Abstract
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 (5min of OA-D followed by 10min of rest; n=8), taVNS (15min; n=9), or no intervention (15min, 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±13pg/mL; p<0.05) than in the time control group (+142±24pg/mL). A similar trend was observed in the taVNS group for TNF-α (+1.7±0.3pg/mL vs. 4.1±1.3pg/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±0.6pg/mL, p<0.05; IL-8: 190±61 vs. 483±125pg/mL, p <0.05; TNF-α: 1.2±0.3 vs. 2.3±0.4pg/mL, p<0.05). OA-D decreased mean blood pressure from the first (100±8mmHg) to the second (92±6mmHg; p<0.05) and third (93±8mmHg; p<0.05) study days and reduced low frequency spectral power of systolic blood pressure variability (19±3mmHg2 after OA-D vs. 28±5mmHg2 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±3.0ms/mmHg) to the second (18.4±4.3ms/mmHg; p<0.05) and third (16.9±4.2ms/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.
Highlights
Context: The parasympathetic-mediated inflammatory reflex inhibits excessive proinflammatory cytokine production
Consistent with these RMSSD responses to transcutaneous auricular vagus nerve stimulation (taVNS), pooling the data from all three study days revealed that taVNS increased high frequency spectral power of heart rate variability (HRV) during the recovery period at the end of the experimental protocol compared to the baseline recording at the beginning of the experimental protocol. These findings suggest that taVNS increases cardiac parasympathetic tone. This cardiac autonomic effect of taVNS did not last into the day because no significant changes in RMSSD or high frequency spectral power of HRV were observed during the baseline recordings of the second and third study days compared to the first study day
TaVNS blunted the increase in salivary interleukin-1β (IL-1β) that was associated with the experimental protocol (Figure 7) and successive applications of occipitoatlantal decompression (OA-D) on three consecutive days reduced salivary IL-6, IL8, and tumor necrosis factor α (TNF-α) baseline levels on the third compared to the first study day (Table 2)
Summary
Context: The parasympathetic-mediated inflammatory reflex inhibits excessive proinflammatory cytokine production. 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 Biological antiinflammatory drugs, such as tumor necrosis factor-α (TNF-α) antagonists, have revolutionized treatment of chronic inflammatory diseases and largely improved prognosis and quality of life for affected patients [1, 2]. Intracerebroventricular administration of the M2-muscarinic antagonist methoctramine inhibited the TNF response to endotoxemia and increased high frequency heart rate variability (HRV) [10], a measure of parasympathetic modulation of cardiac function [11]. The results of the metaanalysis were inconsistent [26], which may be related to the fact that the majority of included studies did not utilize OMT techniques that have the potential to activate the antiinflammatory efferent arc of the inflammatory reflex
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