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[Sympathetic postganglionic innervation of external carotid artery, internal carotid artery, common carotid artery and aorta in the dog--experimental study using HRP and WGA-HRP].

The sympathetic postganglionic innervation of the external carotid artery, internal carotid artery, common carotid artery (CCA) and aorta was studied by using retrograde axonal transport of the horseradish peroxidase (HRP) and wheat germ agglutinin-HRP conjugates (WGA-HRP). When the powder of HRP was applied to the sheaths of internal and external carotid arteries, labeled cells were found only in the ipsilateral superior cervical ganglion (SCG). After injection of WGA-HRP into the walls of the (1) distal, (2) middle, and (3) proximal parts of the CCA, labeled cells were observed in the following ganglia, respectively; (1) the SCG and middle cervical ganglion (MCG), (2) the SCG, MCG and stellate ganglion (SG), and (3) the MCG and SG. These labeled cells were seen in these ganglia of both sides, but they were more marked ipsilaterally. Following injections of WGA-HRP into the walls of ascending and descending aortae, labeled cells were found in the bilateral MCG and SG. These results suggest that the vasodilation of the head and neck after stellate ganglion block using local anesthetic agents is caused by neuronal block of preganglionic sympathetic fibers passing through the stellate ganglion and terminating in the superior cervical ganglion.

Animals↗

Identification of cardiovascular pathways in the sympathetic nervous system.

1. Sympathetic autonomic neurons show distinct patterns of expression of a range of neurochemicals that can be detected immunohistochemically. Often, functionally homologous neurons in the autonomic nervous system express identical combinations of substances that serve as a chemical code that allows them to be identified among other autonomic neurons. 2. In the rat stellate ganglion, where many neurons express either immunoreactivity (IR) to neuropeptide Y (NPY) or the calcium-binding protein calbindin, a population of large post-ganglionic neurons found along the medical border of the stellate ganglion, around the origin of the cardiac nerves, expressed intense IR to both substances at all ages examined, from early postnatal to adult. 3. In the heart, in the first few postnatal weeks, many nerve terminals were IR for both NPY and calbindin, but, with increasing age, calbindin-IR was progressively lost from NPY-IR terminals. Nerve terminals IR for both calbindin and NPY were not seen around pulmonary blood vessels or in the trachea or the thymus. 4. Nerve terminals IR for calretinin, another calcium-binding protein, were present in dense pericellular baskets around neurons in the stellate IR for both calbindin and NPY. The terminals also contained nitric oxide synthase (NOS)-IR. 5. It is suggested that the calbindin- and NPY-IR neurons in the stellate ganglion are the post-ganglionic neurons that innervate the heart and that the nerve terminal containing calretinin and NOS-IR that surround them are the cardiac preganglionic terminals. It thus appears possible, in the rat, to identify the sympathetic cardiac pathway arising in the spinal cord and controlling the heart purely on the basis of chemical coding.

Animals↗

Effect of sympathetic nerve stimulation on cerebral and cephalic blood flow in dogs.

The effect of sympathetic stimulation (stellate ganglion) on dog cerebral and cephalic blood flows was studied via a cervical or a thoracic approach to the stellate ganglion under sodium pentobarbital or chloralose anesthesia. Two different stimulation voltages (3v and 5v) of monophasic pulses were applied for 1 minute. Venous outflow was measured at the confluence of the sagittal, straight and lateral sinuses with the lateral sinuses occluded and with them patent. When the lateral sinuses were occluded, stellate ganglion stimulation resulted in a marked decrease in common carotid blood flow to 38 plus or minus 2.5% (SE) of control and dilation of the ipsilateral pupil, but cerebral blood flow did not change. Similar effects were observed with each of the anatomic approaches, anesthetics, and voltages used and in dogs with low cerebral vascular tone induced by hypercapnia. When the lateral sinuses were kept patent, sympathetic nerve stimulation decreased the venous outflow to 89 plus or minus 2.9% of control and clamping both of the external jugular veins increased venous outflow to 120 plus or minus 2.7% of control. When the lateral sinuses were kept patent and the extracranial venous pressure was increased by clamping both of the external jugular veins, the decrease in venous outflow in response to sympathetic stimulation was even larger: venous outflow was only 65 plus or minus 4.9% of control. We conclude that stimulation of the stellate ganglion has no effect on the cerebral vasculature. Sympathetic stimulation significantly decreases venous blood flow measured at the confluence of the sinuses only when communications between the intracranial and extracranial venous vasculatures are present.

Animals↗

Distribution of preganglionic terminals in the cervical sympathetic ganglia detected by the expression of c-Fos like protein after electric stimulation of the ventral root.

To determine the segmental relationship between the upper thoracic spinal cord and cervical sympathetic ganglia, we observed the distribution pattern of postganglionic cells which expressed c-Fos like protein, one of the products of immediate early genes, after electrical stimulation of ventral roots at the T1-T3 spinal segments. We recognized a clear segmental arrangement of postganglionic cells in the stellate ganglion along its rostrocaudal direction corresponding to the segmental arrangement of preganglionic neurons in the spinal cord. That is, postganglionic neurons which expressed c-Fos like protein after stimulation of the T1 ventral root were distributed in the middle region of the stellate ganglion in the rostrocaudal direction. The c-Fos like protein-positive neurons after stimulation of the T2 ventral root were distributed in a more caudal region of the stellate ganglion than after T1 ventral root stimulation. C-Fos like protein-positive neurons after stimulation of the T3 ventral root were mainly situated in a more caudal region of the stellate ganglion than after T2 ventral root stimulation. There was, however, no segmental relationship between the upper thoracic levels of the spinal cord and superior cervical ganglion in the rostrocaudal direction. These results indicate that the segmental innervation of the upper thoracic spinal cord exists in the stellate ganglion, but not in the superior cervical ganglion.

Animals↗

Autonomous nervous system with respect to dressing of cattle carcasses and its probable role in transfer of PrP(res) molecules.

Pathogen prions are widely recognized as the causative agent in bovine spongiform encephalopathy (BSE) and other transmissible spongiform encephalopathies. However, more research on the possible transmission mutes of this agent once it has reached the host is needed. There is evidence based on the anatomy and physiology of the autonomous nervous system (ANS), as well as observations for different animal species, that the ANS might be involved in the axonal drainage of pathogen prions toward the central nervous system. In this context, more attention should be paid to the cranial cervical ganglion, the stellate ganglion, the chain of paravertebral ganglia next to the first six thoracic vertebrae, the chain of the paravertebral ganglia next to loin vertebrae 1 through 6, the vagus nerve in the neck region and in the mediastine, and the esophagus (because of its close connection to the vagus nerve). For a more detailed risk analysis with respect to these tissues, the ANSs of animals having shown clinical signs of BSE might be examined to corroborate the evidence presented here. In the meantime, as a precautionary measure, the tissue addressed should be taken out of the human food chain, taken out of animal feed, and handled as if it were specified risk material. It is technically possible to remove these parts during cutting and dressing.

Animals↗

[Origin and the functional role of adrenergic fibers of the vagus nerve in cats].

Origin of adrenergic fibres of vagus is studied. They are shown to appear in the thoracic vagus through caudal anastomosis introduction. The observations indicated that axons of spinal neurons and neurons of the ganglion stellate passed through caudal anastomosis and entered a thoracic vagus nerve. Stimulation of the thoracic vagus in cats after atropine sulphate injection increases the heart rate.

Adrenergic Fibers↗

Monoaminergic pathways to the coronary arteries and to the myocardium.

The monoaminergic innervation of the coronary vessels and of the myocardium in dogs was examined by means of degenerative techniques: (i) local perivascular neurotomy was performed at the origin of the left coronary artery; (ii) the stellate ganglion was removed bilaterally. Evaluation of the neural degeneration pattern led the suggestion that three types of neurons at least exist within the heart: (i) neurons innervating the coronary vessels both in the ventricles and in the atria; (ii) neurons innervating the ventricular myocardium, and (iii) neurons innervating the atrial myocardium. The post-ganglionic fibres of the stellate ganglion innervate the vessels of the whole heart. Their contribution to the innervation of the ventricular myocardium represents about 30%.

Animals↗

Effects of unilateral cardiac sympathetic denervation on the ventricular fibrillation threshold.

A train of gated stimuli scanning the entire vulnerable period was delivered to the right anterior or left posterior ventricular surface to study the ventricular fibrillation threshold in anesthetized and vagotomized dogs. Heart rate was held constant by atrial pacing. Measurements were obtained in control conditions and after surgical removal of one stellate ganglion. To avoid the shortcomings associated with an irreversible procedure like stellectomy, control fibrillation threshold measurements were also alternated with determinations during reversible blockade by cooling of one stellate ganglion. The results were similar with both techniques. In nine animals, ablation or cooling of the left stellate ganglion increased ventricular fibrillation threshold by 72 +/- 35 (mean +/- standard deviation) percent compared with control values (P less than 0.001). By contrast, in 11 animals, ablation or cooling of the right stellate ganglion lowered the threshold by 48 +/- 14 percent compared with control values (P less than 0.001). Electrode location did not influence the results. The observed changes depended solely upon unilateral removal of cardiac sympathetic activity and were not demonstrable if such activity was low. These results suggest that right and left cardiac sympathetic nerves may have different and specific effects on cardiac excitability. They also contribute to the understanding of the pathogenesis of the long Q-T syndrome (characterized by episodes of ventricular fibrillation associated with increased sympathetic activity) and increase the rationale for left stellectomy as the specific treatment for this illness. Left stellectomy, by raising the ventricular fibrillation threshold, may also represent an alternative measure in patients at high risk of sudden death from ventricular arrhythmias resistant to medical therapy.

Animals↗

Tissue distribution and subcellular localization of Na+ channel mRNA in the nervous system of the squid, Loligo opalescens.

Recent cloning of a putative Na+ channel alpha subunit cDNA, GFLN1, from the squid stellate ganglion has allowed us to study the expression of this ion channel at a cellular level. In situ hybridizations with a probe derived from and specific to 3' untranslated and coding sequence of GFLN1 were used to determine its tissue distribution as well as its subcellular localization. In sections of the stellate ganglion, the probe labeled all of the cells in the giant fiber lobe (GFL) and most cells in the cellular layer of the main ganglion. In these non-GFL portions of the stellate ganglion, labeling was particularly intense in the ventral large cells and weak or absent in the dorsal small cells. In the optic lobe, only a select group of cells, the second-order visual giant neurons, were intensely labeled. These results are consistent with electrophysiological data that show GFL-like Na+ currents in rare large cells dissociated from the optic lobe and in most but not all cells from the non-GFL part of the stellate ganglion. In sections of the subesophageal mass of the central nervous system, strong labeling for GFLN1 mRNA occurred in the fin lobe, posterior chromatophore lobe, central and latero-ventral palliovisceral lobes, and posterior pedal lobe. In all cases, labeling was detected only in the cellular layer of these tissues and never in nerves or neuropil. In situ hybridization with dissociated GFL neurons maintained in primary culture verified that Na+ channel mRNA is confined to the cell body. These results indicate that GFLN1 is expressed predominately in large cells with large or long axons, and that this mRNA is restricted to the cell bodies of these neurons.

Animals↗

Nitric oxide modulates signaling between cultured adult peripheral cardiac neurons and cardiomyocytes.

To determine whether nitric oxide (NO) modifies cardiomyocytes directly or indirectly via peripheral autonomic neurons, the effects of NO were studied in long-term (3-6 wk) cultures of adult guinea pig ventricular myocytes alone as well as in cocultures with adult extracardiac (stellate ganglion) or intrinsic cardiac neurons. NADPH diaphorase was associated histochemically with cultured intrinsic cardiac and, to a lesser extent, stellate ganglion neurons. The beating frequency of ventricular myocytes cocultured with intrinsic cardiac neurons (M-intrinsic) or stellate ganglion neurons (M-stellate) increased by 20-30% (P < 0.001) after administration of the NO donor S-nitroso-N-acetylpenicillamine (SNAP); this effect was abolished by the guanylate cyclase inhibitor LY-83583. The beating frequency of noninnervated myocyte cultures was not affected by SNAP. The precursor of NO, L-arginine, also increased the beating rate (approximately 20%; P < 0.05) of M-intrinsic cocultures, not affecting that of M-stellate cocultures or noninnervated myocyte cultures. Augmentor effects induced by SNAP were no longer elicited in the presence of tetrodotoxin and were unaffected by beta-adrenergic or muscarinic receptor blockade. It is concluded that 1) NO-sensitive neurons are present in stellate and intrinsic cardiac ganglia, and these neurons increase the beating rate of cardiomyocytes in the presence of NO; 2) more NO-synthesizing neurons are present in M-intrinsic than M-stellate cocultures, since L-arginine increased the beating frequency of myocytes significantly only in M-intrinsic cocultures; and 3) the beating rate of noninnervated myocyte cultures is not directly affected by NO.

Animals↗

[The effects cervicothoracic sympathetic blockade on left ventricular function].

OBJECTIVE: Cervicothoracic sympathetic blocks (stellate ganglion blocks) not only influence pain, but also lead to regional sympathetic denervation of part of the left ventricular wall, while other ventricular regions stay under the control of the unblocked side. What is the influence of these imbalances of sympathetic innervation on ventricular function? METHODS: Thirteen anaesthetised dogs were instrumented for measurement of left ventricular pressure (tip-manometer), cardiac output (ultrasonic flow probe) and regional myocardial function (sonomicrometry) in two left ventricular regions, innervated by the left or right sympathetic system, respectively. Electrical stimulations of the left and right stellate ganglia, and left and right sided stellate ganglion blocks were performed. In eight patients with no cardiac disease, the effects of left stellate ganglion blocks on echocardiographic variables of ventricular function were investigated. RESULTS: In dogs, the unilateral ganglion stimulations led to an increase in regional and global contractility. However, left ventricular wall motion became asynchronous and, despite an increase in contractility, relaxation was impaired. After the ganglion blocks, there was a decrease in regional contractility within the denervated area, also leading to an asynchronous wall motion. As a consequence, relaxation was impaired, but cardiac output was maintained. In the patients, there was an increase in isovolumic relaxation time. This change was also within the compensatory range and cardiac output increased slightly as a consequence of a simultaneous afterload reduction by the ganglion block. CONCLUSION: The studies show a disturbance of diastolic function after stellate ganglion blocks, resulting from an asynchronous wall motion pattern after the regional denervation. However, the changes were within the compensatory range of a healthy ventricle and cardiac output was not reduced.

Anesthesia, Spinal↗

Reflex sympathetic dystrophy.

Early diagnosis of RSD is essential. A keen clinical awareness of this problem is required by all hand surgeons. RSD is a clinical diagnosis that may be supplemented by digital temperature, three-phase bone scan, and digital radiographs of the hand. A thorough examination is necessary to identify untreated or inadequately treated sources of RSD. Once diagnosed, prompt treatment of RSD is beneficial. Patients are referred to our anesthesia department for diagnostic and therapeutic stellate ganglion blocks. A trial of 2 to 3 blocks is attempted initially. After successful block is performed, as measured by a Horner's sign and extremity temperature, the patient is brought to the hand clinic where active range-of-motion exercises are started. A stress loading program is an important and essential part of our treatment protocol. Sympathetic blocks are performed on a biweekly basis until the pain is relieved. Consideration is given to long-acting stellate ganglion blocks with a continuous catheter infusion for patients who show a limited, but short-lived response to stellate ganglion blocks. For RSD that does not respond to the stellate ganglion block, we generally perform a bretylium intravenous regional block. Patients with RSD are referred to our hand psychologist for counseling, psychotherapy, relaxation therapy, and possibly biofeedback. We use a multitherapy approach with all available modalities to achieve the best success in breaking the cycle of pain and returning the patient to normal, productive function.

Autonomic Nerve Block↗

Surgery on the affected upper extremity of patients with a history of complex regional pain syndrome: a retrospective study of 100 patients.

Surgery on the extremity affected with complex regional pain syndrome (CRPS) is generally avoided because of the risk that the symptoms will recur or worsen. Perioperative sympathectomy or stellate ganglion block has previously been recommended for CRPS patients requiring surgery of the affected upper extremity. We evaluated 100 patients with a history of upper extremity CRPS undergoing surgery on the affected extremity. All signs and symptoms of CRPS had resolved before surgery. After completion of the surgical procedure half of the patients (n = 50) underwent a stellate ganglion block; the other half received no intervention. The recurrence rate of CRPS was significantly lower in those patients receiving a postoperative stellate ganglion block (n = 5; 10%) compared with those receiving no intervention (n = 36; 72%). We conclude that performing a perioperative stellate ganglion block in patients with a history of CRPS can significantly reduce the recurrence rate of this disease process.

Anesthetics, Local↗

Organization of the sympathetic postganglionic innervation of the rat heart.

The origins and organization of cardiac sympathetic postganglionic nerves in the rat were identified in the present investigation. The retrograde tracer, Diamidino Yellow, was injected into the right or left ventricles to label somata in the sympathetic chain. Analysis of all sympathetic ganglia from superior cervical ganglion through the 10th thoracic ganglion indicated that the postganglionic innervation of the rat cardiac ventricles originates bilaterally. The majority of these somata were located in the middle and inferior cervical ganglia (middle cervical-stellate ganglion complex) (approximately 92% of all labelled cells), with lesser contributions from the superior cervical and 4th through 6th thoracic ganglia. To confirm and further quantitate these findings, the middle cervical-stellate ganglion complex was removed (MC-S ganglionectomy) bilaterally or ipsilaterally from the left or right sides, and regional cardiac norepinephrine concentration (left and right atrial appendages and left and right ventricles) was analysed 7 or 28 days later. At both times after bilateral MC-S ganglionectomy, regional cardiac norepinephrine was reduced by 89% to 100%, indicating the removal of almost all cardiac noradrenergic cells of origin and possibly fibers of passage. The results of unilateral MC-S ganglionectomy experiments indicated that the atrial appendages and the left ventricle receive bilateral innervation from the middle cervical-stellate ganglion complex. However, the left middle cervical-stellate ganglion complex appears to contribute a majority of the norepinephrine to the right ventricle. Furthermore, between 7 and 28 days after contralateral MC-S ganglionectomy, atrial appendages, but not ventricles, display significant recovery of norepinephrine content. The present data demonstrate: (1) a bilateral locus of origin of cardiac sympathetic postganglionic neurons, limited longitudinally to cervical through mid-thoracic ganglia, and (2) the ability of the cardiac postganglionic innervation to regenerate after partial denervation. These results demonstrate anatomical evidence for significant bilateral integration of cardiac sympathetic activity at the level of the sympathetic ganglion in the rat.

Amidines↗

Regional sympathetic blockade in primary fibromyalgia.

Twenty-eight patients with primary fibromyalgia participated in the study. Eight patients received a stellate ganglion blockade with bupivacaine, and 14 days later an intravenous regional sympathetic blockade with guanethidine. The remaining patients served as controls and were randomly allocated to receive either a sham (placebo) injection with physiologic saline superficial to the stellate ganglion (n = 10) or bupivacaine intramuscularly (n = 10). The efficiency of the stellate ganglion blockade was evaluated by measuring skin blood flow (using a laser Doppler flowmeter), skin temperature, and skin conductance responses ('sympathogalvanic reflex'). Trigger and tender points (TePs) were counted, and rest pain in the arm, shoulder and neck evaluated at intervals up to 4 h after the injection. The guanethidine blockade was evaluated 24 h after the injection by counting TePs and by assessment of rest pain in the hand and forearm. The results indicate that a complete sympathetic blockade, produced by a stellate ganglion blockade, markedly reduced the number of TePs and produced a marked decrease in rest pain. The guanethidine blockade reduced the number of TePs, but had no effect on rest pain. The reduction in pain and TePs produced by a sympathetic blockade may be due to an improvement in microcirculation. Sympathetic activity may, in some patients, contribute to the pathogenesis of primary fibromyalgia.

Adult↗

Differential effects of reserpine and 6-hydroxydopamine on neuropeptide Y (NPY) and noradrenaline in peripheral neurons.

The effects of 6-hydroxydopamine (6-OHDA) and reserpine pretreatment on peripheral neuropeptide Y (NPY)- and noradrenaline (NA)-containing neurons were studied in guinea-pigs. Ten days after 6-OHDA pretreatment, a 60-80% reduction of the NA content was observed in the right atrium of the heart, stellate ganglion and spleen. The content of NPY-like immunoreactivity (LI) was reduced by about 50% in the heart, not changed in the spleen while it increased to 200% of control in the stellate ganglion. Immunohistochemistry showed a pronounced loss of NPY- and tyrosinehydroxylase (TH)-immunoreactive (IR) nerves in the heart but not in the spleen. Increased NPY-IR was seen in axons and cell bodies of the stellate ganglion. Reserpine pretreatment (thereshold dose 0.5 mg X kg-1) caused a dose- and time-dependent reduction of the content of NPY-LI in the heart. A maximal depletion of NPY-LI (about 80%) was observed 5 days after reserpine. Reserpine pretreatment also reduced the content of NPY-LI in the spleen, while no significant change was observed in the adrenal gland or vas deferens. The levels of NPY-LI increased in the stellate ganglion to about 180% of control 5 days after reserpine. Immunohistochemical analysis revealed an almost total loss of NPY-IR nerve fibres in the heart as well as around blood vessels in the lung and skeletal muscle. No detectable changes were observed in perivascular NPY-IR nerves in the spleen, vas deferens or kidney. TH-IR nerves remained unchanged after reserpine, thus indicating that the observed loss of NPY-IR nerves was due to a depletion of NPY and not a degeneration. No change in the levels of substance P-LI was observed in the right atrium 5 days after reserpine. NA was, in contrast to NPY, markedly depleted in all tissues investigated after reserpine treatment. The depletion of NA was more extensive, and occurred more rapidly and at much lower doses as compared to the effects on NPY-LI. Ligations of the sciatic nerve revealed that NPY-LI was transported axonally with a rapid rate (3 mm/h). Reserpine pretreatment significantly increased the amount of accumulated NPY-IR above the ligation, suggesting an increase in axonal transport. High performance liquid chromatography revealed that the NPY-LI consisted of two major peaks in the stellate ganglia, while only one peak closely corresponding to porcine NPY was seen in the right atrium. In conclusion, 6-OHDA pretreatment depletes NPY-LI in certain terminal regions and increases NPY-LI in ganglia.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

[Neural circuit of the cervical sympathetic nervous system with special reference to input and output of the cervical sympathetic ganglia: relationship between spinal cord and cervical sympathetic ganglia and that between cervical sympathetic ganglia and their target organs].

Using anterograde labeling technique with Phaseolus vulgaris leucoagglutinin (PHA-L), we demonstrated the arborization pattern of a single preganglionic axon in the superior cervical ganglion (SCG) and stellate ganglion (STG). These axons expanded in the longitudinal direction, but not for transverse direction. Segmental relationship was identified between the spinal cord and STG, as seen between spinal cord and sympathetic ganglia in the thoraco-lumbar region, but we did not find any segmental relationship between the spinal cord and SCG. Some sympathetic preganglionic neurons in the lateral horn of the thoracic cord, especially in the intermediolateral nucleus (IML) have nitric oxide synthase (NOS) activity. We demonstrated that SCG neurons, which were heavily innervated by these NOS-positive neurons, tended to innervate organs that have some secretory functional tissues. Finally, we showed that the size of neuronal somata does not correlate with the size of target organs, as has been reported in previous studies. We should consider that there are other factors determining the size of neuronal somata, such as the size of dendritic field or volumes of NGF secretory from target tissues.

Animals↗

Cardiac sympathetic afferent cell bodies are located in the peripheral nervous system of the cat.

Studies of the stellate ganglion and middle cervical ganglion indicate that sympathetic efferent nerve activity can be modified by peripheral excitatory inputs and that these neural connections may function as pathways for a peripheral reflex at the level of the thoracic sympathetic ganglia. This excitatory synaptic input could have a soma in either the central or the peripheral nervous system. A study was designed to determine whether chronic decentralization (3 weeks) of the stellate ganglion in cats would 1) abolish sympathetic cardiac afferent nerve activity recorded at the stellate cardiac nerve and 2) abolish local thoracic reflexes that are generated by stimulation of peripheral nerves. The ansae subclaviae, T3 and T4 rami, and stellate ganglion were also examined by electron microscopy for the extent of Wallerian degeneration. Afferent cardiac activation of the axon collaterals arising from cell bodies located in the dorsal root ganglia was abolished due to degeneration. However, sympathetic afferent nerve activity from the left ventricular receptors was still present and was recorded from the stellate cardiac nerve in all cats. Cardiac receptors were sensitive to mechanical distortion, increases in the left ventricular pressure, and epicardial application of veratrine hydrochloride. These data imply that 1) cardiovascular afferent input to the stellate ganglion persists following chronic decentralization and 2) the sensory neurons are located in the peripheral sympathetic nervous system. Thus, we find that regulation of the heart occurs in part via thoracic ganglia, independently of the central nervous system.

Afferent Pathways↗