Surgical Isolation of Stellate Ganglia and Electrophysiology v1

The purpose of the present study was to determine whether thoracic veins may act as ectopic pacemakers and whether nodelike cells and rich sympathetic innervation are present at the ectopic sites. We used a 1,792-electrode mapping system with 1-mm resolution to map ectopic atrial arrhythmias in eight normal dogs during in vivo right and left stellate ganglia (SG) stimulation before and after sinus node crushing. SG stimulation triggered significant elevations of transcardiac norepinephrine levels, sinus tachycardia in all dogs, and atrial tachycardia in two of eight dogs. Sinus node crushing resulted in a slow junctional rhythm (51 ± 6 beats/min). Subsequent SG stimulation induced 20 episodes of ectopic beats in seven dogs and seven episodes of pulmonary vein tachycardia in three dogs (cycle length 273 ± 35 ms, duration 16 ± 4 s). The ectopic beats arose from the pulmonary vein ( n = 11), right atrium ( n = 5), left atrium ( n = 2), and the vein of Marshall ( n = 2). There was no difference in arrhythmogenic effects of left vs. right SG stimulation (13/29 vs. 16/29 episodes, P = nonsignificant). There was a greater density of periodic acid Schiff-positive cells ( P < 0.05) and sympathetic nerves ( P < 0.05) at the ectopic sites compared with other nonectopic atrial sites. We conclude that, in the absence of a sinus node, thoracic veins may function as subsidiary pacemakers under heightened sympathetic tone, becoming the dominant sites of initiation of focal atrial arrhythmias that arise from sites with abundant sympathetic nerves and periodic acid Schiff-positive cells.

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Macrophage Activation in Stellate Ganglia Contributes to Lung Injury‐Induced Arrhythmogenesis in Male Rats

Acta Physiologica ◽

10.1111/apha.13657 ◽

2021 ◽

Author(s):

Juan Hong ◽

Ryan J. Adam ◽

Lie Gao ◽

Taija Hahka ◽

Zhiqiu Xia ◽

...

Keyword(s):

Lung Injury ◽

Macrophage Activation ◽

Male Rats ◽

Stellate Ganglia

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To the Editor—Sympathetic innervation of the anterior left ventricular wall by the right and left stellate ganglia

Heart Rhythm ◽

10.1016/j.hrthm.2012.08.048 ◽

2012 ◽

Vol 9 (11) ◽

pp. e21

Author(s):

James Winter ◽

Kieran E. Brack ◽

John H. Coote ◽

G. André Ng

Keyword(s):

Sympathetic Innervation ◽

Left Ventricular ◽

Left Ventricular Wall ◽

Ventricular Wall ◽

Stellate Ganglia ◽

The Right

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Abstract 1372: Characterization Of The Rejuvenation Of Cardiac Sympathetic Nerves In Cardiac Hypertrophy

Circulation ◽

10.1161/circ.116.suppl_16.ii_281-d ◽

2007 ◽

Vol 116 (suppl_16) ◽

Author(s):

Kensuke Kimura ◽

Masaki Ieda ◽

Hideaki Kanazawa ◽

Takahide Arai ◽

Takashi Kawakami ◽

...

Keyword(s):

Cardiac Hypertrophy ◽

Fluorescent Protein ◽

Sympathetic Neurons ◽

Weight Ratio ◽

Sympathetic Nerves ◽

Marker Genes ◽

List Type ◽

Stellate Ganglia ◽

Immature Neuron

Background : Cardiac hypertrophy induces the fetal isoform of genes (rejuvenation), including contractile proteins, ion channels, and natriuretic peptides. Cardiac sympathetic nerve function is known to be altered in cardiac hypertrophy and congestive heart failure. We recently reported that alteration of cardiac sympathetic nerves (CSN) was caused by their rejuvenation (Circ Res, 2007). The present study was designed to examine the precise characterization of the rejuvenation of CSN in cardiac hypertrophy. Methods and Results : RV hypertrophy was produced by consistent hypoxia (10% O 2 ) in C57/BL6 mice. RV pressure increased to 47 mmHg, and RV/(body weight) ratio increased by 1.6 fold. Nerve growth factor protein was augmented in hypertrophic RV, but was unchanged in LV. Double-transgenic mice, which specifically express eGFP (enhanced green fluorescent protein) in the sympathetic neurons, was generated by crossing dopamine β-hydroxylase (DBH)-Cre mice with Floxed-eGFP mice. The eGFP-positive CSN were markedly increased in hypertrophic RV, but not in LV. Nerve density, quantitated by immunostained area with eGFP and GAP43 (growth-associated corn marker), increased by 8.1 and 9.3 fold, respectively, in RV, but not in LV. (4) Catecholamine content was attenuated in RV. (5) Western blot revealed that tyrosine hydroxylase was markedly down-regulated in RV. (6) Immunostaining clearly demonstrated that the immature neuron markers, PSA-NCAM (highly polysialylated neural cell adhesion molecule) and Ulip-1 (Unc-33-like phosphoprotein 1), were expressed in CSN in hypertrophic RV and stellate ganglia. Basic helix-loop-helix transcription factor, Mash-1 (mammalian achaete-scute complex homolog 1) was strongly expressed in the stellate ganglia. (7) Immature neuron marker-immunopositive cells in stellate ganglia had a markedly decreased TH expression. Conclusion : The rejuvenated CSN showed various immature and fetal neuron marker genes at not only the peripheral axons but also the cellular bodies at the stellate ganglia. Rejuvenation of CSN might be critically involved in the alteration of sympathetic neuronal function in cardiac hypertrophy, including depressed norepinephrine synthesis and hyperinnervation.

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Synaptic transmission in the chronically decentralized middle cervical and stellate ganglia of the dog

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y83-171 ◽

1983 ◽

Vol 61 (10) ◽

pp. 1149-1155 ◽

Cited By ~ 15

Author(s):

J. A. Armour

Keyword(s):

Central Nervous System ◽

Action Potentials ◽

Autonomic Nerves ◽

Autonomic Ganglia ◽

Afferent Nerves ◽

Stellate Ganglia ◽

Compound Action Potentials ◽

The Central Nervous System ◽

Compound Action ◽

Stimulation Of

Afferent stimulation of one thoracic cardiopulmonary nerve generated compound action potentials in the efferent axons of other ipsilateral cardiopulmonary nerves in dogs, 14 days after their thoracic autonomic ganglia had been decentralized. The compound action potentials were influenced by the frequency of activation and (in 5 of 12 dogs) by pharmacological autonomic blocking agents (hexamethonium, atropine, phentolamine, and propranolol). Moreover, they were abolished transiently when chymotrypsin was injected locally into the ganglia, and extendedly when manganese was injected. Thus, synapses that can be activated by stimulation of afferent nerves exist in chronically decentralized thoracic autonomic nerves and ganglia. It is proposed that regulation of the heart and lungs occurs in part via thoracic autonomic neural elements independent of the central nervous system.

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Depressor responses to stimulation of sympathetic afferents in monkeys and dogs

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1981.240.1.r23 ◽

1981 ◽

Vol 240 (1) ◽

pp. R23-R28 ◽

Cited By ~ 2

Author(s):

D. R. Kostreva ◽

F. A. Hopp ◽

J. P. Kampine

Keyword(s):

Fiber Type ◽

Depressor Response ◽

Stellate Ganglia ◽

Afferent Fibers ◽

Pressor Responses ◽

Conduction Velocities ◽

C Fiber ◽

Cervical Vagotomy ◽

Left And Right ◽

Stimulation Of

In dogs and monkeys anesthetized with pentobarbital sodium, stimulation of the cut central ends of the stellate cardiac nerve, the left and right anterior ansae subclavia, and the stellate ganglia resulted in a depressor response when stimulating fibers with conduction velocities in the range of 2.5-10 m/s. These afferents are in the A delta-fiber-type range. Pressor responses could be elicited by stimulating afferent fibers with conduction velocities in the range of 0.5-3.0 m/s. These fibers are in the C-fiber-type range. Stimulation of the abdominal sympathetic afferents always resulted in a depressor response regardless of the conduction velocities of the fibers. No changes in heart rate were observed. Bilateral cervical vagotomy did not alter the pressor or depressor responses.

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Responses of neurons in rostral ventrolateral medulla to activation of cardiac receptors in rats

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.2000.279.5.h2549 ◽

2000 ◽

Vol 279 (5) ◽

pp. H2549-H2557 ◽

Cited By ~ 21

Author(s):

De-Pei Li ◽

Hui-Lin Pan

Keyword(s):

Rostral Ventrolateral Medulla ◽

Ventrolateral Medulla ◽

Single Unit Activity ◽

Afferent Pathways ◽

Sympathetic Control ◽

Stellate Ganglia ◽

Cervical Vagotomy ◽

The Mean ◽

Cardiac Receptors ◽

Stimulation Of

Ischemic stimulation of cardiac receptors reflexly excites the cardiovascular system. However, the supraspinal mechanisms involved in this reflex are not well defined. This study examined the responses of barosensitive neurons in the rostral ventrolateral medulla (RVLM) to stimulation of cardiac receptors and the afferent pathways involved in these responses. Single-unit activity of RVLM neurons was recorded in α-chloralose-anesthetized rats. Cardiac receptors were stimulated by epicardial application of 10 μg/ml of bradykinin (BK). Barosensitive neurons were silenced by stimulation of baroreceptors. Application of BK increased the mean arterial pressure from 65.2 ± 1.9 to 89.3 ± 2.9 mmHg and excited RVLM barosensitive neurons from 6.2 ± 0.7 to 10.7 ± 0.9 impulses/s ( P < 0.05, n = 40). BK had no effect on 21 nonbarosensitive neurons. Blockade of stellate ganglia abolished the response of barosensitive neurons to BK. Cervical vagotomy significantly increased the baseline discharges of RVLM barosensitive neurons but had no effect on their responses to BK. Thus this study indicates that stimulation of cardiac receptors selectively activates RVLM barosensitive neurons through sympathetic afferent pathways. This information suggests that the RVLM barosensitive neurons are likely involved in the sympathetic control of circulation during myocardial ischemia.

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