title: The sympathetic-vagal balance against endotoxemia.
abstract: The goal of this study was to establish a convenient and effective approach to anti-inflammation treatment by rebalancing the sympathetic-vagal system via vagal nerve stimulation (VNS). We established an endotoxemia model in Sprague-Dawley rats using lipopolysaccharide (LPS) injection. Electrical discharges in the vagal system, including the nucleus tractus solitarii (NTS) and afferent and efferent cervical vagal nerves, were detected. The condition of sympathetic-vagal balance, presented as heart rate variability (HRV) and hepatic norepinephrine/acetylcholine (NE/ACh), was measured following endotoxemia with and without VNS. Discharges in afferent and efferent vagal nerves increased significantly following LPS injection compared with the basis level and corresponding time points in the control group. Discharges in the NTS also increased significantly following LPS injection. The HRV components, including normalized high frequency (HFnm), normalized low frequency (LFnm), LF/HF, and very low frequency (VLF), increased significantly following LPS injection. HFnm values in the LPS + VNS group increased significantly compared with the LPS group. Conversely, LFnm, LF/HF, and VLF in the LPS + VNS group decreased significantly compared with the LPS group. Hepatic NE and ACh significantly decreased within 6 h after LPS injection compared with the basal level and the control groups (P < 0.05). VNS did not significantly improve hepatic NE, but the ACh levels in the LPS + VNS group were higher than those in other groups. Sympathetic and vagal nervous systems are enhanced following endotoxemia. The overexcitation of the sympathetic system leads to sympathetic-vagal disequilibrium. The rebalance of the sympathetic and vagal system is crucial for critically ill patients.
authors.affiliation: Intensive Care Unit, Trauma center of PLA, Institute of Surgery Research, Daping Hospital, Third Military Medical University, Chongqing 400042, China. huajcn@yahoo.com.cn
authors.forename: Jian
authors.initials: J
authors.lastname: Huang
authors.forename: Yaoli
authors.initials: Y
authors.lastname: Wang
authors.forename: Dongbo
authors.initials: D
authors.lastname: Jiang
authors.forename: Jian
authors.initials: J
authors.lastname: Zhou
authors.forename: Xiankai
authors.initials: X
authors.lastname: Huang
mesh_terms: D000109:Acetylcholine / Q000378:metabolism; D000200:Action Potentials / Q000502:physiology; D000704:Analysis of Variance; D000818:Animals; D004195:Disease Models, Animal; D019446:Endotoxemia / Q000139:chemically induced / Q000473:pathology* / Q000503:physiopathology*; D005260:Female; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D008070:Lipopolysaccharides; D008099:Liver / Q000378:metabolism; D008297:Male; D009638:Norepinephrine / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D017552:Solitary Nucleus / Q000187:drug effects / Q000502:physiology; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D013997:Time Factors; D014630:Vagus Nerve / Q000503:physiopathology*; D055536:Vagus Nerve Stimulation
chemical_list: D008070:Lipopolysaccharides; D000109:Acetylcholine; D009638:Norepinephrine
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