Burn-induced organ dysfunction: Vagus nerve stimulation attenuates organ and serum cytokine levels

Niederbichler, Andreas D.; Papst, Stephan; Claaßen, Leif; Jokuszies, Andreas; Steinstraesser, Lars; Hirsch, Tobias; Altintas, M.A.; Ipaktchi, Kyros; Reimers, Kerstin; Kraft, Theresia; Vogt, Peter M.

doi:10.1016/j.burns.2008.08.023

Cited by 28 publications

(18 citation statements)

References 26 publications

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“…Dominance of sympathetic activities causes high FFA, because β receptor signal stimulates lypolysis. Moreover, stimulation of parasympathetic activities attenuates the increase in TNFα responded in response to inflammation (36,37). These findings suggest that HBA increases parasympathetic activities, leading to lipid homeostasis.…”

Section: Discussionmentioning

confidence: 85%

Long-term treatment with hyperbaric air improves hyperlipidemia of db/db mice

et al. 2010

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Section: Discussionmentioning

confidence: 85%

Long-term treatment with hyperbaric air improves hyperlipidemia of db/db mice

et al. 2010

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“…For the past 20 years, our laboratory and others have investigated how the inflammatory reflex and the CAP monitor and regulate systemic inflammation (Figure 1) [23,24]. Activation of the CAP via either VNS or administration of a pharmacological cholinergic agonist limits proinflammatory cytokine production, inhibits apoptosis of critical immune cells, limits vital organ damage and improves survival in multiple models of systemic future science group www.futuremedicine.com inflammation and sepsis, including collagen-induced arthritis, burns, colitis, myocardial ischemia, pancreatitis, stroke and polymicrobial abdominal sepsis [25][26][27][28][29][30][31] . Electrical stimulation of the cervical vagus nerve in rodents significantly reduces systemic and organ specific proinflammatory cytokine production during endotoxic shock, with the greatest reduction coming in the spleen [32,33].…”

Section: Future Indicationsmentioning

confidence: 99%

The Inflammatory Reflex and Neural Tourniquet: Harnessing the Healing Power of the Vagus Nerve

Fritz

2017

Bioelectron. Med.

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The CNS helps protect against tissue injury. The most important priorities include limiting blood loss and systemic inflammation. We elucidated two endogenous neural pathways that rapidly and specifically improve hemostasis and decrease inflammation through vagus nerve signaling. Activation of the neural tourniquet or inflammatory reflex via electrical vagus nerve stimulation (VNS) significantly improves outcomes in preclinical disease models. Currently, VNS is clinically approved for the treatment of medically refractory epilepsy and depression. The growing field of bioelectronic medicine will help physicians harness the Neural Tourniquet™ and inflammatory reflex for clinical use as well. Considering the substantial harm caused by uncontrolled bleeding and inflammation, electrical VNS may dramatically improve the care of millions of patients.

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“…It is now well accepted that signaling from the vagus nerve has potent anti-inflammatory effects [25]. Electrical VNS against a burn injury model reduced serum levels of TNF-α and IL-6 [26], [27], and in a traumatic brain injury model, the suppressive effect of VNS on TNF-α was shown in intestine [28]. In the present study, we also showed that induction of serum TNF-α and IL-6 was significantly suppressed by electrical VNS treatment in our rat model of heatstroke.…”

Section: Discussionmentioning

confidence: 99%

Electrical Vagus Nerve Stimulation Attenuates Systemic Inflammation and Improves Survival in a Rat Heatstroke Model

et al. 2013

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This study was performed to gain insights into novel therapeutic approaches for the treatment of heatstroke. The central nervous system regulates peripheral immune responses via the vagus nerve, the primary neural component of the cholinergic anti-inflammatory pathway. Electrical vagus nerve stimulation (VNS) reportedly suppresses pro-inflammatory cytokine release in several models of inflammatory disease. Here, we evaluated whether electrical VNS attenuates severe heatstroke, which induces a systemic inflammatory response. Anesthetized rats were subjected to heat stress (41.5°C for 30 minutes) with/without electrical VNS. In the VNS-treated group, the cervical vagus nerve was stimulated with constant voltage (10 V, 2 ms, 5 Hz) for 20 minutes immediately after completion of heat stress. Sham-operated animals underwent the same procedure without stimulation under a normothermic condition. Seven-day mortality improved significantly in the VNS-treated group versus control group. Electrical VNS significantly suppressed induction of pro-inflammatory cytokines such as tumor necrosis factor-α and interleukin-6 in the serum 6 hours after heat stress. Simultaneously, the increase of soluble thrombomodulin and E-selectin following heat stress was also suppressed by VNS treatment, suggesting its protective effect on endothelium. Immunohistochemical analysis using tissue preparations obtained 6 hours after heat stress revealed that VNS treatment attenuated infiltration of inflammatory (CD11b-positive) cells in lung and spleen. Interestingly, most cells with increased CD11b positivity in response to heat stress did not express α7 nicotinic acetylcholine receptor in the spleen. These data indicate that electrical VNS modulated cholinergic anti-inflammatory pathway abnormalities induced by heat stress, and this protective effect was associated with improved mortality. These findings may provide a novel therapeutic strategy to combat severe heatstroke in the critical care setting.

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Burn-induced organ dysfunction: Vagus nerve stimulation attenuates organ and serum cytokine levels

Cited by 28 publications

References 26 publications

Long-term treatment with hyperbaric air improves hyperlipidemia of db/db mice

Long-term treatment with hyperbaric air improves hyperlipidemia of db/db mice

The Inflammatory Reflex and Neural Tourniquet: Harnessing the Healing Power of the Vagus Nerve

Electrical Vagus Nerve Stimulation Attenuates Systemic Inflammation and Improves Survival in a Rat Heatstroke Model

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