Vagal modulation of catecholamines in the adrenal gland controls systemic inflammation in experimental sepsis (INM2P.437)
2014; American Association of Immunologists; Volume: 192; Issue: 1_Supplement Linguagem: Inglês
10.4049/jimmunol.192.supp.56.20
ISSN1550-6606
AutoresLuis Ulloa, Juan M. Inclan-Rico, Patrick Morcillo, Geber Peña, Rafael Torres‐Rosas,
Tópico(s)Anesthesia and Neurotoxicity Research
ResumoAbstract Sepsis is the leading cause of mortality in non-coronary Intensive Care Units accounting for 9.3% of overall deaths in the USA. Sepsis and other critical conditions like hemorrhage, resuscitation, shock, and trauma are characterized by overzealous inflammatory responses that cause lethal multiple organ failure. Despite its recent identification, multiple investigators have already reported that the vagus nerve controls systemic inflammation in experimental ischemia and reperfusion, hemorrhage and resuscitation, pancreatitis, colitis, endotoxemia, septic shock and severe sepsis. Vagus nerve stimulation controls systemic inflammation, but its clinical use is precluded by the surgical exposure of the vagus nerve, the use of anesthetics, and its temporal effect(1,2). Transcutaneous activation of the vagus nerve improves survival in experimental sepsis without surgery. Transcutaneous activation of the vagus nerve inhibits the production of multiple inflammatory cytokines including TNFα, IL6 and INFγ. This anti-inflammatory potential has a lasting effect and does not merely delay the pathogenesis of sepsis. Transcutaneous activation of the vagus nerve controls systemic inflammation by modulating catecholamine's production in the adrenal gland. Studies funded by NIH-GM084125 to LU. REFERENCES 1. Wang, H., et al. Nature medicine 10, 1216-1221 (2004). 2. Wang, H., et al. Nature 421, 384-388 (2003).
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