09-01 Epub Date: 2023-05-09 DOI:10.1080/10790268.2023.2203535
Michelle Trbovich, Yubo Wu, Wouker Koek, Jill Wecht, Dean Kellogg
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引用次数: 0

Abstract

Objective: Persons 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.

Design: Prospective interventional trial.

Setting: laboratory.

Participants: 22 veterans with SCI.

Interventions: Skin 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 measures: Laser 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.

Results: CVC rise in BR sites was significantly less than CON sites in areas with intact (P = 0.03) and impaired (P = 0.04) thermoregulatory vasodilation.

Conclusion: Cutaneous 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.

阐明脊髓损伤患者在被动热应激时皮肤血管扩张减弱的机制。
目的:脊髓损伤(SCI)患者在全身被动热应激(PHS)时,无法像健全人那样通过体温调节血管扩张来有效散热。皮肤血流(SkBF)由双重交感血管运动系统控制:去甲肾上腺素能血管收缩神经(VC)和胆碱能血管舒张神经(VD)。因此,血管舒张功能受损可能是由于去甲肾上腺素能血管收缩神经张力的不适当增加与胆碱能血管舒张神经张力的竞争或胆碱能神经张力的减弱所致。为了解决这个问题,我们使用了选择性阻断去甲肾上腺素神经释放从而降低去甲肾上腺素能血管张力的乙酰胆碱(BR)。如果 PHS 期间血管扩张受损是由于不适当的血管张力增加所致,那么 BR 治疗将改善 PHS 期间的 SkBF 反应:设计:前瞻性干预试验。设置:实验室。参与者:22 名患有 SCI 的退伍军人:干预措施:对先前定义为体温调节血管扩张完好与受损的皮肤表面区域进行 BR 离子透入治疗,附近未治疗的部位作为对照/CON。参与者接受 PHS 治疗,直到核心温度上升 1°C:激光多普勒血流计测量体温调节血管扩张受损和完好区域的 BR 和 CON 点的 SkBF。计算所有部位的皮肤血管电导率(CVC)。峰值-PHS CVC与基线(BL)进行归一化:(CVC peak-PHS/CVC BL)以量化SkBF的变化:结果:在体温调节血管扩张完好(P = 0.03)和受损(P = 0.04)的区域,BR 位点的 CVC 上升明显低于 CON 位点:结论:对影响血管收缩的去甲肾上腺素能神经递质的神经释放进行皮肤阻断并不能增强 SCI 患者在 PHS 期间的体温调节血管扩张;相反,BR 会减弱这种反应。阻断影响血管收缩的去甲肾上腺素能神经递质的皮肤释放并不能恢复 SCI 患者在 PHS 期间的皮肤主动血管扩张。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Journal of Spinal Cord Medicine
Journal of Spinal Cord Medicine 医学-临床神经学
CiteScore
4.20
自引率
5.90%
发文量
101
审稿时长
6-12 weeks
期刊介绍: For more than three decades, The Journal of Spinal Cord Medicine has reflected the evolution of the field of spinal cord medicine. From its inception as a newsletter for physicians striving to provide the best of care, JSCM has matured into an international journal that serves professionals from all disciplines—medicine, nursing, therapy, engineering, psychology and social work.
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