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Báo cáo y học: "Neuroimmune perspectives in sepsis"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Critical Care giúp cho các bạn có thêm kiến thức về ngành y học đề tài: Neuroimmune perspectives in sepsis. | Available online http ccforum.eom content 13 2 133 Commentary Neuroimmune perspectives in sepsis Luis Ulloa and Edwin A Deitch Department of Surgery UMDNJ - New Jersey Medical School 185 South Orange Avenue PO Box 1709 Newark NJ 07103 USA Corresponding author Luis Ulloa Mail@LuisUlloa.com Published 23 April 2009 This article is online at http ccforum.com content 13 2 133 2009 BioMed Central Ltd Critical Care 2009 13 133 doi 10.1186 cc7758 See related research by Hofer et al. http ccforum.com content 13 1 R11 Abstract Physiologic anti-inflammatory mechanisms are selected by evolution to control the immune system and to prevent infectious and inflammatory disorders. Central-acting a2-agonists attenuate systemic inflammation and improve survival in experimental sepsis. This anti-inflammatory and therapeutic mechanism of central sym-patholytics appears to be mediated by an unexpected vagomimetic potential of the a2-agonists to activate the vagus nerve. Recent studies however rule out a cholinergic anti-inflammatory mechanism based on a direct cholinergic interaction between the vagus nerve and the immune system. Since the nervous system is the principal regulator of the immune system physiologic studies understanding the neuroimmune connections can provide major advantages to design novel therapeutic strategies for sepsis. In the previous issue of Critical Care Hofer and colleagues reported that central sympatholytics attenuate systemic inflammation and improve survival in experimental sepsis 1 . -Adrenoceptors close a negative feedback loop in the neuronal synapses to limit catecholamine production. a2-Agonists clonidine and dexmedetomidine therefore mimic a physiological condition of high levels of catecholamines and inhibit the noradrenergic neurotransmission in the medulla oblongata. The clinical implications of the central-acting a2-agonists reveal an unexpected sedative potential that is in part mediated by a proposed vagomimetic potential of these agonists to .