Rapid saline infusion and/or drinking enhance skin sympathetic nerve activity components reduced by hypovolaemia and hyperosmolality in hyperthermia

Rapid saline infusion and/or drinking enhance skin sympathetic nerve activity components reduced by hypovolaemia and hyperosmolality in hyperthermia
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快速盐水输注和/或饮用可增强因热疗时低血容量和高渗透压而减少的皮肤交感神经活动成分

DOI:
10.1113/jp276633
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发表时间:
2018
期刊:
The Journal of Physiology
影响因子:
--
通讯作者:
Nose Hiroshi
Nose Hiroshi
中科院分区:
--
文献类型:
--
作者:
Kamijo Yoshi-ichiro;Okazaki Kazunobu;Ikegawa Shigeki;Okada Yoshiyuki;Nose Hiroshi

文献摘要

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在热疗中,血浆高渗透压抑制皮肤血管舒张和出汗反应,这种抑制可通过口咽刺激(如饮酒)消除。低血容量仅抑制皮肤血管舒张,在高温下快速输注可增强皮肤血管舒张。我们最近的研究表明,皮肤交感神经活动(SSNA)涉及与心脏周期同步和非同步的成分,这些成分分别与活跃的血管扩张剂和sudomotor相关。在目前的研究中,血浆高渗抑制了这两种成分;饮酒消除了高渗透压引起的抑制,同时增加了皮肤血管舒张和出汗,而不改变血浆容量和渗透压。此外,快速生理盐水输注增加了低血容量和高热人群的同步成分和皮肤血管舒张。结果支持了我们的观点,即SSNA涉及活跃的皮肤血管扩张器和压迫运动器,并且渗透压信号被投射到控制体温调节的部位比来自压力感受器的信号被投射到延髓的位置更优越。摘要我们报道了皮肤交感神经活动(SSNA)与心脏周期同步和非同步的成分;这两种成分在高温下都增加,我们的研究结果表明,这两种成分分别与活性血管扩张剂和抗强心剂有关。在本研究中,我们研究了热疗中这些成分的增加是否会被血浆高渗透压抑制,同时抑制皮肤血管扩张和出汗,以及这种抑制是否会通过口咽刺激(饮酒)释放。此外,在低血容量和高热受试者中测试了快速生理盐水输注对皮肤血管扩张和出汗的成分和反应的影响。我们发现(1)血浆高渗透压抑制了热疗中的这两种成分,(2)同时饮用200 mL水可以释放这种抑制,同时增强皮肤血管舒张和出汗反应,(3)在前10分钟和后20分钟分别以1.0和0.2 mL min - 1kg - 1快速输注,利尿剂诱导的低血容量血症中的同步成分和皮肤血管舒张比时间对照组更大。在0.1 ml min - 1kg - 1的情况下,快速输注30分钟,与时间对照组相比,未观察到非同步成分和出汗反应的增加。结果支持这样的观点,即SSNA涉及与心脏周期同步和非同步的成分,与活跃的皮肤血管舒张剂和压迫运动有关,并且渗透压诱导的体温调节调节位点位于压力感受器信号投射的延髓之上。
Key pointsIn hyperthermia, plasma hyperosmolality suppresses both cutaneous vasodilatation and sweating responses and this suppression is removed by oropharyngeal stimulation such as drinking. Hypovolaemia suppresses only cutaneous vasodilatation, which is enhanced by rapid infusion in hyperthermia.Our recent studies suggested that skin sympathetic nerve activity (SSNA) involves components synchronized and non‐synchronized with the cardiac cycle, which are associated with an active vasodilator and a sudomotor, respectively.In the present study, plasma hyperosmolality suppressed both components; drinking removed the hyperosmolality‐induced suppressions, simultaneously with increases in cutaneous vasodilatation and sweating, while not altering plasma volume and osmolality.Furthermore, a rapid saline infusion increased the synchronized component and cutaneous vasodilatation in hypovolaemic and hyperthermic humans.The results support our idea that SSNA involves an active cutaneous vasodilator and a sudomotor, and that a site where osmolality signals are projected to control thermoregulation is located more superior than the medulla where signals from baroreceptors are projected.AbstractWe reported that skin sympathetic nerve activity (SSNA) involved components synchronized and non‐synchronized with the cardiac cycle; both components increased in hyperthermia and our results suggested that the components are associated with an active vasodilator and a sudomotor, respectively. In the present study, we examined whether the increases in the components in hyperthermia would be suppressed by plasma hyperosmolality simultaneously with suppression of cutaneous vasodilatation and sweating and whether this suppression was released by oropharyngeal stimulation (drinking). Also, effects of a rapid saline infusion on both components and responses of cutaneous vasodilatation and sweating were tested in hypovolaemic and hyperthermic subjects. We found that (1) plasma hyperosmolality suppressed both components in hyperthermia, (2) the suppression was released by drinking 200 mL of water simultaneously with enhanced cutaneous vasodilatation and sweating responses, and (3) a rapid infusion at 1.0 and 0.2 ml min−1kg−1for the first 10 min and the following 20 min, respectively, increased the synchronized component and cutaneous vasodilatation in diuretic‐induced hypovolaemia greater than those in a time control; at 0.1 ml min−1kg−1for 30 min no greater increases in the non‐synchronized component and sweating responses were observed during rapid infusion than in the time control. The results support the idea that SSNA involves components synchronized and non‐synchronized with the cardiac cycle, associated with the active cutaneous vasodilator and sudomotor, and a site of osmolality‐induced modulation for thermoregulation is located superior to the medulla where signals from baroreceptors are projected.