Stellate ganglion block relieves acute lung injury induced by severe acute pancreatitis via the miR-155-5p/SOCS5/JAK2/STAT3 axis.

Acute lung injury (ALI), a prevalent complication of severe acute pancreatitis (SAP), is also a leading contributor to respiratory failure and even death of SAP patients. Here, we intended to investigate the function and mechanism of stellate ganglion block (SGB) in ameliorating SAP-induced ALI (SAP-ALI). We engineered an SAP-ALI model in rats and treated them with SGB. HE staining and the dry and wet method were implemented to evaluate pathological alterations in the tissues and pulmonary edema. The rats serum changes of the profiles of TNF-α, IL-6, IL-1ß, and IL-10 were examined. The profiles of miR-155-5p and SOCS5/JAK2/STAT3 were detected. Functional assays were performed for confirming the role of miR-155-5p in modulating the SOCS5/JAK2/STAT3 pathway in pulmonary epithelial cells. Our findings revealed that SGB vigorously alleviated SAP rat lung tissue damage and lung edema and lessened the generation of pro-inflammatory cytokines TNF-α, IL-6, and IL-1ß. SGB enhanced SOCS5 expression, hampered miR-155-5p, and suppressed JAK2/STAT3 pathway activation. As evidenced by mechanism studies, miR-155-5p targeted the 3'UTR of SOCS5 and repressed its expression, hence resulting in JAK2/STAT3 pathway activation. During animal trials, we discovered that SGB ameliorated SAP-ALI, boosted SOCS5 expression, and mitigated the levels of pro-inflammatory factors and miR-155-5p in the plasma. In vitro, miR-155-5p overexpression substantially facilitated pulmonary epithelial cell apoptosis, inflammation, and JAK2/STAT3 pathway activation and restrained SOCS5 expression. All in all, our work hinted that SGB could modulate the miR-155-5p/SOCS5/JAK2/STAT3 axis to alleviate SAP-ALI.

Effects of local cardiac denervation on cardiac innervation and ventricular arrhythmia after chronic myocardial infarction.

BACKGROUND: Modulation of the autonomic nervous system (ANS) has already been demonstrated to display antiarrhythmic effects in patients and animals with MI. In this study, we investigated whether local cardiac denervation has any beneficial effects on ventricular electrical stability and cardiac function in the chronic phase of MI. METHODS: Twenty-one anesthetized dogs were randomly assigned into the sham-operated, MI and MI-ablation groups, respectively. Four weeks after local cardiac denervation, LSG stimulation was used to induce VPCs and VAs. The ventricular fibrillation threshold (VFT) and the incidence of inducible VPCs were measured with electrophysiological protocol. Cardiac innervation was determined with immunohistochemical staining of growth associated protein-43 (GAP43) and tyrosine hydroxylase (TH). The global cardiac and regional ventricular function was evaluated with doppler echocardiography in this study. RESULTS: Four weeks after operation, the incidence of inducible VPC and VF in MI-ablation group were significantly reduced compared to the MI dogs (p<0.05). Moreover, local cardiac denervation significantly improved VFT in the infarcted border zone (p<0.05). The densities of GAP43 and TH-positive nerve fibers in the infarcted border zone in the MI-ablation group were lower than those in the MI group (p<0.05). However, the local cardiac denervation did not significantly improve cardiac function in the chronic phase of MI, determined by the left ventricle diameter (LV), left atrial diameter (LA), ejection fraction (EF). CONCLUSIONS: Summarily, in the chronic phase of MI, local cardiac denervation reduces the ventricular electrical instability, and attenuates spatial heterogeneity of sympathetic nerve reconstruction. Our study suggests that this methodology might decrease malignant ventricular arrhythmia in chronic MI, and has a great potential for clinical application.

Granular cell tumor of the stellate ganglion presenting with Horner's syndrome.

We report a granular cell tumor (GCT) that occurred within the stellate ganglion of a 26-year-old woman who initially presented with a unilateral Horner's syndrome and progressive right upper extremity pain. We also review the literature related to the differential diagnoses of such a cervicothoracic tumor, with particular emphasis on the embryologic origin of these possibilities. GCT are rare tumors of Schwann cell origin which are more often found in subcutaneous locations than in relation to neural elements. In this woman, a mass identified on preoperative imaging was positioned anterolateral to the T1 vertebral body and displaced the vertebral artery anteriorly. During surgery, the lesion was observed within the sympathetic chain in the area of the stellate ganglion. The sympathetic chain was transected above and below the mass in order to achieve an adequate resection. The pathology demonstrated polygonal cells with diffuse eosinophilic granular cytoplasm positive for CD68 (a marker of lysosomes) and S-100 (a marker of neural crest derivatives) which established the diagnosis of GCT. This is the first patient, to our knowledge, with a granular cell tumor arising from the stellate ganglion.

Sympathetic nerve fibers and ganglia in canine cervical vagus nerves: localization and quantitation.

BACKGROUND: Cervical vagal nerve (CVN) stimulation may improve left ventricular ejection fraction in patients with heart failure. OBJECTIVES: To test the hypothesis that sympathetic structures are present in the CVN and to describe the location and quantitate these sympathetic components of the CVN. METHODS: We performed immunohistochemical studies of the CVN from 11 normal dogs and simultaneously recorded stellate ganglion nerve activity, left thoracic vagal nerve activity, and subcutaneous electrocardiogram in 2 additional dogs. RESULTS: A total of 28 individual nerve bundles were present in the CVNs of the first 11 dogs, with an average of 1.87±1.06 per dog. All CVNs contain tyrosine hydroxylase-positive (sympathetic) nerves, with a total cross-sectional area of 0.97±0.38 mm(2). The sympathetic nerves were nonmyelinated, typically located at the periphery of the nerve bundles and occupied 0.03%-2.80% of the CVN cross-sectional area. Cholineacetyltransferase-positive nerve fibers occupied 12.90%-42.86% of the CVN cross-sectional areas. Ten of 11 CVNs showed tyrosine hydroxylase and cholineacetyltransferase colocalization. In 2 dogs with nerve recordings, we documented heart rate acceleration during spontaneous vagal nerve activity in the absence of stellate ganglion nerve activity. CONCLUSIONS: Sympathetic nerve fibers are invariably present in the CVNs of normal dogs and occupy in average up to 2.8% of the cross-sectional area. Because sympathetic nerve fibers are present in the periphery of the CVNs, they may be susceptible to activation by electrical stimulation. Spontaneous activation of the sympathetic component of the vagal nerve may accelerate the heart rate.

Lipoma gigante cervico -torácico. Abordaje mixto por cervicotomía y toracoscopia: Reporte de un caso / Cervico-thoracic giant lipoma: mixed approach by cervicotomy and thoracoscopy: a case report

Se presenta un caso de lipoma cervicotorácico gigante en paciente femenino de 45 años de edad, quien consultó por aumento de volumen cervical, odinodisfagia y disnea. Una radiografía de tórax y tomografía computarizada reveló una masa gigante intratorácica bilateral, ocupando la cavidad torácica izquierda con extensión al mediastino anterosuperior y al cuello, desplazando la tráquea y la faringe hacia la porción anterior y derecha. La paciente se llevó a resección quirúrgica del tumor cervico-torácico, con examen histológico que confirmó el diagnóstico de un lipoma gigante, con peso de 475 gramos y medidas de 30 x 20 cm. Este es el lipoma cervico-torácico más grande documentado en la literatura moderna y con abordaje mixto cervicotomía más toracoscopia

Female patient 45 years old with giant cervicothoracic lipoma, that consulted by increase of cervical volume, odinodysphagia and dyspnea. An x-ray thorax and computerized tomography revealed a bilateral intrathoracic giant mass, occupying the left thoracic cavity extending to the anterosuperior mediastinum and the neck, causing displacement of the trachea and the pharynx towards the previous and right portion. The patient took to surgical resection of the cervical thoracic tumor, with histological examination that confirmed the diagnosis of a giant lipoma, with weight of 475 grams and measures of 30 x 20 cm. It is largest cervical thoracic lipoma documented in modern literature and with cervicotomy and thoracoscopic approach

Cervicothoracic neuroblastoma arising from the stellate ganglion in children: the use of muscle and bone sparing transmanubrial transcostal approach.

Cervicothoracic neuroblastoma arising from the stellate ganglion in children has always been a challenge to the pediatric surgeon. Localized thoracic neuroblastoma in children has a very good prognosis if excised completely even without adjuvant therapy. Several approaches have been described to resect cervicothoracic neuroblastoma arising from the stellate ganglion with limited success. The muscle and bone sparing transmanubrial transcostal approach which spares the clavicle and the sternomastoid muscle provides excellent exposure for the complete excision of the tumor and excellent functional outcome. We report a 2-year-old girl with cervicothoracic neuroblastoma who had an excellent outcome with this approach.

Myocardial ischemic nociceptive signaling mediated by P2X3 receptor in rat stellate ganglion neurons.

Adenosine 5'-triphosphate (ATP) is implicated in peripheral pain signaling through activation of P2X receptors. P2X(3) receptors have a high level of expression in, and selective location on sensory afferents. P2X receptors, particularly the P2X(3) subtype, are identified as targets for novel analgesics. The stellate ganglion (SG) is peripheral sympathetic ganglia involved in heart function. Surgical interventions of sympathetic afferent pathways abolish or relieve angina pectoris, so it is showed that cardiac pain is mediated by the activation of afferents in sympathetic nerves. The cervicothoracic sympathetic ganglia, including the stellate ganglion, are implicated in sensations associated with myocardial ischemia or cardiac pain. In the present study we have examined P2X(3) involvement in cardiac nociceptive transmission. P2X receptor agonists activated currents (I(ATP)) in SG neurons. The I(ATP) amplitude and P2X(3) mRNA expression in myocardial ischemic injury group were much larger than those obtained in control group. Prostaglandin E(2) (PGE(2)) and substance P (SP) increased ATP-activated currents. P2X(3) receptor antagonist A-317491 reduced P2X agonist activated currents and P2X(3) mRNA expression. The results revealed that the myocardial ischemia induced the upregulation of P2X(3) receptor in function and morphous and P2X(3) receptor antagonist A-317491 inhibited P2X agonist activated currents and P2X(3) mRNA expression. The facts indicated that P2X(3) receptor in SG neurons was involved in cardiac nociceptive transmission.

Intractable cryptogenic frontal lobe epilepsy in a patient with MURCS association.

The MURCS association is a rare, nonrandom association of müllerian duct aplasia, renal aplasia and cervicothoracic somite dysplasia. The etiology is unknown. Although it is usually a sporadic disorder, familial cases with uterovaginal anomalies have been reported. Occasionally, it may be accompanied by abnormalities involving various other organs or systems. Malformations related to the central nervous system are very rare and the presence of seizures has not been reported previously. We present a 26-year-old female with MURCS association who had late onset, drug resistant partial seizures presumably originating in the frontal lobe.

Expression of vasoactive intestinal polypeptide and calcitonin gene-related peptide in human stellate ganglia after acute myocardial infarction.

Using the method of indirect immunofluorescence the distribution of vasoactive intestinal polypeptide (VIP) and calcitonin gene-related peptide (CGRP) was investigated in autopsy specimens of human stellate ganglia following acute myocardial infarction (AMI). The dramatic increase of both VIP- and CGRP-immunoreactivities in principal ganglionic neurons as well as of calcitonin gene-related peptide in perineuronal nets was revealed. It was concluded that hypoxia and myocardial ischaemia following AMI are the main inducing factors for activation of both vasoactive regulatory neuropeptide synthesis. The upregulation of VIP and CGRP expression in sympathetic ganglionic neurons may provide regulatory and trophic support to the ischaemic heart.

Upregulation of vasoactive intestinal polypeptide (VIP) and calcitonin gene-related peptide (CGRP) expression in stellate ganglia of children with congenital cardiovascular lesions.

The distribution patterns of vasoactive intestinal polypeptide (VIP) and calcitonin gene-related peptide (CGRP) immunoreactivities (IR) in stellate ganglia of human neonates and infants with congenital heart and vascular lesions were investigated by the method of indirect immunohistochemistry. The results demonstrated upregulation of VIP and CGRP expression in principal ganglionic neurons independently of the type of lesion. It is suggested that the activation of neuropeptide synthesis in stellate ganglia is a compensatory reaction of ganglionic neurons in response to congenital cardiovascular lesions, in regulation of heart contractility, and as a trophic influence on the ischemic myocardium. Hypoxia is the main inducing factor for the upregulation of VIP and CGRP expression in sympathetic neurons.

Distribution of vasoactive intestinal polypeptide-, calcitonin gene-related peptide-, somatostatin- and neurofilament-immunoreactivities in sympathetic ganglia of human fetuses and premature neonates.

The distribution patterns of vasoactive intestinal polypeptide (VIP), calcitonin gene-related peptide (CGRP), somatostatin (SOM) and neurofilament (NF) immunoreactivities (IR) were studied in the stellate ganglia of human fetuses and neonates at 24-26 weeks gestation. Sizeable populations with some quantitative variations of VIP-, CGRP- and SOM immunoreactive nerve cells were detected in all ganglia studied. In marked contrast, neurofilament expression was down-regulated. The upregulation of VIP, CGRP and SOM expression suggested their inductor effect on growth and differentiation neurons as well as on the development of their neurotransmitter properties. The main neuropeptides-inducing factor of sympathetic ganglia in human prenatal ontogenesis may be considered as a relative hypoxia.

Nerve sprouting and sudden cardiac death.

The factors that contribute to the occurrence of sudden cardiac death (SCD) in patients with chronic myocardial infarction (MI) are not entirely clear. The present study tests the hypothesis that augmented sympathetic nerve regeneration (nerve sprouting) increases the probability of ventricular tachycardia (VT), ventricular fibrillation (VF), and SCD in chronic MI. In dogs with MI and complete atrioventricular (AV) block, we induced cardiac sympathetic nerve sprouting by infusing nerve growth factor (NGF) to the left stellate ganglion (experimental group, n=9). Another 6 dogs with MI and complete AV block but without NGF infusion served as controls (n=6). Immunocytochemical staining revealed a greater magnitude of sympathetic nerve sprouting in the experimental group than in the control group. After MI, all dogs showed spontaneous VT that persisted for 5.8+/-2.0 days (phase 1 VT). Spontaneous VT reappeared 13.1+/-6.0 days after surgery (phase 2 VT). The frequency of phase 2 VT was 10-fold higher in the experimental group (2.0+/-2.0/d) than in the control group (0.2+/-0.2/d, P<0.05). Four dogs in the experimental group but none in the control group died suddenly of spontaneous VF. We conclude that MI results in sympathetic nerve sprouting. NGF infusion to the left stellate ganglion in dogs with chronic MI and AV block augments sympathetic nerve sprouting and creates a high-yield model of spontaneous VT, VF, and SCD. The magnitude of sympathetic nerve sprouting may be an important determinant of SCD in chronic MI.

Signs of sympathetic denervation associated with a thoracic melanoma in a horse.

Sympathetic denervation in a 20-year-old, gray, Thoroughbred-Percheron gelding was manifested by cutaneous hyperthermia and sweating over the right side of the body, demarcated by a line from the withers to the elbow and extending cranially. There was cutaneous hyperthermia over the right side of the head, but other signs of Horner's syndrome (sweating, ptosis, miosis, enophthalmos) were not present. The pattern of cutaneous hyperthermia and sweating was consistent with sympathetic denervation localized to the cervicothoracic ganglion, and thoracic radiographs revealed increased density in the craniodorsal thorax. Cytologic evaluation of a sample of pleural effusion revealed mesothelial cells containing melanin and cells suggestive of melanocytes or melanoblasts. Treatment with oral cimetidine and intrapleural cisplatin was not successful. A necropsy was not performed, but the clinical findings supported a diagnosis of thoracic melanoma involving the cervicothoracic ganglion.

[Changes in the adrenergic structures of the human stellate ganglia in pathological states]. / Izmeneniia adrenergicheskikh struktur zvezdchatykh gangliev cheloveka pri nekotorykh patologicheskikh sostoianiiakh.

Stellate ganglia from patients who had succumbed to various diseases were examined by a fluorescent histochemical technique using 2% glyoxylic acid. Catecholamines were detectable in the major neurons, in small intensely fluorescent cells, and in adrenergic fibers with varicosities at levels that varied with the patient's age, cause of death, duration of the agonal period, the treatment administered, and the time when the material had been taken after death. All adrenergic structures of the ganglia were clearly demonstrable after early autopsies of those who had died suddenly from pulmonary artery thromboembolism in the absence of other abnormalities. The ganglia were found to be greatly depleted of catecholamines in cases of sudden cardiac death in the presence of ischemic heart disease before the development of myocardial infarction as well as in those of rapid death from stroke.