2021
DOI: 10.1016/j.autneu.2021.102893
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Effects of transcutaneous auricular vagus nerve stimulation on cardiovascular autonomic control in health and disease

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Cited by 34 publications
(24 citation statements)
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“…The mechanism for the HR suppression via tVNS is suggested to be the activation of excitatory inputs to the caudal ventrolateral medulla medulla by afferent fibers via the NTS; this would consequently suppress the rostral ventrolateral medulla, the source of excitatory drive of the sympathetic nervous system [ 30 ]. Previous studies indicate that tVNS activates a wide range of brain regions involved in the autonomic nervous system control [ 13 , 14 , 31 ] and that the heart-evoked potential, which reflects the cardiac interoceptive input, increases in these areas during tVNS.…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…The mechanism for the HR suppression via tVNS is suggested to be the activation of excitatory inputs to the caudal ventrolateral medulla medulla by afferent fibers via the NTS; this would consequently suppress the rostral ventrolateral medulla, the source of excitatory drive of the sympathetic nervous system [ 30 ]. Previous studies indicate that tVNS activates a wide range of brain regions involved in the autonomic nervous system control [ 13 , 14 , 31 ] and that the heart-evoked potential, which reflects the cardiac interoceptive input, increases in these areas during tVNS.…”
Section: Discussionmentioning
confidence: 99%
“…Therefore, the HR rebound after the termination of stimulation in Experiment 1 was not due to homeostatic plasticity, but rather to the physiological reaction to the verbal NRS response. In animal studies on the application of tVNS for cardiac disease, high-intensity stimulation to vagal efferent fibers induces atrial fibrillation and low-intensity VNS has been shown to suppress atrial fibrillation [ 7 , 10 , 24 , 30 , 33 , 34 , 35 , 36 ]. However, atrial fibrillation cannot be induced unless the HR is reduced by 40% or more [ 36 ].…”
Section: Discussionmentioning
confidence: 99%
“…Several other studies found a decreased HRV in SLE [ 126 , 127 , 128 , 129 , 130 ]. It is widely known that ANS dysfunction is associated with the development of cardiovascular diseases (CVDs), where the sympathetic activity is a mediator of both the onset and progression of CVDs while on the other hand, the parasympathetic control seems to have a protective role with reduced mortality in CVDs [ 131 , 132 , 133 ]. In SLE patients, CVDs are a high cause of mortality, especially related to atherosclerosis, and CVD risk is doubled with respect to the general population [ 134 , 135 ].…”
Section: Autonomic Nervous System and Its Interplay With Inflammation...mentioning
confidence: 99%
“…This includes pharmacologic therapies directed toward modulation of sympathetic nervous system activation such as beta-blockers, while recognizing limitations of off-target action and long-term side effects. Nonpharmacologic interventions such as vagal nerve stimulation, renal and carotid body denervation, and stellectomy are other options; however, they are invasive, expensive, and also associated with side effects ( 2 ). Furthermore, there are limitations with human model systems including heart rate, heart rate variability (HRV), plasma catecholamines, and noradrenaline spillover that can have limitations in terms of largescale implementation, can be confounded in certain states such as heart failure (HF), and have age- and sex-specific influences that need to be considered ( 3 ).…”
mentioning
confidence: 99%