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.

Activation of Cholinergic Anti-Inflammatory Pathway Contributes to the Protective Effects of 100% Oxygen Inhalation on Zymosan-Induced Generalized Inflammation in Mice

“…Furthermore, Huang et al reported that both sympathetic and vagal nervous systems are significantly depressed within 6 h after intravenous injection of lipopolysaccharide (5 mg/kg) in rats [34]. In our recently published article, we proved that 100% oxygen inhalation protects against zymosan-induced generalized inflammation in mice partly through activation of b2 adrenergic receptor pathway [11].…”

Experimental examination of anti-inflammatory effects of a 5-HT3 receptor antagonist, tropisetron, and concomitant effects on autonomic nervous function in a rat sepsis model

“…Sympathetic overstimulation in an LPS-induced sepsis model reportedly lead to sympathetic-vagal disequilibrium [39]. Furthermore, almost all immunocompetent cells have adrenergic receptors [40], and catecholamines exhibit substantial immunomodulatory effects [41][42][43][44].…”

Neurochemistry in the Pathophysiology of Septic Encephalopathy

“…In lipopolysaccharide-injected rat (i.e., an animal model of sepsis), electrical threshold to induce action potentials are increased (i.e., hard neuronal firing) in vagus nerve (Huang J et al, 2010). This finding suggests that the vagus nerve activity is reduced after sepsis.…”