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Review

The Role of Vagus Nerve Stimulation in Sepsis

ORCID Icon, , , , &
Pages 51-62 | Received 30 Jun 2020, Accepted 22 Sep 2020, Published online: 21 Oct 2020
 

Abstract

Sepsis is a life-threatening organ dysfunction due to a dysregulated host response to infection. The infection triggers a host response with an early hyperinflammatory and subsequent anti-inflammatory phase, both regulated by homeostatic mechanisms. A breakdown of these regulatory mechanisms can result in an exaggerated immune response which leads to complications. The vagus nerve plays a central role in regulating inflammation and the balance between the sympathetic and parasympathetic arms of the autonomic nervous system through the “cholinergic anti-inflammatory pathway”. Several experimental models support the notion that external stimulation of the vagus nerve can modulate inflammation and restore the sympatho-vagal balance which may translate to improved outcomes in sepsis. Here, we review the pathophysiologic basis and evidence behind vagus nerve stimulation in sepsis.

Author contributions

ZUA Asad contributed toward writing the first draft. A Przebinda contributed toward drafting section on the role of inflammation. AMD Chaudhary contributed toward drafting section on Animal and Human studies and creating . S Farooqui contributed toward drafting section on the role of autonomic nervous system. H Youness & S Stavrakis contributed toward reviewing/editing.

Financial & competing interests disclosure

Supported by a Veterans Affairs Medical Center Oklahoma City pilot grant (grant#A002) to ZUA Asad and H Youness. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Additional information

Funding

Supported by a Veterans Affairs Medical Center Oklahoma City pilot grant (grant#A002) to ZUA Asad and H Youness. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

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