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0095. Transvenous vagus nerve stimulation does not modulate the innate immune response in humans in vivo during experimental endotoxemia
© Kox et al; licensee Springer. 2014
Published: 26 September 2014
In a variety of conditions excessive and/or persistent activation of the innate immune system has detrimental effects. In animals, electrical vagus nerve stimulation (VNS) inhibits the innate immune response in models of endotoxemia (administration of lipopolysaccharide [LPS]), sepsis, trauma, and hemorrhagic shock, via the so-called cholinergic anti-inflammatory pathway. However, human in vivo evidence is lacking. Up till now, VNS was possible through implantation of a cuff electrode wrapped around the nerve, which limits its use in acute inflammatory situations frequently encountered on the ICU. A novel, less invasive VNS method is transvenous VNS (tVNS).
To determine whether tVNS exerts anti-inflammatory effects during experimental human endotoxemia.
A parallel randomized double-blind sham-controlled study in healthy male volunteers was performed. Subjects were randomized to receive either tVNS (n=10) or sham tVNS (n=10).
In both groups, a stimulation catheter with multiple circular electrode pairs was inserted in the left internal jugular vein at C5-C7 spinal level to be situated adjacent to the vagal nerve. In the tVNS group, stimulation (0-10 V, 1 ms, 20 Hz) was continuously performed during 30 minutes, starting 10 minutes before intravenous administration of 2 ng/kg E. Coli LPS. In sham subjects, the exact same procedures were performed, but the stimulator was not switched on by an unblinded team member.
Thirty-minute transvenous vagus nerve stimulation is feasible and safe but does not modulate the innate immune response in humans in vivo during experimental human endotoxemia.
This study was sponsored by Medtronic Inc.
This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.