Department of Clinical Medicine, Burrell College of Osteopathic Medicine, Las Cruces, NM, USA.
Department of Biomedical Sciences, Burrell College of Osteopathic Medicine, Las Cruces, NM, USA.
J Osteopath Med. 2021 Feb 24;121(4):401-415. doi: 10.1515/jom-2020-0071.
The parasympathetic-mediated inflammatory reflex inhibits excessive proinflammatory cytokine production. Noninvasive techniques, including occipitoatlantal decompression (OA-D) and transcutaneous auricular vagus nerve stimulation (taVNS), have been demonstrated to increase parasympathetic tone.
To test the hypothesis that OA-D and taVNS increase parasympathetic nervous system activity and inhibit proinflammatory cytokine mobilization and/or production.
Healthy adult participants were randomized to receive OA-D (5 min of OA-D followed by 10 min of rest; n=8), taVNS (15 min; n=9), or no intervention (15 min, time control; n=10) on three consecutive days. Before and after these interventions, saliva samples were collected for determination of the cytokines interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor α (TNF-α). Arterial blood pressure and the electrocardiogram were recorded for a 30-min baseline, throughout the intervention, and during a 30-min recovery period to derive heart rate and blood pressure variability markers as indices of vagal and sympathetic control.
OA-D and taVNS increased root mean square of successive RR interval differences (RMSSD) and high frequency heart rate variability, which are established markers for parasympathetic modulation of cardiac function. In all three groups, the experimental protocol was associated with a significant increase in salivary cytokine concentrations. However, the increase in IL-1β was significantly less in the taVNS group (+66 ± 13 pg/mL; p<0.05) than in the time control group (+142 ± 24 pg/mL). A similar trend was observed in the taVNS group for TNF-α (+1.7 ± 0.3 pg/mL vs. 4.1 ± 1.3 pg/mL; p<0.10). In the OA-D group baseline IL-6, IL-8, and TNF-α levels on the third study day were significantly lower than on the first study day (IL-6: 2.3 ± 0.4 vs. 3.2 ± 0.6 pg/mL, p<0.05; IL-8: 190 ± 61 vs. 483 ± 125 pg/mL, p <0.05; TNF-α: 1.2 ± 0.3 vs. 2.3 ± 0.4 pg/mL, p<0.05). OA-D decreased mean blood pressure from the first (100 ± 8 mmHg) to the second (92 ± 6 mmHg; p<0.05) and third (93 ± 8 mmHg; p<0.05) study days and reduced low frequency spectral power of systolic blood pressure variability (19 ± 3 mmHg after OA-D vs. 28 ± 5 mmHg before OA-D; p<0.05), a marker of sympathetic modulation of vascular tone. OA-D also increased baroreceptor-heart rate reflex sensitivity from the first (13.7 ± 3.0 ms/mmHg) to the second (18.4 ± 4.3 ms/mmHg; p<0.05) and third (16.9 ± 4.2 ms/mmHg; p<0.05) study days.
Both OA-D and taVNS elicited antiinflammatory responses that were associated with increases in heart rate variability-derived markers for parasympathetic function. These findings suggest that OA-D and taVNS activate the parasympathetic antiinflammatory reflex. Furthermore, an antihypertensive effect was observed with OA-D that may be mediated by reduced sympathetic modulation of vascular tone and/or increased baroreceptor reflex sensitivity.
副交感神经介导的炎症反射抑制过度的促炎细胞因子产生。非侵入性技术，包括枕髁减压术（OA-D）和经皮耳迷走神经刺激（taVNS），已被证明可以增加副交感神经张力。
检验假设，即 OA-D 和 taVNS 增加副交感神经系统活动并抑制促炎细胞因子的动员和/或产生。
将健康成年参与者随机分为三组，分别接受 OA-D（5 分钟 OA-D 后休息 10 分钟；n=8）、taVNS（15 分钟；n=9）或无干预（15 分钟，时间对照；n=10），连续三天。在这些干预措施之前和之后，采集唾液样本以测定细胞因子白细胞介素-1β（IL-1β）、白细胞介素-6（IL-6）、白细胞介素-8（IL-8）和肿瘤坏死因子-α（TNF-α）。在 30 分钟的基线、整个干预期间和 30 分钟的恢复期内记录动脉血压和心电图，以得出心率和血压变异性标志物作为迷走神经和交感神经控制的指标。
OA-D 和 taVNS 增加了均方根连续 RR 间隔差异（RMSSD）和高频心率变异性，这是心脏功能副交感神经调节的既定标志物。在所有三组中，实验方案均与唾液细胞因子浓度的显著增加相关。然而，与时间对照组（+142±24pg/mL）相比，taVNS 组的 IL-1β 增加量明显减少（+66±13pg/mL；p<0.05）。在 taVNS 组中也观察到 TNF-α 的类似趋势（+1.7±0.3pg/mL 与+4.1±1.3pg/mL；p<0.10）。在 OA-D 组中，第三次研究日的基线 IL-6、IL-8 和 TNF-α 水平明显低于第一次研究日（IL-6：2.3±0.4 与 3.2±0.6pg/mL，p<0.05；IL-8：190±61 与 483±125pg/mL，p<0.05；TNF-α：1.2±0.3 与 2.3±0.4pg/mL，p<0.05）。OA-D 使平均血压从第一次（100±8mmHg）降至第二次（92±6mmHg；p<0.05）和第三次（93±8mmHg；p<0.05）研究日，并且降低了收缩压变异性的低频谱功率（19±3mmHg 后 OA-D 与 28±5mmHg 前 OA-D；p<0.05），这是血管张力交感神经调节的标志物。OA-D 还增加了从第一次（13.7±3.0ms/mmHg）到第二次（18.4±4.3ms/mmHg；p<0.05）和第三次（16.9±4.2ms/mmHg；p<0.05）研究日的压力感受器-心率反射敏感性。
OA-D 和 taVNS 均引起抗炎反应，与心率变异性衍生的副交感神经功能标志物增加相关。这些发现表明，OA-D 和 taVNS 激活了副交感神经抗炎反射。此外，OA-D 观察到降压作用，这可能是通过降低血管张力的交感神经调节和/或增加压力感受器反射敏感性来介导的。
