Effects of mildly increasing dialysis sodium removal on renin and sympathetic system in hemodialysis patients

Background It has been argued that the benefits of reducing sodium loading may be offset by increased activation of the renin-angiotensin-aldosterone system （RAAS） and sympathetic nervous system. This study aimed to investigate the long-term effects of an increase in dialysis sodium removal on circulating RAAS and sympathetic system in hypertensive hemodialysis （HD） patients with ＂normal＂ post-HD volume status. Methods Thirty hypertensive HD patients were enrolled in this pilot trial. After one month period of dialysis with standard dialysate sodium of 138 mmol/L, the patients were followed up for a four months period with dialysate sodium set at 136 retool/L, without changes in instructions regarding dietary sodium control. During the period of study, the dry weight was adjusted monthly under the guidance of bioimpedance spectroscopy to maintain post-HD volume status in a steady state; 44-hour ambulatory blood pressure, plasma renin, angiotensin II （Ang II）, aldosterone, and norepinephrine （NE） were measured. Results After four months of HD with low dialysate sodium of 136 mmol/L, 44-hour systolic and diastolic blood pressures （BPs） were significantly lower （-10 and -6 mmHg）, in the absence of changes in antihypertensive medications. No significant changes were observed in plasma renin, Ang II, aldosterone, and NE concentrations. The post-HD volume parameters were kept constant. Conclusion Mildly increasing dialysis sodium removal over 4 months can significantly improve BP control and does not activate circulating RAAS and sympathetic nervous system in hypertensive HD patients. Chin Med J 2014;127 （14）： 2628-2631

Sympathetic nervous system activation and heart failure:Current state of evidence and the pathophysiology in the light of novel biomarkers

Heart failure(HF)is a complex clinical syndrome characterized by the activation of at least several neurohumoral pathways that have a common role in maintaining cardiac output and adequate perfusion pressure of target organs and tissues.The sympathetic nervous system(SNS)is upregulated in HF as evident in dysfunctional baroreceptor and chemoreceptor reflexes,circulating and neuronal catecholamine spillover,attenuated parasympathetic response,and augmented sympathetic outflow to the heart,kidneys and skeletal muscles.When these sympathoexcitatory effects on the cardiovascular system are sustained chronically they initiate the vicious circle of HF progression and become associated with cardiomyocyte apoptosis,maladaptive ventricular and vascular remodeling,arrhythmogenesis,and poor prognosis in patients with HF.These detrimental effects of SNS activity on outcomes in HF warrant adequate diagnostic and treatment modalities.Therefore,this review summarizes basic physiological concepts about the interaction of SNS with the cardiovascular system and highlights key pathophysiological mechanisms of SNS derangement in HF.Finally,special emphasis in this review is placed on the integrative and up-to-date overview of diagnostic modalities such as SNS imaging methods and novel laboratory biomarkers that could aid in the assessment of the degree of SNS activation and provide reliable prognostic information among patients with HF.

Renal sympathetic nervous system and the effects of denervation on renal arteries

Resistant hypertension is associated with chronic activation of the sympathetic nervous system resulting in various comorbidities. The prevalence of resistant hypertension is often under estimated due to various reasons. Activation of sympathetic nervous system at the renal-as well as systemic-level contributes to the increased level of catecholamines and resulting increase in the blood pressure. This increased activity was demonstrated by increased muscle sympathetic nerve activity and renal and total body noradrenaline spillover. Apart from the hypertension, it is hypothesized to be associated with insulin resistance, congestive heart failure and obstructive sleep apnea. Renal denervation is a novel procedure where the sympathetic afferent and efferent activity is reduced by various techniques and has been used successfully to treat drug-resistant hypertension improvement of various metabolic derangements.Renal denervation has the unique advantage of offering the denervation at the renal level, thus mitigating the systemic side effects. Renal denervation can be done by various techniques including radiofrequency ablation, ultrasound guided ablation and chemical ablation. Various trials evaluated the role of renal denervation in the management of resistant hypertension and have found promising results. More studies are underway to evaluate the role of renal denervation in patients presenting with resistant hypertension in different scenarios. Appropriate patient selection might be the key in determining the effectiveness of the procedure.

Effects of spinal cord stimulation on cerebrovascular flow: role of sym-pathetic and parasympathetic innervations

Objective Cervical spinal cord stimulation （SCS） has been found to augment cerebral blood flow （CBF） in a number of animal models. However, the effective use of SCS is hampered by a lack of understanding of its mechanism（s） of action. In this paper, we focus on the sympathetic and parasympathetic effects of SCS on CBF. Method SpragueDawley rats were selected for the experimental series. The animals were divided into 5 groups to underwent SCS and laser Doppler flowmeter （LDF） recordings. Control group, the animal underwent SCS and LDF recordings without any surgery of the nerve fibers and ganglia. V 1 group, the animal underwent bilateral resection of the nasociliary and post-ganglionic parasympathetic nerve fibbers. SCG group, the animal underwent bilateral resection of supper cervical ganglion. V 1 ＋ SCG group, the animal underwent both surgeries as V1- and SCG-group animals did. Sham group, the animal underwent the carotid manipulation with blunt-tipped forceps as well as the dissection of nasociliary and post-ganglionic parasympathetic nerve fibers around the ethmoidal foramen, but without cutting any nerves. Results During the SCS, the LDF was no statistical difference between the V 1 or SCG group and the control group. Yet, the effects of SCS on CBF are completely abolished in V1＋ SCG group. Conclusions Surgical interruption of both the parasympathetic and sympathetic pathways has the contradict effect on SCS-induced CBF augmentation.

Electroacupuncture at ST36 modulates gastric motility via vagovagal and sympathetic reflexes in rats

BACKGROUND Electroacupuncture(EA) at ST36 can significantly improve gastrointestinal symptoms, especially in promoting gastrointestinal motility. The automatic nervous system plays a main role in EA, but few studies exist on how vagovagal and sympathetic reflexes affect EA to regulate gastrointestinal motility.AIM To study the role of vagovagal and sympathetic reflexes in EA at ST36, as well as the associated receptor subtypes that are involved.METHODS Gastric motility was measured with a manometric balloon placed in the gastric antrum area in anesthetized animals. The peripheral nervous discharge was measured using a platinum electrode hooking the vagus or greater splanchnic nerve, and the central nervous discharge was measured with a glass microelectrode in the dorsal motor nucleus of the vagus(DMV). The effects and mechanisms of EA at ST36 were explored in male Sprague-Dawley rats which were divided in to a control group, vagotomy group, sympathectomy group, and microinjection group [including an artificial cerebrospinal fluid group, glutamate(L-Glu) group, and γ-aminobutyric acid(GABA) group] and in genetically modified male mice [β1β2 receptor-knockout(β1β2^(-/-)) mice, M2M3 receptorknockout(M2M3^(-/-)) mice, and wild-type control mice].RESULTS EA at ST36 promoted gastric motility during 30-120 s. During EA, both vagus and sympathetic nerve discharges increased, with a much higher frequency of vagus nerve discharge than sympathetic discharge. The gastric motility mediated by EA at ST36 was interdicted by vagotomy. However, gastric motility mediated by EA at ST36 was increased during 0-120 s by sympathectomy, which eliminated the delay effect of EA during 0-30 s, but it was lower than the control group during 30-120 s. Using gene knockout mice and their wild-type controls to explore the receptor mechanisms, we found that EA at ST36 decreased gastric motility in M2/3^(-/-) mice, and promoted gastric motility in β1/2^(-/-) mice. Extracellular recordings showed that EA at ST36 increased spikes of the DMV. Microinjection of L-Glu into the DMV increased gastric motility, while EA at ST36 decreased gastric motility during 0-60 s, and promoted gastric motility during 60-120 s.Injection of GABA reduced or increased gastric motility, and reduced the promoting gastric motility effect of EA at ST36.CONCLUSION These data suggest that EA at ST36 modulates gastric motility via vagovagal and sympathetic reflexes mediated through M2/3 and β1/2 receptors, respectively.Sympathetic nerve activity mediated through β1/2 receptors is associated with an early delay in modulation of gastric motility by EA at ST36.

Electroacupuncture at ST25 inhibits jejunal motility:Role ofsympathetic pathways and TRPV1

AIM: To investigate whether electroacupuncture(EA) at ST25 affects jejunal motility in vivo and if so, whether a sympathetic pathway is involved.METHODS: Jejunal motility was assessed using a manometric balloon placed in the jejunum approximately about 3-5 cm away from the suspensory ligament of the duodenum in anesthetized animals. The effects of EA at ST25 were measured in male Sprague-Dawley rats, some of which were treated with propranolol or clenbuterol(EA intensities: 1, 3, 5, 7, and 9 m A), and in male transient receptor potential vanilloid-1(TRPV1)(capsaicin receptor) knockout mice(EA intensities: 1, 2, and 4 m A).RESULTS: Anesthetized rats exhibited three types of fasting jejunal motor patterns(types A, B, and C), and only type C rats responded to EA stimulation. In type C rats, EA at ST25 significantly suppressed the motor activity of the jejunum in an intensity-dependent manner. The inhibitory effect of EA was weakened by propranolol(β adrenoceptor antagonist) and disappeared with clenbuterol(β adrenoceptor agonist) induced inhibition of motility, suggesting that the effect of EA on motility is mediated via a sympathetic pathway. Compared with wild-type mice, EA at ST25 was less effective in TRPV1 knockout mice, suggesting that this multi-modal sensor channel participates in the mechanism. CONCLUSION: EA at ST25 was found to inhibit jejunal motility in an intensity-dependent manner, via a mechanism in which sympathetic nerves and TRPV1 receptors play an important role.

Sympathetic skin response:a new test to diagnose erectile dysfunction

Aim: Electrophysiological monitoring of the activity of the penile sympathetic skin responses (PSSR) in healthy menand patients with erectile dysfunction (ED). Methods: PSSR were recorded from the skin of penis with disk elec-trodes at the time of electric stimulation of left median nerves. Results: PSSR were recorded from all the healthymen and almost all the patients. In healthy men the latency of P_0, the latency of N_1, the duration of N_1 and the ampli-tude of N_1 were 1249 ± 111 ms, 2239 ± 286 ms, 1832 ± 505 ms and 470 μV (median), respectively. In ED patientsthe latency of P_0, the latency of N_1, the duration of N_1 and the amplitude of N_1 were 1467 ± 183 ms ( P < 0.01), 2561± 453 ms (P < 0.05), 2560 ± 861 ms (P < 0.01 ) and 91 μV (P < 0.01), respectively. The normal latency of Powas less than 1471 ms. The normal amplitude of N1 was more than 235μV. According to this normal value, of 20 pa-tients 11 showed longer latency of P_0, and 14 showed lower amplitude of N_1 as compared with those of normal subjects.Conclusion: PSSR can be used as an electrophysiological method in assisting the diagnosis of ED.(Asian J Androl 2001; Mar; 3: 45-48)

Effects of neuregulin-1 on autonomic nervous system remodeling post-myocardial infarction in a rat model

Sympathetic nerve and vagus nerve remodeling play an important part in cardiac function post-myocardial infarction （MI）. Increasing evidence indicates that neuregulin-1 （NRG-1） improves cardiac function following heart failure. Since its impact on cardiac function and neural remodeling post-MI is poorly understood, we aimed to investigate the role of NRG-1 in autonomic nervous system remodeling post-MI. Forty-five Sprague-Dawley rats were equally randomized into three groups： sham （with the left anterior descending coronary artery exposed but without ligation）, MI （left anterior descending coronary artery ligation）, and MI plus NRG-1 （left anterior descending coronary artery ligation followed by intraperitoneal injection of NRG-1 （10 lag/kg, once daily for 7 days））. At 4 weeks after MI, echocardi- ography was used to detect the rat cardiac function by measuring the left ventricular end-systolic inner diameter, left ventricular diastolic diameter, left ventricular end-systolic volume, left ventricular end-diastolic volume, left ventricular ejection fraction, and left ventricular fractional shortening, mRNA and protein expression levels of tyrosine hydroxylase, growth associated protein-43 （neuronal specific pro- tein）, nerve growth factor, choline acetyltransferase （vagus nerve marker）, and vesicular acetylcholine transporter （cardiac vagal nerve fiber marker） in ischemic myocardia were detected by real-time PCR and western blot assay to assess autonomous nervous remodeling. After MI, the rat cardiac function deteriorated significantly, and it was significantly improved after NRG-1 injection. Compared with the MI group, mRNA and protein levels of tyrosine hydroxylase and growth associated protein-43, as well as choline acetyltransferase mRNA level significantly decreased in the MI plus NRG-1 group, while mRNA and protein levels of nerve growth factor and vesicular acetylcholine transporters, as well as choline acetyltransferase protein level slightly decreased. Our results indicate that NRG- 1 can improve cardiac function and regulate sympathetic and vagus nerve remodeling post-MI, thus reaching a new balance of the autonomic nervous system to protect the heart from injury.

Dynamic Radiographic Analysis of Sympathetic Cervical Spondylosis Instability

Objective To investigate the correlation between subaxial cervical spine instability and cervical spondylotic sympathetic symptoms as well as the difference of cervical spondylotic subaxial instability between male and female patients. Methods We analyzed retrospectively 318 surgical cases of cervical spondylosis treated at Department of Orthopedic Surgery of Peking Union Medical College Hospital between July 2003 and December 2007. All cases were divided into group A without sympathetic symptoms (n=284) and group B with sympathetic symptoms (n=34). Angular and horizontal translation values between two adjacent vertebral bodies from C2 to C7 were measured separately on hyperflexion and hyperextension lateral cervical spine radiographs. Fisher's exact test was used to evaluate the correlation between subaxial cervical instability and sympathetic symptoms. Intragroup correlation between patient gender and subaxial cervical instability was also evaluated. Results Subaxial instability incidences in groups A and B were 21.8% (62/284) and 55.9% (19/34), respectively. Statistical analysis indicated a definite correlation between subaxial cervical instability and sympathetic symptoms (P=0.000). Among patients without sympathetic symptoms, subaxial instability incidences were 21.4% (37/173) in males and 22.5% (25/111) in females, respectively (P=0.883). While among patients with sympathetic symptoms, subaxial instability incidences were 27.3% (3/11) in males and 69.6% (16/23) in females, respectively, indicating significant difference (P=0.030). Subaxial instability was most commonly seen at C4-C5 intervertebral space in sympathetic cervical spondylosis patients. Conclusions High correlation exists between subaxial cervical spine instability and cervical spondylotic sympathetic symptoms, especially in female patients. Hyperextension and hyperflexion radiographs of cervical spine are important to assess sympathetic cervical spondylotic subaxial instability.

Olfactory ensheathing cell transplantation improves sympathetic skin responses in chronic spinal cord injury

Forty-three patients with chronic spinal cord injury for over 6 months were transplanted with bryonic olfactory ensheathing cells, 2-4 × 106, into multiple sites in the injured area under the sur-gical microscope. The sympathetic skin response in patients was measured with an electromyo-graphy/evoked potential instrument 1 day before transplantation and 3-8 weeks after trans-tion. Spinal nerve function of patients was assessed using the American Spinal Injury Association impairment scale. The sympathetic skin response was elicited in 32 cases before olfactory en-sheathing celltransplantation, while it was observed in 34 cases after transplantation. tantly, sympathetic skin response latency decreased significantly and amplitude increased cantly after transplantation. Transplantation of olfactory ensheathing cells also improved American Spinal Injury Association scores for movement, pain and light touch. Our findings indicate that factory ensheathing celltransplantation improves motor, sensory and autonomic nerve functions in patients with chronic spinal cord injury.

Renal sympathetic denervation in therapy resistant hypertension-pathophysiological aspects and predictors for treatment success

Many forms of human hypertension are associated with an increased systemic sympathetic activity. Especially the renal sympathetic nervous system has been found to play a prominent role in this context. Therefore, catheterinterventional renal sympathetic denervation(RDN) has been established as a treatment for patients suffering from therapy resistant hypertension in the past decade. The initial enthusiasm for this treatment was markedly dampened by the results of the Symplicity-HTN-3 trial, although the transferability of the results into clinical practice to date appears to be questionable. In contrast to the extensive use of RDN in treating hypertensive patients within or without clinical trial settings over the past years, its effects on the complex pathophysiological mechanisms underlying therapy resistant hypertension are only partly understood and are part of ongoing research. Effects of RDN have been described on many levels in human trials: From altered systemic sympathetic activity across cardiac and metabolic alterations down to changes in renal function. Most of these changes could sustainably change long-term morbidity and mortality of the treated patients, even if blood pressure remains unchanged. Furthermore, a number of promising predictors for a successful treatment with RDN have been identified recently and further trials are ongoing. This will certainly help to improve the preselection of potential candidates for RDN and thereby optimize treatment outcomes. This review summarizes important pathophysiologic effects of renal denervation and illustrates the currently known predictors for therapy success.

Renal sympathetic denervation in resistant hypertension

Resistant hypertension remains a major clinical problem despite the available multidrug therapy.Over the next decades,its incidence will likely increase given that it is strongly associated with older age and obesity.Resistant hypertension patients have an increased cardiovascular risk,thus effective antihypertensive treatment will provide substantial health benefits.The crosstalk between sympathetic nervous system and kidneys plays a crucial role in hypertension.It influences several pathophysiological mechanisms such as the central sympathetic tone,the sodium balance and the systemic neurohumoral activation.In fact,studies using several animal models demonstrated that the renal denervation prevented and attenuated hypertension in multiple species.Large reductions in blood pressure were also observed in malignant hypertension patients submitted to sympathectomy surgeries.However,these approaches had an unacceptably high rates of periprocedural complications and disabling adverse events.Recently,an innovative non-pharmacological therapy that modulates sympathetic activation has been successfully developed.Renal sympathetic percutaneous denervation is an endovascular procedure that uses radiofrequency energy to destroy the autonomic renal nerves running inside the adventitia of renal arteries.This method represents a promising new approach to the strategy of inhibiting the sympathetic nervous system.The aim of this review is to examine the background knowledge that resulted in the development of this hypertension treatment and to critically appraise the available clinical evidence.

Neuroanatomy and clinical analysis of the cervical sympathetic trunk and longus colli

Anterior cervical surgery is commonly used for cervical vertebral body lesions. However, the structure of blood vessels and nerve tissues along the route of anterior cervical surgery is complex. We aimed to measure the data of the longus colli, the sympathetic trunk and the cervical sympathetic trunk （CST） ganglia in Chinese cadaver speci- mens. A total of 32 adult cadavers were studied. We delineated the surgical anatomy of the CST. The superior and inferior/cervicothoracic ganglia of the sympathetic trunk consistently appeared. The middle ganglion was observed in 28.1% of the specimens and there were 2 cases of unilateral double middle cervical ganglia. The inferior ganglion was observed in 25.0% of the specimens and the cervicothoracic ganglion was observed in the remaining speci- mens. The distance between the CST gradually decreased from the top to the bottom, and the distance between the medial edges of the longus colli gradually broadened from the top down. The average angle between the bilat- eral CST and the midline of the vertebra was 11.2°± 1.8° on the left side and 10.3°± 1.4° on the right side. The average angle between the medial margins of longus colli of both sides was 11.1°± 1.9°. The CST is at high risk when LC muscle is cut transversely or is dragged heavily, especially at the levels of C6 and C7. Awareness of the regional anatomy of the CST could help surgeons to identify and preserve it during anterior cervical surgeries.

A retrograde apoptotic signal originating in NGF-deprived distal axons of rat sympathetic neurons in compartmented cultures

Previous investigations of retrograde survival signaling by nerve growth factor （NGF） and other neurotrophins have supported diverse mechanisms, but all proposed mechanisms have in common the generation of survival signals retrogradely transmitted to the neuronal cell bodies. We report the finding of a retrograde apoptotic signal in axons that is suppressed by local NGF signaling. NGF withdrawal from distal axons alone was sufficient to activate the pro-apoptotic transcription factor, c-jun, in the cell bodies. Providing NGF directly to cell bodies, thereby restoring a source of NGF-induced survival signals, could not prevent c-jun activation caused by NGF withdrawal from the distal axons. This is evidence that c-jun is not activated due to loss of survival signals at the cell bodies. Moreover, blocking axonal transport with colchicine inhibited c-jun activation caused by NGF deprivation suggesting that a retrogradely transported pro-apoptotic signal, rather than loss of a retrogradely transported survival signal, caused c-jun activation. Additional experiments showed that activation of c-jun, pro-caspase-3 cleavage, and apoptosis were blocked by the protein kinase C inhibitors, rottlerin and chelerythrine, only when applied to distal axons suggesting that they block the axon-specific pro-apoptotic signal. The rottlerin-sensitive mechanism was found to regulate glyco- gen synthase kinase 3 （GSK3） activity. The effect of siRNA knockdown, and pharmacological inhibition of GSK3 suggests that GSK3 is required for apoptosis caused by NGF deprivation and may function as a retrograde carrier of the axon apoptotic signal. The existence of a retrograde death signaling system in axons that is suppressed by neurotro- phins has broad implications for neurodevelopment and for discovering treatments for neurodegenerative diseases and neurotrauma.

Enhanced sympathetic activity and cardiac sympathetic afferent reflex in rats with heart failure induced by adriamycin

Our previous studies have shown that the cardiac sympathetic afferent reflex is enhanced in rats with chronic heart failure （CHF） induced by coronary artery ligation and contributes to the over-excitation of sympathetic ac- tivity. We sought to determine whether sympathetic activity and cardiac sympathetic afferent reflex were en- hanced in adriamycin-induced CHF and whether angiotensin II （Ang II） in the paraventricular nucleus （PVN） was involved in enhancing sympathetic activity and cardiac sympathetic afferent reflex. Heart failure was induced by intraperitoneal injection of adriamycin for six times during 2 weeks （15 mg/kg）. Six weeks after the first injec- tion, the rats underwent anesthesia with urethane and a-chloralose. After vagotomy and baroreceptor denervation, cardiac sympathetic afferent reflex was evaluated by renal sympathetic nerve activity and mean arterial pressure （MAP） response to epicardial application of capsaicin （1.0 nmol）. The response of MAP to ganglionic blockade with hexamethonium in conscious rats was performed to evaluate sympathetic activity. The renal sympathetic nerve activity and cardiac sympathetic afferent reflex were enhanced in adriamycin rats and the maximum depres- sor response of MAP induced by hexamethonium was significantly greater in adriamycin rats than that in control rats. Bilateral PVN microinjection of angiotensin II （Ang II） caused larger responses of the cardiac sympathetic afferent reflex, baseline renal sympathetic nerve activity and MAP in adriamycin rats than control rats. These re- sults indicated that both sympathetic activity and cardiac sympathetic afferent reflex were enhanced and Ang II in the PVN was involved in the enhanced sympathetic activity and cardiac sympathetic afferent reflex in rats with adriamycin-induced heart failure.

Computed tomography-guided chemical renal sympathetic nerve modulation in the treatment of resistant hypertension: A case report

BACKGROUND Resistant hypertension(RH)has always been a difficult problem in clinical diagnosis and treatment.At present,there is no recognized safe and effective minimally invasive treatment.CASE SUMMARY An 80-year-old woman was admitted to hospital due to trigeminal neuralgia(TN).The patient had a history of RH for more than 10 years and her blood pressure(BP)was not well-controlled.Before the treatment for TN,we decided to perform chemical renal sympathetic denervation with ethanol in the Pain Department of our hospital.One year after the operation,she stopped taking antihypertensive drugs,and her BP was satisfactorily controlled within 4 years after surgery.CONCLUSION Computed tomography-guided chemical renal sympathetic modulation may be a feasible method for the treatment of RH.

Sympathetic Cooling of ^(40)Ca^(+_27)Al^+ Ion Pair Crystal in a Linear Paul Trap

The 27Al＋ ion optical clock is one of the most attractive optical clocks due to its own advantages such as low black-body radiation shift at room temperature and insensitivity to the magnetic drift. However, it cannot be laser-cooled directly in the absence of 167nm laser to date. This problem can be solved by sympathetic cooling. In this work, a linear Paul trap is used to trap both 40Ca＋ and 27A1＋ ions simultaneously, and a single Dopplercooled 40Ca＋ ion is employed to sympathetically cool a single 27A1＋ ion. Thus a ＇bright-dark＇ two-ion crystal has been successfully synthesized. The temperature of the crystal has been estimated to be about 7mK by measuring the ratio of carrier and sideband spectral intensities. Finally, the dark ion is proved to be an 27Al＋ ion by precise measuring of the ion crystal＇s secular motion frequency, which means that it is a great step for our 2Z Al＋ quantum logic clock.

Recovery of sympathetic nerve function after lumbar sympathectomy is slower in the hind limbs than in the torso

Local sympathetic denervation by surgical sympathectomy is used in the treatment of lower limb ulcers and ischemia,but the restoration of cutaneous sympathetic nerve functions is less clear.This study aims to explore the recovery of cutaneous sympathetic functions after bilateral L2-4 sympathectomy.The skin temperature of the left feet,using a point monitoring thermometer,increased intraoperatively after sympathectomy.The cytoplasm of sympathetic neurons contained tyrosine hydroxylase and dopamineβ-hydroxylase,visualized by immunofluorescence,indicated the accuracy of sympathectomy.Iodine starch test results suggested that the sweating function of the hind feet plantar skin decreased 2 and 7 weeks after lumbar sympathectomy but had recovered by 3 months.Immunofluorescence and western blot assay results revealed that norepinephrine and dopamineβ-hydroxylase expression in the skin from the sacrococcygeal region and hind feet decreased in the sympathectomized group at 2 weeks.Transmission electron microscopy results showed that perinuclear space and axon demyelination in sympathetic cells in the L5 sympathetic trunks were found in the sympathectomized group 3 months after sympathectomy.Although sympathetic denervation occurred in the sacrococcygeal region and hind feet skin 2 weeks after lumbar sympathectomy,the skin functions recovered gradually over 7 weeks to 3 months.In conclusion,sympathetic functional recovery may account for the recurrence of hyperhidrosis after sympathectomy and the normalization of sympathetic nerve trunks after incomplete injury.The recovery of sympathetic nerve function was slower in the limbs than in the torso after bilateral L（2-4） sympathectomy.

Effects of transection of cervical sympathetic trunk on cerebral infarct volume and oxygen free radical levels in rats with focal cerebral ischemia/reperfusion injury

BACKGROUND： Stellate ganglion block （SGB） plays a protective role on the brain, but the precise mechanism of action is not clear. OBJECTIVE： To simulate SGB by transection of the cervical sympathetic trunk （TCST） and to investigate the TCST effects on changes in cerebral infarct volume and oxygen free radical levels in rats with focal cerebral ischemia/reperfusion injury. DESIGN, TIME AND SETTING： A complete randomized control animal experiment was performed at the Institute of Neurological Diseases of Taihe Hospital, Yunyang Medical College from February to December 2005. MATERIALS： A total of 101 healthy Wistar rats, weighing 280-320 g, of both genders, aged 17-18 weeks, were used in this study. 2, 3, 5-triphenyltetrazolium chloride （TTC） was purchased from Changsha Hongyuan Biological Company. Superoxide dismutase （SOD）, malondialdehyde （MDA） and nitric oxide （NO） assay kits were provided by Nanjing Jiancheng Bioengineering Institute. METHODS： Rats were randomly divided into a TCST group, a model group and a sham operation group. Successful models were included in the final analysis, with at least 20 rats in each group. After TCST, rat models of focal cerebral ischemia/reperfusion injury were established in the TCST group by receiving middle cerebral artery occlusion （MCAO） by the intraluminal suture method for 2 hours, followed by 24 hours of reperfusion. Rat models of focal cerebral ischemia/reperfusion injury were made in the model group. Rats in the sham operation group underwent experimental procedures as for the model group, threading depth of 10 mm, and middle cerebral artery was not ligated. MAIN OUTCOME MEASURES： Brain tissue sections of ten rats from each group were used to measure cerebral infarct volume by TTC staining. Brain tissue homogenate of another ten rats from each group was used to detect SOD activities, MDA contents and NO levels. Rat neurological function was assessed by neurobehavioral measures. RESULTS： Cerebral infarct volume was bigger in the model group than in the TCST group （P 〈 0.05）. Twenty four hours after cerebral ischemia/reperfusion, SOD activities were lower, whereas MDA contents and NO levels were higher in the TCST and model groups, compared with the sham operation group （P 〈 0.05 or P 〈 0.01）. Compared with the model group, SOD activities were higher, whereas MDA contents and NO levels were lower in the TCST group （P 〈 0.05）. CONCLUSION： After TCST, cerebral infarct volume is reduced, SOD activities are increased, and MDA contents and NO levels are decreased compared to the model group in rats with focal cerebral ischemia/reperfusion injury. These changes may be associated with TCST.

The sensitivity of neurons with non-periodic activity to sympathetic stimulation in rat injured dorsal root ganglion

Objective The relationship between compressed dorsal root ganglion （DRG） neurons and firing pattern and sensitivity of neurons was studied in chronically the Hindmarsh-Rose （HR） neuronal model. Methods Spontane- ous activities from single fibers of chronically compressed DRG neurons in rats were recorded, and divided into periodic and non-periodic firing patterns. The sensitivity of the two kinds of firing pattern neuron to sympathetic stimulation （SS） was compared. Result It was found that 27.3% of periodic firing neurons and 93.2% of non-periodic firing neurons responded to SS respectively （ periodic vs non-periodic, P 〈 0.01 ）. The responses to SS with different stimulation time were greater non-periodic firing neurons than periodic firing neurons （P 〈 0.01 ）. The non-periodic firing neurons obviously responded to SS. After the firing pattern of these neurons transformed to periodic firing pattern, their responses to SS disappeared or decreased obviously. The HR neuronal model exhibited a significantly greater response to perturbation in non-periodic （chaotic） firing pattern than in periodic firing pattern. Conelusion The non-periodic firing neurons with deterministic chaos are more sensitive to external stimuli than the periodic firing neurons.