Baroreflex activation in conscious rats modulates the joint inflammatory response via sympathetic function

The baroreflex is a critical physiological mechanism controlling cardiovascular function by modulating both the sympathetic and parasympathetic activities. Here, we report that electrical activation of the baroreflex attenuates joint inflammation in experimental arthritis induced by the administration of zymosan into the femorotibial cavity. Baroreflex activation combined with lumbar sympathectomy, adrenalectomy, celiac subdiaphragmatic vagotomy or splenectomy dissected the mechanisms involved in the inflammatory modulation, highlighting the role played by sympathetic inhibition in the attenuation of joint inflammation. From the immunological standpoint, baroreflex activation attenuates neutrophil migration and the synovial levels of inflammatory cytokines including TNF, IL-1β and IL-6, but does not affect the levels of the anti-inflammatory cytokine IL-10. The anti-inflammatory effects of the baroreflex system are not mediated by IL-10, the vagus nerve, adrenal glands or the spleen, but by the inhibition of the sympathetic drive to the knee. These results reveal a novel physiological neuronal network controlling peripheral local inflammation.     

卒中后抑郁患者的交感神经皮肤反应与事件相关电位对照研究

目的探讨交感神经皮肤反应(SSR)与事件相关电位(ERP)对卒中后抑郁患者的诊断价值。方法对55例卒中后抑郁患者和52例正常健康者分别进行了SSR和ERP测定,并将结果加以比较。结果卒中后抑郁组中SSR和ERP测定中的P300成分异常率分别为87.3%(48/55)和83.6%(46/55),两者异常吻合率为76.4%(42/55)。卒中后抑郁组SSR测定结果中,SSR潜伏期和波幅值较对照组延长和降低,其差异具有显著性(P<0.01),ERP测定中N2、P3波潜伏期和P3波幅较对照组分别延长和降低,存在显著性差异(P<0.01)。其中N2、P3波潜伏期与SSR测定中潜伏期以及波幅与波幅之间呈正相关(r=0.29~0.36,P<0.01),而两者潜伏期与波幅之间呈负相关(r=-0.32~-0.33,P<0.01)。结论交感神经皮肤反应和事件相关电位测定可作为卒中后抑郁患者的诊断指标应用于临床。     

The influx of Ca and the release of noradrenaline evoked by the stimulation of presynaptic nicotinic receptors of chick sympathetic neurons in culture are not mediated via L-, N-, or P-type calcium channels

We have shown earlier that nicotinic agonists induce the release of noradrenaline from chick sympathetic neurons in culture in two ways: (a) by activating the postsynaptic nicotinic receptors on nerve cell bodies, giving rise to spreading electrical activity and opening of voltage operated calcium channels in neuronal processes; (b) by activating the presynaptic nicotinic receptors on neuronal processes. In the present work, we investigated the contribution of various pathways to the observed Ca²⁺ influx and subsequent noradrenaline release. Sympathetic neurons in culture were stimulated either by the nicotinic agonist dimethylphenylpiperazinium or electrically, in the presence or absence of tetrodotoxin and of specific blockers of calcium or nicotinic channels, and the effects on [Ca²⁺]_i in the area of neuronal processes and on noradrenaline release were measured. Under control conditions, the N-type channel blocker ω-conotoxin (0.1 μmol/1) diminished the release of noradrenaline and the increase of intraterminal Ca²⁺ by 48% and 55%, respectively, whereas the L-type channel blocker (+)Bay k 8644 (1 μmol/1) diminished the release of noradrenaline by 25% and the increase of [Ca²⁺]_i by 39%. The P-type channel blocker ω-agatoxin (0.3 μmol/1) had no effect. The effects of the L-type channel ligands were complex and could only be explained on the assumption that, at high concentrations, these drugs also act as nicotinic antagonists. Tetrodotoxin blocked the Ca²⁺ response evoked by electrical stimulation whereas DMPP applied in the presence of tetrodotoxin still evoked an increase of [Ca²⁺]_i and the release of noradrenaline (27% and 30% of control without tetrodotoxin, respectively). These residual responses were not blocked by any of the calcium channel blockers used or by their combination. Apparently, a substantial part of the influx of Ca²⁺ induced by the activation of presynaptic nicotinic receptors is not carried by the N-, L- or P-type channels and probably occurs directly via the open channels of nicotinic receptors.     

Daily changes in presynaptic cholinergic activity of rat sympathetic superior cervical ganglion

The in vitro capacity of sympathetic superior cervical ganglia (SCG) to take up [³H]choline from the extracellular medium, to synthesize acetylcholine from [³H]choline, and to release [³H]acetylcholine in response to a high K⁺ concentration, were examined in rats throughout a 24-h cycle. Both the release of [³H]acetylcholine and the synthesis of [³H]acetylcholine from [³H]choline exhibited significant diurnal variations, showing maxima during the first half of the night. After these maxima, nocturnal acetylcholine release and synthesis decayed to daytime levels and remained low until the end of the night. [³H]Choline uptake by rat SCG did not vary significantly throughout a 24-h period. A 1.5-h exposure of rats to darkness at the 5th hour of light phase of the daily photoperiod did not change significantly any parameter studied. A 20-min, 5-Hz, electrical stimulation of the preganglionic trunk of SCG excised from rats at noon increased significantly subsequent K⁺-induced [³H]acetylcholine release but did not change [³H]acetylcholine synthesis. In decentralized SCG of rats subjected to a unilateral SCG decentralization and a contralateral sham-operation 7 days earlier, [³H]acetylcholine release and synthesis were highly reduced or abolished at the decentralized side, while [³H]choline uptake remained unaltered. The present results suggest that an activation of preganglionic rat SCG neurons takes place during the first half of the scotophase.     

100例2型糖尿病患者交感神经皮肤反应研究

目的探讨交感神经皮肤反应(SSR)检测在评价2型糖尿病(T2DM)自主神经损害中的价值.方法对100例T2DM患者进行SSR检测,30例健康志愿者作为对照.结果2组SSR的起始潜伏期、N波潜伏期、波幅、面积比较差异有显著性意义(P＜0.05),P波潜伏期差异无显著性意义(P＞0.05).T2DM组72例(72%)患者至少有一肢SSR异常.血糖控制满意组和血糖控制不良组比较,起始和N波潜伏期差异有统计学意义(P＜0.05),波幅和面积无显著性意义(P＞0.05).T2DM组病程＜5年与病程≥5年比较,潜伏期、波幅、面积差异均无统计学意义(P＞0.05).结论SSR可作为评价T2DM自主神经损害的客观电生理指标;T2DM患者SSR与血糖控制水平相关,与病程无关.     

A Management of Early CRPS I Caused by Ankle Sprain: A Case Report

Abstract:   We present a case of a 13-year-old boy who developed signs and symptoms of neuropathic pain/early Complex Regional Pain Syndrome (CRPS) Type I, formerly known as Reflex Sympathetic Dystrophy (RSD), after spraining his ankle while wrestling. Aggressive pain control, using medications and sympatholytic blocks, with physical therapy and rehabilitation, led to the resolution of his painful condition. This prevented the disease from possibly progressing to a full-blown case of CRPS I (RSD) that is very challenging to treat.     

Whole-cell recordings from sympathetic preganglionic neurons in rat spinal cord slices

Whole-cell patch-clamp recordings (WCR) were made from sympathetic preganglionic neurons (SPN) in neonate rat spinal cord slices. SPN were identified histologically by filling them with the fluorescent dye Lucifer Yellow contained within the patch pipette solution. Current clamp recordings were obtained from SPN with a potassium based pipette solution. The cells exhibited many of the characteristic properties of SPN seen previously with intracellular recordings in both the rat and the cat. However, we found an order of magnitude increase in both cell input resistance (950 MΩ) and time constant (118 ms) over those seen with conventional recordings. We believe these values approximate better the situation in intact cells, and will have a vital bearing upon how SPN integrate inputs. We conclude that WCR in spinal cord slices provides a powerful tool for investigating the cellular properties of SPN.     

Cardiovascular autonomic dysfunction in normotensive awake subjects with obstructive sleep apnoea syndrome

Cardiovascular autonomic function in normotensive awake patients with obstructive sleep apnoea syndrome was studied in 21 normotensive (mean age 48 ± 14 years), drug-free men with obstructive sleep apnoea syndrome. Cardiovascular reflex tests with continuous blood pressure monitoring and biochemical indices were performed the morning after a standard polygraphic sleep recording. A group of 20 agematched (mean age 49 ± 19 years) normal subjects was used as controls. The obstructive sleep apnoea syndrome patients showed higher heart rate and noradrenaline plasma levels (p < 0.05) at rest and a higher blood pressure response to head-up tilt (p < 0.01), suggesting sympathetic overactivity. Respiratory arrhythmia, baroreflex sensitivity index and Valsalva ratio were significantly lower in the obstructive sleep apnoea syndrome group (p < 0.01) whereas the decrease in heart rate induced by the cold face test was significantly higher (p < 0.05) showing a blunting of reflexes dependent on baroreceptor or pulmonary afferents with normal or increased cardiac vagal efferent activity. These abnormalities in autonomic regulation may predispose obstructive sleep apnoea syndrome patients to cardiovascular complications like hypertension and cardiac arrhythmias.     

Intracranial trajectories of sympathetic nerve fibers originating in the superior cervical ganglion in the rat: WGA-HRP anterograde labeling study

Intracranial trajectories of sympathetic nerve fibers originating in the superior cervical ganglion (SCG) in the rat were investigated by means of anterograde labeling following the injection of wheat germ agglutinin-horseradish peroxidase conjugate (WGA-HRP) into the unilateral SCG. The trajectory of the sympathetic fiber innervating the pineal gland and its continuing structures was found advancing along the abducent nerve, through the cavernous plexus, then along the trochlear nerve. Labeled sympathetic fibers showed two patterns of distribution in the blood vessels on the basal surface of the brain. The sympathetic fibers originating in the unilateral SCG were intermingled with those fibers from the contralateral SCG in the pineal gland, its continuing structures and the choroid plexus of the third ventricle as well as in the cerebral blood vessels.