Temporomandibular joint osteoarthritis(TMJ-OA)is a common disease often accompanied by pain,seriously affecting physical and mental health of patients.Abnormal innervation at the osteochondral junction has been consid...Temporomandibular joint osteoarthritis(TMJ-OA)is a common disease often accompanied by pain,seriously affecting physical and mental health of patients.Abnormal innervation at the osteochondral junction has been considered as a predominant origin of arthralgia,while the specific mechanism mediating pain remains unclear.To investigate the underlying mechanism of TMJ-OA pain,an abnormal joint loading model was used to induce TMJ-OA pain.We found that during the development of TMJ-OA,the increased innervation of sympathetic nerve of subchondral bone precedes that of sensory nerves.Furthermore,these two types of nerves are spatially closely associated.Additionally,it was discovered that activation of sympathetic neural signals promotes osteoarthritic pain in mice,whereas blocking these signals effectively alleviates pain.In vitro experiments also confirmed that norepinephrine released by sympathetic neurons promotes the activation and axonal growth of sensory neurons.Moreover,we also discovered that through releasing norepinephrine,regional sympathetic nerves of subchondral bone were found to regulate growth and activation of local sensory nerves synergistically with other pain regulators.This study identified the role of regional sympathetic nerves in mediating pain in TMJ-OA.It sheds light on a new mechanism of abnormal innervation at the osteochondral junction and the regional crosstalk between peripheral nerves,providing a potential target for treating TMJ-OA pain.展开更多
OBJECTIVE:To investigate the mechanism of electroacupuncture of sympathetic nerve activity and blood pressure reduction in the hypothalamic paraventricular nucleus(PVN)of spontaneous hypertensive rats(SHRs).METHODS:A ...OBJECTIVE:To investigate the mechanism of electroacupuncture of sympathetic nerve activity and blood pressure reduction in the hypothalamic paraventricular nucleus(PVN)of spontaneous hypertensive rats(SHRs).METHODS:A total of 64 male SHRs were divided into four groups:model,sham-operated(Sham),electroacupuncture(EA),and N-methyl-D-aspartate receptor antagonist and electroacupuncture(NRA+EA).In addition,16 Wistar-Kyoto rats were used as controls.PVN stereotaxic surgery was performed in both the Sham and NRA+EA groups,while the EA and NRA+EA groups received 14 d of electroacupuncture.Blood pressure(BP)and heart rate(HR)were measured the day before the intervention and every other day.After 14 d of intervention,the rats in each group were tested for renal sympathetic nerve activity(RSNA).The associated factor levels were determined using Western blotting,reverse transcription-polymerase chain reaction(RTPCR),enzyme-linked immunosorbent assay(ELISA)and immunofluorescence assays.RESULTS:In comparison to the model group,the EA and NRA+EA groups had significantly lower BP,HR,and RSNA(P<0.01).The expression of N-methyl-Daspartate receptor(NMDAR),angiotensin II(Ang II),angiotensin II type 1(AT1),tumor necrosis factor-α,interleukin-1β,norepinephrine and arginine vasopressin was significantly lower in the EA and NRA+EA groups(P<0.01).Moreover,the antihypertensive effect of NRA+EA group outperformed to the EA group.CONCLUSIONS:Electroacupuncture effectively reduced the BP and sympathetic nerve excitability in SHRs.The mechanism was linked to the inhibition of NMDARmediated Ang II/AT1 and the inflammatory response in PVN.展开更多
BACKGROUND Diabetic gastroparesis(DGP)disrupts gastric motility.Electroacupuncture(EA)at Zusanli(ST36)may alleviate DGP symptoms via neural pathways.AIM To investigate how EA current intensities at ST36 regulate neura...BACKGROUND Diabetic gastroparesis(DGP)disrupts gastric motility.Electroacupuncture(EA)at Zusanli(ST36)may alleviate DGP symptoms via neural pathways.AIM To investigate how EA current intensities at ST36 regulate neural pathways and improve gastric motility in DGP models.METHODS A DGP model was established using intraperitoneal injection of streptozotocin.Gastrointestinal motility was measured in rats after 2 weeks of continuous EA at ST36.Current intensity was selected as 0.5 mA,1 mA,and 3 mA.Gastric electrodynamics were detected by recording and analyzing the number of gastric discharges.The gastric emptying rate and propulsion rate of the small intestine were measured to assess dynamic gastrointestinal function.Hematoxylin-eosin staining was conducted to measure histopathological changes in the gastric sinus.Reverse transcription-polymerase chain reaction was conducted to determine mRNA levels of Rho guanine nucleotide-binding protein A and Rho-associated coiled-coil forming protein kinase.Western blotting was conducted to determine the expression levels of choline acetyltransferase,tyrosine hydroxylase,Rho guanine nucleotide-binding protein A,and Rho-associated coiled-coil forming protein kinase.Immunofluorescence staining in the stomach was conducted to detect the distribution of C-kit,an interstitial cell of Cajal marker.An enzymelinked immunosorbent assay was conducted to detect serum levels of acetylcholine and norepinephrine.RESULTS Treatment with EA improved gastric emptying and gastric smooth muscle disorders in rats with DGP,mitigated pathological damage,and restored the function of interstitial cells of Cajal.In addition,different current intensities of EA affected gastrointestinal function of rats with DGP.The 0.5 mA,1 mA,and 3 mA EA groups all improved gastrointestinal function.0.5 mA EA increased acetylcholine levels by increasing protein expression of choline acetyltransferase(P<0.05),thereby upregulating vagus nerve activity and enhancing parasympathetic nerve regulation.3 mA EA increased norepinephrine levels(P<0.05)by increasing protein expression of tyrosine hydroxylase,thereby activating the sympathetic nervous pathway.1 mA coordinated the function of the vagus and sympathetic nerves to improve gastrointestinal motility.CONCLUSION EA with ST36 improved gastric motility in rats with DGP.0.5 mA EA activated the vagus nerve,while 3 mA EA regulated gastrointestinal motility by activating the sympathetic nerves.展开更多
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 me...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.展开更多
Objective To investigate the effects of histamine receptor antagonists on vasoconstriction induced by electrical stimulation （ES） on posterior auricular nerve,and to explore the pre-and post-synaptic effects of symp...Objective To investigate the effects of histamine receptor antagonists on vasoconstriction induced by electrical stimulation （ES） on posterior auricular nerve,and to explore the pre-and post-synaptic effects of sympathetic histamine on the vasomotor responses of vascular smooth muscle in rabbit ear.Methods ES was applied to posterior auricular nerves of the whole rabbit ear at 10 Hz,20 Hz and 40 Hz,respectively.Besides,the whole ear was perfused with different histamine receptor antagonists under constant perfusion pressure,and the changes in the flow rate of perfusate were observed.Results The flow rate of venous outflow was decreased by ES at all the 3 frequencies.The ES-induced vasoconstriction at 20 Hz and 40 Hz could be partly inhibited by H1 receptor antagonist chlorpheniramine （P0.05） .After exhaustion of histamine in mast cells by pretreatment with specific mast cell degranulator compound 48/80,chlorpheniramine could still inhibit the ES-induced flow rate reduction.In contrast,H2 receptor antagonist cimetidine could enhance the 40-Hz ES-induced flow rate reduction （P 0.05） .Moreover,ES-induced vasoconstriction at the 3 frequencies could all be enhanced by H3 receptor antagonist thioperamide （P0.05） .Conclusion Stimulation on the auricular nerve may evoke histamine release from sympathetic nerves rather than from mast cells.Moreover,the functions of sympathetic histamine vary from pre-synaptic modulation to post-synaptic vasoconstriction or vasodilatation,via activation of different histamine receptors.展开更多
Greater fluctuations in office blood pressure increase the risk of stroke and blood pressure volatility is an important risk factor for cardiovascular events. Effects of sympathetic and parasympathetic nerve on blood ...Greater fluctuations in office blood pressure increase the risk of stroke and blood pressure volatility is an important risk factor for cardiovascular events. Effects of sympathetic and parasympathetic nerve on blood pressure regulation are well known, however, those on visit-to visit variation remains unclear. Aim of this study is to clarify the contribution of sympathetic and parasympathetic balance on blood pressure fluctuation. Methods: We enrolled 23 outpatients with essential hypertension. We measured blood pressure, and pulse rate at clinic 14 times in a row and calculated coefficient of variance (CV) as visit-to-visit variability. The velocity of pupil contraction, miosis (VC) and dilation, mydriasis (VD) was determined from pupillary function test. Results: Systolic blood pressure and diastolic blood pressure were not significantly correlated with VC, VD and VD/VC. Heart rate was not correlated with VC and VD, but significantly correlated with VD/VC. CV of systolic blood pressure, diastolic blood pressure and heart rate were not significantly correlated with VC or VD. Ratio of VD to VC significantly negative correlated with CV of blood pressure, diastolic blood pressure, and heart. Value of VD was significantly correlated with value of VC. Conclusion: Visit-to-visit variability of blood pressure and heart rate is not related with sympathetic or parasympathetic tone independently but augmented by the impaired sympathetic and parasympathetic balance.展开更多
Objective: To study sympathetic-sensory coupling in chronically compressed dorsal root ganglion (DRG) neurons in rats. Methods: In chronically compressed DRG model, the spontaneous activity of single fiber from the in...Objective: To study sympathetic-sensory coupling in chronically compressed dorsal root ganglion (DRG) neurons in rats. Methods: In chronically compressed DRG model, the spontaneous activity of single fiber from the injured DRG neuron was recorded, and lumbar sympathetic trunk was electrical stimulated to study the sympathetic modulation of spontaneous activities in injured DRG neurons. Results: Fifty-seven percent of spontaneous active neurons of injured DRG responded to sympathetic stimulation. The responses included simple excitation, excitation followed by inhibition and simple inhibition. The responses enhanced with the increase of sympathetic stimulation time. The responses to sympathetic stimula- tion could be blocked by intravenously injection of phentolamine, a-adrenorecepor antagonist. Fifty-three percent of injured DRG responded to norepinephrine (NE). The responses to NE were similar to those induced by sympathetic stimulation. Conclusion: Sympathetic-sensory coupling is virtually present in chronic compressed DRG neurons. NE released from sympathetic nerve terminals acts on a-adrenorecepor to influence spontaneous activities of injured DRG neurons.展开更多
Previous studies have shown that sympathetic nerves are related to certain types of pain, and this phenomenon is referred to as sympathetic-sensory coupling. Chronic pain resulting from nerve injury can be exacerbated...Previous studies have shown that sympathetic nerves are related to certain types of pain, and this phenomenon is referred to as sympathetic-sensory coupling. Chronic pain resulting from nerve injury can be exacerbated by sympathetic stimulation or relieved by sympathetic inhibition. In the present study, the correlation between pain and sympathetic nerves was analyzed in patients with severe pain in lower limbs, as we^l as in a chronically compressed dorsa~ root ganglion ~CCD） rat model （model of low back pain and sciatica）. Patients with severe pain in the lower limbs underwent chemical lumbar sympathectomy （CLS）, and the analgesic effects of CLS were compared with painkillers. Results demonstrated significantly relieved lower limb pain following CLS, and the analgesic effects of CLS were superior to those seen with painkillers. In the CCD rat model, dorsal root ganglion neuronal activity significantly increased as a result of electrical stimulation to the sympathetic nerves. These results suggest that sympathetic nerves are closely associated with pain and sympathetic-sensory coupling is likely in lower limb pain in both patients and rat models of CCD.展开更多
To study whether the sympathetic nerves coordinate with the parasympathetic nerves during micturition in the rat. We used antegrade neural tracing with biotinylated dextran amine (BDA) injected into the pontine mictur...To study whether the sympathetic nerves coordinate with the parasympathetic nerves during micturition in the rat. We used antegrade neural tracing with biotinylated dextran amine (BDA) injected into the pontine micturition center (PMC) to label the terminals in the L6-S1 cord. Preganglionic parasympathetic neurons (PPNs) in the L6-S1 segment were labelled by retrograde transport of Fluorogold (FG) from the major pelvic ganglion (MPG).We detected retrograde neurons in L6-S1 using retrograde transport of horseradish peroxidase (HRP) from the intermediolateral cell column (IML) of the L1-L2 segment where sympathetic preganglionic neurons (SPNs) are located. Immunohistochemical methods showed that PPNs were identified to be choline acetyltransferase-immunoreactive (ChAT-IR). HRP-labelled neurons were not ChAT-IR and located dorsal to PPNs. BDA-labelled terminals were located mainly in the bilateral IML of L6-S1, some of which had synaptic contact with the HRP-labelled neurons. In addition, there were some wheat germ agglutinin-horseradish peroxidase (WGA-HRP) labelled terminals in the ipsilateral IML of the L1-L2 segment after WGA-HRP was microinjected into SPN. We conclude that PMC may control the preganglionic neurons of sympathetic nerves through the interneurons located dorsal to PPNs.展开更多
Background:A common assumption with autonomic assessment is that one branch opposes the other.With independent measures of parasympathetic (P) and sympathetic (S) ac tivity,based on concurrent time-frequency analysis ...Background:A common assumption with autonomic assessment is that one branch opposes the other.With independent measures of parasympathetic (P) and sympathetic (S) ac tivity,based on concurrent time-frequency analysis of respiratory activity and heart rate variability,this assumption has been challenged.Clinical observations of unprovoked P-excess during S-stimulation have been associated with treatable,abnormal responses.Method:Serial autonomic profiling of 12,967 patients was performed using the P&S method (ANX-3.0 Autonomic Monitor by ANSAR Medical Technologies,Inc.,Philadelphia,PA) over a five-year period.Treatment protocols are very low-dose and depend on patient history.For cardiovascular disease patients,Carvedilol was prescribed.For non-CVD patients,Nortriptyline was prescribed.In some cases where end-organ effects were not yet presented or relieved,patients were weaned of therapy once PE was relieved.Alternative therapies included Specific Chiropractic Adjustment,better known in the literature as Chiropractic Manipulative Therapy and intensive zero-impact,cardiovascular exercise.Results:PE patients present with normal HR and BP and no other apparent symptoms at rest.However,they reported symptoms of:sleep difficulties,palpitations,poor peripheral circulation,general malaise,depression (often with anxiety or ADD-like symptoms),frequent headache or migraines,menopause difficulties in women,hypothyroidism,cognitive difficulties,gastrointestinal upset,persistent weight-gain,and dizziness after standing.Conclusion:Normalizing PE,regardless of method,stabilizes the patient,relieves symptoms,improves quality of life,and improves patient outcomes.展开更多
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 e...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.展开更多
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...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.展开更多
The hypothalamic paraventricular nucleus(PVN) is a crucial region involved in maintaining homeostasis through the regulation of cardiovascular, neuroendocrine, and other functions. The PVN provides a dominant source o...The hypothalamic paraventricular nucleus(PVN) is a crucial region involved in maintaining homeostasis through the regulation of cardiovascular, neuroendocrine, and other functions. The PVN provides a dominant source of excitatory drive to the sympathetic outflow through innervation of the brainstem and spinal cord in hypertension. We discuss current findings on the role of the PVN in the regulation of sympathetic output in both normotensive and hypertensive conditions. The PVN seems to play a major role in generating the elevated sympathetic vasomotor activity that is characteristic of multiple forms of hypertension, including primary hypertension in humans. Recent studies in the spontaneously hypertensive rat model have revealed an imbalance of inhibitory and excitatory synaptic inputs to PVN presympathetic neurons as indicated by impaired inhibitory and enhanced excitatory synaptic inputs in hypertension.This imbalance of inhibitory and excitatory synaptic inputs in the PVN forms the basis for elevated sympathetic outflow in hypertension. In this review, we discuss the disruption of balance between glutamatergic and GABAergic inputs and the associated cellular and molecular alterations as mechanisms underlying the hyperactivity of PVN pre-sympathetic neurons in hypertension.展开更多
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...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.展开更多
The rostral ventrolateral medulla(RVLM) is a key region in cardiovascular regulation. It has been demonstrated that cholinergic synaptic transmission in the RVLM is enhanced in hypertensive rats. Angiotensinconverting...The rostral ventrolateral medulla(RVLM) is a key region in cardiovascular regulation. It has been demonstrated that cholinergic synaptic transmission in the RVLM is enhanced in hypertensive rats. Angiotensinconverting enzyme 2(ACE2) in the brain plays beneficial roles in cardiovascular function in hypertension. The purpose of this study was to determine the effect of ACE2 overexpression in the RVLM on cholinergic synaptic transmission in spontaneously hypertensive rats(SHRs).Four weeks after injecting lentiviral particles containing enhanced green fluorescent protein and ACE2 bilaterally into the RVLM, the blood pressure and heart rate were notably decreased. ACE2 overexpression significantly reduced the concentration of acetylcholine in microdialysis fluid from the RVLM and blunted the decrease in blood pressure evoked by bilateral injection of atropine into the RVLM in SHRs. In conclusion, we suggest that ACE2 overexpression in the RVLM attenuates the enhanced cholinergic synaptic transmission in SHRs.展开更多
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 d...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)展开更多
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 reaso...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.展开更多
Injury to peripheral nerves can lead to neuropathic pain, along with well-studied effects on sensory neurons, including hyperexcitability, abnormal spontaneous activity, and neuroinflammation in the sensory ganglia. N...Injury to peripheral nerves can lead to neuropathic pain, along with well-studied effects on sensory neurons, including hyperexcitability, abnormal spontaneous activity, and neuroinflammation in the sensory ganglia. Neuropathic pain can be enhanced by sympathetic activity. Peripheral nerve injury may also damage sympathetic axons or expose them to an inflammatory environment. In this study, we examined the lumbar sympathetic ganglion responses to two rat pain models： ligation of the L5 spinal nerve, and local inflammation of the L5 dorsal root ganglion （DRG）, which does not involve axotomy. Both models resulted in neuroinflammatory changes in the sympathetic ganglia, as indicated by macrophage responses, satellite glia activation, and increased numbers of T cells, along with very modest increases in sympathetic neuron excitability （but not spontaneous activity） measured in ex vivo recordings. The spinal nerve ligation model generally caused larger responses than DRG inflammation. Plasticity of the sympathetic system should be recognized in studies of sympathetic effects on pain.展开更多
Evidence suggests that the deterioration of communication between the sympathetic nervous system and cardiovascular system always accompanies the aging of human and animals. Cardiac sympathetic norepinephrine(NE) tran...Evidence suggests that the deterioration of communication between the sympathetic nervous system and cardiovascular system always accompanies the aging of human and animals. Cardiac sympathetic norepinephrine(NE) transporter(NET) on presynaptic membrane is a predominant component to eliminate released NE in the synaptic cleft and maintains the sensitivity of the β-adrenergic receptor(β-AR). In the present study,we investigated NET and β1-AR mRNA levels and sympathetic nerve density in cardiac sympathetic ganglion and left ventricular myocardium in 2-and 16-month-old rats with Northern blot analysis and immunohistochemistry. The expression levels of NET mRNA,NET protein and β1-AR mRNA in the ganglia or myocardia of 16-month-old rats were markedly reduced by 67%,26%,and 43%,respectively,in comparison with those in 2-month-old rats. Our results also show that aging induces a strong decrease of the catecholaminergic nerve fiber density.展开更多
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 an...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.展开更多
基金National Nature Science Foundation of China 82471000(to K.J.)National Nature Science Foundation of China 82170978(to K.J.)+1 种基金National Nature Science Foundation of China 82325012(to L.N.N.)National Key Research and Development Program 2023YFC2509100(to K.J.)。
文摘Temporomandibular joint osteoarthritis(TMJ-OA)is a common disease often accompanied by pain,seriously affecting physical and mental health of patients.Abnormal innervation at the osteochondral junction has been considered as a predominant origin of arthralgia,while the specific mechanism mediating pain remains unclear.To investigate the underlying mechanism of TMJ-OA pain,an abnormal joint loading model was used to induce TMJ-OA pain.We found that during the development of TMJ-OA,the increased innervation of sympathetic nerve of subchondral bone precedes that of sensory nerves.Furthermore,these two types of nerves are spatially closely associated.Additionally,it was discovered that activation of sympathetic neural signals promotes osteoarthritic pain in mice,whereas blocking these signals effectively alleviates pain.In vitro experiments also confirmed that norepinephrine released by sympathetic neurons promotes the activation and axonal growth of sensory neurons.Moreover,we also discovered that through releasing norepinephrine,regional sympathetic nerves of subchondral bone were found to regulate growth and activation of local sensory nerves synergistically with other pain regulators.This study identified the role of regional sympathetic nerves in mediating pain in TMJ-OA.It sheds light on a new mechanism of abnormal innervation at the osteochondral junction and the regional crosstalk between peripheral nerves,providing a potential target for treating TMJ-OA pain.
基金Doctoral Research Fund Project of Qilu Hospital of Shandong University(Qingdao):Mechanistic Study on the Improvement of Vertigo Caused by Posterior Circulation Ischemia by Acupuncture through Regulating Cerebral Blood Flow in Rats with Posterior Circulation Ischemia Vertigo(No.QDKY2023BS19)National Natural Science Foundation of China:From Microrna 9 Regulate P2X7 Receptor of Microglia in Paraventricular Nucleus of Hypothalamus to Explore the Effect of Electroacupuncture on Sympathetic Nerve Excitability in Spontaneously Hypertensive Rats(No.82074553)。
文摘OBJECTIVE:To investigate the mechanism of electroacupuncture of sympathetic nerve activity and blood pressure reduction in the hypothalamic paraventricular nucleus(PVN)of spontaneous hypertensive rats(SHRs).METHODS:A total of 64 male SHRs were divided into four groups:model,sham-operated(Sham),electroacupuncture(EA),and N-methyl-D-aspartate receptor antagonist and electroacupuncture(NRA+EA).In addition,16 Wistar-Kyoto rats were used as controls.PVN stereotaxic surgery was performed in both the Sham and NRA+EA groups,while the EA and NRA+EA groups received 14 d of electroacupuncture.Blood pressure(BP)and heart rate(HR)were measured the day before the intervention and every other day.After 14 d of intervention,the rats in each group were tested for renal sympathetic nerve activity(RSNA).The associated factor levels were determined using Western blotting,reverse transcription-polymerase chain reaction(RTPCR),enzyme-linked immunosorbent assay(ELISA)and immunofluorescence assays.RESULTS:In comparison to the model group,the EA and NRA+EA groups had significantly lower BP,HR,and RSNA(P<0.01).The expression of N-methyl-Daspartate receptor(NMDAR),angiotensin II(Ang II),angiotensin II type 1(AT1),tumor necrosis factor-α,interleukin-1β,norepinephrine and arginine vasopressin was significantly lower in the EA and NRA+EA groups(P<0.01).Moreover,the antihypertensive effect of NRA+EA group outperformed to the EA group.CONCLUSIONS:Electroacupuncture effectively reduced the BP and sympathetic nerve excitability in SHRs.The mechanism was linked to the inhibition of NMDARmediated Ang II/AT1 and the inflammatory response in PVN.
基金Supported by National Natural Science Foundation of China,No.82205298Natural Science Foundation of Hunan Province,No.2023JJ30462+1 种基金Hunan Provincial Department of Science and Technology,No.2023SK2045,No.22JBZ007,No.Z2023XJYQ07,No.B2024007,and No.Z2023JB012024 Graduate Innovation Topics,No.2024CX031.
文摘BACKGROUND Diabetic gastroparesis(DGP)disrupts gastric motility.Electroacupuncture(EA)at Zusanli(ST36)may alleviate DGP symptoms via neural pathways.AIM To investigate how EA current intensities at ST36 regulate neural pathways and improve gastric motility in DGP models.METHODS A DGP model was established using intraperitoneal injection of streptozotocin.Gastrointestinal motility was measured in rats after 2 weeks of continuous EA at ST36.Current intensity was selected as 0.5 mA,1 mA,and 3 mA.Gastric electrodynamics were detected by recording and analyzing the number of gastric discharges.The gastric emptying rate and propulsion rate of the small intestine were measured to assess dynamic gastrointestinal function.Hematoxylin-eosin staining was conducted to measure histopathological changes in the gastric sinus.Reverse transcription-polymerase chain reaction was conducted to determine mRNA levels of Rho guanine nucleotide-binding protein A and Rho-associated coiled-coil forming protein kinase.Western blotting was conducted to determine the expression levels of choline acetyltransferase,tyrosine hydroxylase,Rho guanine nucleotide-binding protein A,and Rho-associated coiled-coil forming protein kinase.Immunofluorescence staining in the stomach was conducted to detect the distribution of C-kit,an interstitial cell of Cajal marker.An enzymelinked immunosorbent assay was conducted to detect serum levels of acetylcholine and norepinephrine.RESULTS Treatment with EA improved gastric emptying and gastric smooth muscle disorders in rats with DGP,mitigated pathological damage,and restored the function of interstitial cells of Cajal.In addition,different current intensities of EA affected gastrointestinal function of rats with DGP.The 0.5 mA,1 mA,and 3 mA EA groups all improved gastrointestinal function.0.5 mA EA increased acetylcholine levels by increasing protein expression of choline acetyltransferase(P<0.05),thereby upregulating vagus nerve activity and enhancing parasympathetic nerve regulation.3 mA EA increased norepinephrine levels(P<0.05)by increasing protein expression of tyrosine hydroxylase,thereby activating the sympathetic nervous pathway.1 mA coordinated the function of the vagus and sympathetic nerves to improve gastrointestinal motility.CONCLUSION EA with ST36 improved gastric motility in rats with DGP.0.5 mA EA activated the vagus nerve,while 3 mA EA regulated gastrointestinal motility by activating the sympathetic nerves.
文摘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.
基金supported by the National Natural Science Foundation of China(No.30770669,30800310)
文摘Objective To investigate the effects of histamine receptor antagonists on vasoconstriction induced by electrical stimulation （ES） on posterior auricular nerve,and to explore the pre-and post-synaptic effects of sympathetic histamine on the vasomotor responses of vascular smooth muscle in rabbit ear.Methods ES was applied to posterior auricular nerves of the whole rabbit ear at 10 Hz,20 Hz and 40 Hz,respectively.Besides,the whole ear was perfused with different histamine receptor antagonists under constant perfusion pressure,and the changes in the flow rate of perfusate were observed.Results The flow rate of venous outflow was decreased by ES at all the 3 frequencies.The ES-induced vasoconstriction at 20 Hz and 40 Hz could be partly inhibited by H1 receptor antagonist chlorpheniramine （P0.05） .After exhaustion of histamine in mast cells by pretreatment with specific mast cell degranulator compound 48/80,chlorpheniramine could still inhibit the ES-induced flow rate reduction.In contrast,H2 receptor antagonist cimetidine could enhance the 40-Hz ES-induced flow rate reduction （P 0.05） .Moreover,ES-induced vasoconstriction at the 3 frequencies could all be enhanced by H3 receptor antagonist thioperamide （P0.05） .Conclusion Stimulation on the auricular nerve may evoke histamine release from sympathetic nerves rather than from mast cells.Moreover,the functions of sympathetic histamine vary from pre-synaptic modulation to post-synaptic vasoconstriction or vasodilatation,via activation of different histamine receptors.
文摘Greater fluctuations in office blood pressure increase the risk of stroke and blood pressure volatility is an important risk factor for cardiovascular events. Effects of sympathetic and parasympathetic nerve on blood pressure regulation are well known, however, those on visit-to visit variation remains unclear. Aim of this study is to clarify the contribution of sympathetic and parasympathetic balance on blood pressure fluctuation. Methods: We enrolled 23 outpatients with essential hypertension. We measured blood pressure, and pulse rate at clinic 14 times in a row and calculated coefficient of variance (CV) as visit-to-visit variability. The velocity of pupil contraction, miosis (VC) and dilation, mydriasis (VD) was determined from pupillary function test. Results: Systolic blood pressure and diastolic blood pressure were not significantly correlated with VC, VD and VD/VC. Heart rate was not correlated with VC and VD, but significantly correlated with VD/VC. CV of systolic blood pressure, diastolic blood pressure and heart rate were not significantly correlated with VC or VD. Ratio of VD to VC significantly negative correlated with CV of blood pressure, diastolic blood pressure, and heart. Value of VD was significantly correlated with value of VC. Conclusion: Visit-to-visit variability of blood pressure and heart rate is not related with sympathetic or parasympathetic tone independently but augmented by the impaired sympathetic and parasympathetic balance.
基金Supported by National Natural Science Foundation of China, No. 39970242
文摘Objective: To study sympathetic-sensory coupling in chronically compressed dorsal root ganglion (DRG) neurons in rats. Methods: In chronically compressed DRG model, the spontaneous activity of single fiber from the injured DRG neuron was recorded, and lumbar sympathetic trunk was electrical stimulated to study the sympathetic modulation of spontaneous activities in injured DRG neurons. Results: Fifty-seven percent of spontaneous active neurons of injured DRG responded to sympathetic stimulation. The responses included simple excitation, excitation followed by inhibition and simple inhibition. The responses enhanced with the increase of sympathetic stimulation time. The responses to sympathetic stimula- tion could be blocked by intravenously injection of phentolamine, a-adrenorecepor antagonist. Fifty-three percent of injured DRG responded to norepinephrine (NE). The responses to NE were similar to those induced by sympathetic stimulation. Conclusion: Sympathetic-sensory coupling is virtually present in chronic compressed DRG neurons. NE released from sympathetic nerve terminals acts on a-adrenorecepor to influence spontaneous activities of injured DRG neurons.
基金the Natural Science Foundation of Guangdong Province,No. 05300503
文摘Previous studies have shown that sympathetic nerves are related to certain types of pain, and this phenomenon is referred to as sympathetic-sensory coupling. Chronic pain resulting from nerve injury can be exacerbated by sympathetic stimulation or relieved by sympathetic inhibition. In the present study, the correlation between pain and sympathetic nerves was analyzed in patients with severe pain in lower limbs, as we^l as in a chronically compressed dorsa~ root ganglion ~CCD） rat model （model of low back pain and sciatica）. Patients with severe pain in the lower limbs underwent chemical lumbar sympathectomy （CLS）, and the analgesic effects of CLS were compared with painkillers. Results demonstrated significantly relieved lower limb pain following CLS, and the analgesic effects of CLS were superior to those seen with painkillers. In the CCD rat model, dorsal root ganglion neuronal activity significantly increased as a result of electrical stimulation to the sympathetic nerves. These results suggest that sympathetic nerves are closely associated with pain and sympathetic-sensory coupling is likely in lower limb pain in both patients and rat models of CCD.
基金This project was supported by a grant fromthe Ministry ofSicience and Technology of China (No .2003CB515300) .
文摘To study whether the sympathetic nerves coordinate with the parasympathetic nerves during micturition in the rat. We used antegrade neural tracing with biotinylated dextran amine (BDA) injected into the pontine micturition center (PMC) to label the terminals in the L6-S1 cord. Preganglionic parasympathetic neurons (PPNs) in the L6-S1 segment were labelled by retrograde transport of Fluorogold (FG) from the major pelvic ganglion (MPG).We detected retrograde neurons in L6-S1 using retrograde transport of horseradish peroxidase (HRP) from the intermediolateral cell column (IML) of the L1-L2 segment where sympathetic preganglionic neurons (SPNs) are located. Immunohistochemical methods showed that PPNs were identified to be choline acetyltransferase-immunoreactive (ChAT-IR). HRP-labelled neurons were not ChAT-IR and located dorsal to PPNs. BDA-labelled terminals were located mainly in the bilateral IML of L6-S1, some of which had synaptic contact with the HRP-labelled neurons. In addition, there were some wheat germ agglutinin-horseradish peroxidase (WGA-HRP) labelled terminals in the ipsilateral IML of the L1-L2 segment after WGA-HRP was microinjected into SPN. We conclude that PMC may control the preganglionic neurons of sympathetic nerves through the interneurons located dorsal to PPNs.
文摘Background:A common assumption with autonomic assessment is that one branch opposes the other.With independent measures of parasympathetic (P) and sympathetic (S) ac tivity,based on concurrent time-frequency analysis of respiratory activity and heart rate variability,this assumption has been challenged.Clinical observations of unprovoked P-excess during S-stimulation have been associated with treatable,abnormal responses.Method:Serial autonomic profiling of 12,967 patients was performed using the P&S method (ANX-3.0 Autonomic Monitor by ANSAR Medical Technologies,Inc.,Philadelphia,PA) over a five-year period.Treatment protocols are very low-dose and depend on patient history.For cardiovascular disease patients,Carvedilol was prescribed.For non-CVD patients,Nortriptyline was prescribed.In some cases where end-organ effects were not yet presented or relieved,patients were weaned of therapy once PE was relieved.Alternative therapies included Specific Chiropractic Adjustment,better known in the literature as Chiropractic Manipulative Therapy and intensive zero-impact,cardiovascular exercise.Results:PE patients present with normal HR and BP and no other apparent symptoms at rest.However,they reported symptoms of:sleep difficulties,palpitations,poor peripheral circulation,general malaise,depression (often with anxiety or ADD-like symptoms),frequent headache or migraines,menopause difficulties in women,hypothyroidism,cognitive difficulties,gastrointestinal upset,persistent weight-gain,and dizziness after standing.Conclusion:Normalizing PE,regardless of method,stabilizes the patient,relieves symptoms,improves quality of life,and improves patient outcomes.
基金Supported by the National Natural Science Foundation of China,No.81373749No.81574071,and No.81673883
文摘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.
基金Supported by The National Key Basic Research Program(973 Program)No.2011CB505206+3 种基金the National Natural Science Foundation of ChinaNo.81202744No.81373749 and No.81574071Jiangsu Provincial Qinglan Project Sci-tech Innovation Team
文摘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.
基金supported by National Institutes of Health Grants HL131161,HL139523,and HL142133
文摘The hypothalamic paraventricular nucleus(PVN) is a crucial region involved in maintaining homeostasis through the regulation of cardiovascular, neuroendocrine, and other functions. The PVN provides a dominant source of excitatory drive to the sympathetic outflow through innervation of the brainstem and spinal cord in hypertension. We discuss current findings on the role of the PVN in the regulation of sympathetic output in both normotensive and hypertensive conditions. The PVN seems to play a major role in generating the elevated sympathetic vasomotor activity that is characteristic of multiple forms of hypertension, including primary hypertension in humans. Recent studies in the spontaneously hypertensive rat model have revealed an imbalance of inhibitory and excitatory synaptic inputs to PVN presympathetic neurons as indicated by impaired inhibitory and enhanced excitatory synaptic inputs in hypertension.This imbalance of inhibitory and excitatory synaptic inputs in the PVN forms the basis for elevated sympathetic outflow in hypertension. In this review, we discuss the disruption of balance between glutamatergic and GABAergic inputs and the associated cellular and molecular alterations as mechanisms underlying the hyperactivity of PVN pre-sympathetic neurons in hypertension.
文摘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.
基金supported by the National Natural Science Foundation of China(81470534,81770419,81630012,and 81570385)the Key Laboratory of Medical Electrophysiology(Southwest Medical University)Ministry of Education of China-No201709(KeyME-2017-09)
文摘The rostral ventrolateral medulla(RVLM) is a key region in cardiovascular regulation. It has been demonstrated that cholinergic synaptic transmission in the RVLM is enhanced in hypertensive rats. Angiotensinconverting enzyme 2(ACE2) in the brain plays beneficial roles in cardiovascular function in hypertension. The purpose of this study was to determine the effect of ACE2 overexpression in the RVLM on cholinergic synaptic transmission in spontaneously hypertensive rats(SHRs).Four weeks after injecting lentiviral particles containing enhanced green fluorescent protein and ACE2 bilaterally into the RVLM, the blood pressure and heart rate were notably decreased. ACE2 overexpression significantly reduced the concentration of acetylcholine in microdialysis fluid from the RVLM and blunted the decrease in blood pressure evoked by bilateral injection of atropine into the RVLM in SHRs. In conclusion, we suggest that ACE2 overexpression in the RVLM attenuates the enhanced cholinergic synaptic transmission in SHRs.
文摘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)
文摘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.
基金supported in part by National Institutes of Health Grants NS045594,NS055860,and AR068989 to J.M.Z.
文摘Injury to peripheral nerves can lead to neuropathic pain, along with well-studied effects on sensory neurons, including hyperexcitability, abnormal spontaneous activity, and neuroinflammation in the sensory ganglia. Neuropathic pain can be enhanced by sympathetic activity. Peripheral nerve injury may also damage sympathetic axons or expose them to an inflammatory environment. In this study, we examined the lumbar sympathetic ganglion responses to two rat pain models： ligation of the L5 spinal nerve, and local inflammation of the L5 dorsal root ganglion （DRG）, which does not involve axotomy. Both models resulted in neuroinflammatory changes in the sympathetic ganglia, as indicated by macrophage responses, satellite glia activation, and increased numbers of T cells, along with very modest increases in sympathetic neuron excitability （but not spontaneous activity） measured in ex vivo recordings. The spinal nerve ligation model generally caused larger responses than DRG inflammation. Plasticity of the sympathetic system should be recognized in studies of sympathetic effects on pain.
基金supported by the Postdoctoral Fellow Foundation of the Science and Technology Committee of Shanghai (No. 98-10)the Natural Science Foundation of Chinese People's Armed Police Force (Nos. WKH2006-5 and WKH2008ZO4), China
文摘Evidence suggests that the deterioration of communication between the sympathetic nervous system and cardiovascular system always accompanies the aging of human and animals. Cardiac sympathetic norepinephrine(NE) transporter(NET) on presynaptic membrane is a predominant component to eliminate released NE in the synaptic cleft and maintains the sensitivity of the β-adrenergic receptor(β-AR). In the present study,we investigated NET and β1-AR mRNA levels and sympathetic nerve density in cardiac sympathetic ganglion and left ventricular myocardium in 2-and 16-month-old rats with Northern blot analysis and immunohistochemistry. The expression levels of NET mRNA,NET protein and β1-AR mRNA in the ganglia or myocardia of 16-month-old rats were markedly reduced by 67%,26%,and 43%,respectively,in comparison with those in 2-month-old rats. Our results also show that aging induces a strong decrease of the catecholaminergic nerve fiber density.
文摘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.
