Burn-induced organ dysfunction: vagus nerve stimulation attenuates organ and serum cytokine levels.
BACKGROUND
The interaction of the CNS and the immune system is well known. A parasympathetic anti-inflammatory pathway has recently been described. Both electrical and pharmacological parasympathetic stimulation attenuate proinflammatory mediator generation. Burn induces abacterial cytokine generation and we sought to evaluate whether parasympathetic stimulation after experimental burn decreases cardiodepressive mediator generation.


METHODS
A 30% TBSA full-thickness rat burn model was used. After microsurgical preparation of the cervical portion of the vagus nerve, we performed electric vagus nerve stimulation. Serum was harvested and organ samples of heart and liver were homogenized. Samples were subjected to sandwich-ELISA specific for TNF-alpha, IL-1beta and IL-6. Heart rate measurements were done using left ventricular microcatheterization. Statistical analysis was done using Student's t-tests and analysis of variance (ANOVA).


RESULTS
Burn induced a significant rise of TNF-alpha, IL-1beta and IL-6 in organ homogenates and serum. After cervical vagal electrostimulation, serum and organ homogenate levels of proinflammatory cytokines were markedly reduced compared to burn controls. Left ventricular microcatheter assessment demonstrated no cardiodepressive effect of the vagal stimulation itself.


CONCLUSIONS
Our results encourage further research regarding the neuroimmunologic background of burn, possibly leading to the development of a novel therapeutic approach to burn-induced organ dysfunction and immunodysregulation.
Niederbichler
Andreas D
AD
Department of Plastic, Hand and Reconstructive Surgery, Burn Center, Medizinische Hochschule Hannover, Germany. niederbichler.andreas@mh-hannover.de
Papst
Stephan
S
Claassen
Leif
L
Jokuszies
Andreas
A
Steinstraesser
Lars
L
Hirsch
Tobias
T
Altintas
Mehmet A
MA
Ipaktchi
Kyros R
KR
Reimers
Kerstin
K
Kraft
Theresia
T
Vogt
Peter M
PM
D000818:Animals; D002056:Burns / Q000276:immunology* / Q000503:physiopathology / Q000628:therapy; D016207:Cytokines / Q000097:blood / Q000378:metabolism*; D006339:Heart Rate; D018836:Inflammation Mediators / Q000097:blood / Q000378:metabolism; D053583:Interleukin-1beta / Q000097:blood / Q000378:metabolism; D015850:Interleukin-6 / Q000097:blood / Q000378:metabolism; D008099:Liver / Q000276:immunology; D008297:Male; D009206:Myocardium / Q000276:immunology; D051381:Rats; D017207:Rats, Sprague-Dawley; D014409:Tumor Necrosis Factor-alpha / Q000097:blood / Q000378:metabolism; D055536:Vagus Nerve Stimulation / Q000379:methods*
D016207:Cytokines; D018836:Inflammation Mediators; D053583:Interleukin-1beta; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha