Para-sympathetic vagal activation has profound influence on heart rate and other cardiovascular parameters. We tested the hypothesis that transcutaneous Vagal Nerve Stimulation (tVNS) through the auricular branch of the vagus nerve would attenuate the normal sympathetic response to central blood volume reduction by lower body negative pressure (LBNP). 10 healthy volunteers (6 female; age 21 ± 2 years; weight 62 ± 13 kg; height 167 ± 12 cm) were included in this cross-over design trial. After 15 min rest in supine position, subjects underwent three 15-min periods of 30 mmHg LBNP intervention with and without cyclic tVNS stimulation. Continuous cardiovascular parameters (Nexfin) were recorded. Overall tVNS did not convincingly attenuate sympathetic response to central hypovolemia. Deactivation of the tVNS during LBNP resulted in increased MAP at 2.3 ± 0.5 mmHg (P < 0.001). Comparing the cyclic actual active stimulation periods to periods with pause during tVNS intervention showed a decrease in HR by 72.9 ± 11.2 to 70.2 ± 11.6 bpm (mean ± SD; P < 0.05), and concomitant increases in SV (86.0 ± 12.1 to 87.2 ± 12.6 mL; P < 0.05), MAP (82.9 ± 6.3 to 84.0 ± 6.2 mmHg; P < 0.05) and TPR (1116.0 ± 111.1 to 1153 ± 104.8 dyn*s/cm5; P < 0.05). tVNS in 30 s cycles during LBNP can selectively attenuate HR, prompting a compensatory augmented sympathetic response. It would appear the method used in this study at least, has an isolated cardiac inhibitory effect probably mediated by augmented vagal activity on the sinoatrial or atrio-ventricular node, possibly in combination with reduced activity in the sympathetic cardiac nerve.

中文翻译：

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下半身负压时经皮迷走神经刺激


副交感迷走神经激活对心率和其他心血管参数具有深远的影响。我们测试了这样的假设：通过迷走神经耳支的经皮迷走神经刺激（tVNS）会减弱对下半身负压（LBNP）导致的中枢血容量减少的正常交感神经反应。本交叉设计试验包括 10 名健康志愿者（6 名女性；年龄 21 ± 2 岁；体重 62 ± 13 kg；身高 167 ± 12 cm）。仰卧位休息 15 分钟后，受试者接受 3 个 15 分钟的 30 mmHg LBNP 干预，有或没有循环 tVNS 刺激。记录连续心血管参数（Nexfin）。总体而言，tVNS 并没有令人信服地减弱对中枢血容量不足的交感神经反应。 LBNP 期间 tVNS 失活导致 MAP 增加至 2.3 ± 0.5 mmHg (P < 0.001)。将循环实际主动刺激周期与 tVNS 干预期间的暂停周期进行比较，结果显示 HR 下降 72.9 ± 11.2 至 70.2 ± 11.6 bpm（平均值 ± SD；P < 0.05），并且 SV 随之增加（86.0 ± 12.1 至 87.2 ± 12.6 mL；P < 0.05）、MAP（82.9 ± 6.3 至 84.0 ± 6.2 mmHg；P < 0.05）和 TPR（1116.0 ± 111.1 至 1153 ± 104.8 dyn*s/cm5；P < 0.05）。 LBNP 期间 30 秒周期的 tVNS 可以选择性减弱 HR，促使补偿性增强交感神经反应。看来本研究中使用的方法至少具有孤立的心脏抑制作用，可能是由窦房结或房室结迷走神经活动增强介导的，可能与交感心脏神经活动减少相结合。