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PubMed1987

Spinal segmental preganglionic outflow to cervical sympathetic trunk and postganglionic cardiac sympathetic nerves.

The aim of this study was to verify in which spinal cord segments the preganglionic neurones projecting to the cervical sympathetic trunk or converging onto the somata of the postganglionic cardiac sympathetic neurones are located in cats. The thoracic white rami T1 to T5 were electrically stimulated and the evoked responses were recorded in the cervical sympathetic trunks and postganglionic cardiac nerves. The responses were mostly evoked by electrical stimulation of group B preganglionic fibres. The maximum amplitude of evoked responses in the cervical sympathetic trunk was obtained when the T2 white ramus was stimulated and decreased gradually when followed by the stimulation of T1, T3, T4 and T5 white rami. In most cases the maximum amplitude of evoked responses in the left inferior cardiac nerve, right inferior cardiac nerve and left middle cardiac nerve was obtained when the T3 white ramus was stimulated. The size of the responses decreased when more cranial and caudal white rami were stimulated. It was found that the somata of the postganglionic neurones of the right and left inferior cardiac nerves were placed in the right and left stellate ganglion, respectively. Somata of the postganglionic neurones with axons in the left middle cardiac nerve were mainly located in the left middle cervical ganglion and some in the left stellate ganglion.

Action Potentials↗
PubMed1984

Pressure and flow in epicardial coronary veins of the dog heart: responses to positive inotropism.

Peripheral coronary venous pressures and coronary sinus venous flow were measured in the canine heart as well as intramyocardial, intraventricular, aortic, and coronary artery pressures. Maximum coronary venous flow occurred after maximum intramyocardial and peripheral coronary artery pressures had been reached. Maximum venous flow occurred at or following the maximum peripheral coronary vein pressure. Positive inotropic changes induced by stimulation of the right or left stellate ganglia or infusing isoproterenol, norepinephrine, or dobutamine significantly increased intramyocardial pressure, systolic epicardial coronary venous pressure, and systolic coronary venous flow. Mean coronary sinus flow was augmented by all interventions except isoproterenol. The estimated systolic vein resistance was slightly increased following right stellate ganglion stimulation, but not following left stellate ganglion stimulation, isoproterenol, or dobutamine. Norepinephrine reduced this parameter minimally. These data indicate that coronary veins respond differently to a variety of different positive inotropic interventions.

Animals↗
PubMed1999

The effects of combined sympathetic block and intravascular infusion of prostaglandin E1 on brachial arterial blood flow in dogs.

UNLABELLED: We compared the effects of stellate ganglion block (SGB) with those of SGB combined with an intravascular infusion of prostaglandin E1 (PGE1) on brachial arterial blood flow (BABF) in 24 mongrel dogs. The experimental protocol was designed so that the dogs received one of the following: SGB with 0.5% mepivacaine 1.0 mL (n = 8); combined SGB and IV infusion of PGE1 at a rate of 150 ng x kg(-1) x min(-1) for 10 min (n = 8); or combined SGB and intraarterial (IA) infusion of PGE1 at a rate of 0.1 ng x kg(-1) x min(-1) for 10 min (n = 8). BABF increased significantly in all groups and reached a maximum of 67% 10 min after SGB, 124% with the combined SGB and IV infusion of PGE1, and 117% with the combined SGB and IA infusion of PGE1. We conclude that combined SGB and IV or IA infusion of PGE1 increases BABF significantly compared with SGB alone. IMPLICATIONS: Combined stellate ganglion block and intraarterial or IV infusion of prostaglandin E1 increases brachial arterial blood flow significantly compared with stellate ganglion block alone.

Alprostadil↗
PubMed1994

Purinergic modulation of adult guinea pig cardiomyocytes in long term cultures and co-cultures with extracardiac or intrinsic cardiac neurones.

OBJECTIVE: To determine the capacity of ATP to modify cardiomyocytes directly or indirectly via peripheral autonomic neurones, the effects of various purinergic agents were studied on long term cultures of adult guinea pig ventricular myocytes and their co-cultures with extracardiac (stellate ganglion) or intrinsic cardiac neurones. METHODS: Ventricular myocytes and cardiac neurones were enzymatically dissociated and plated together or alone (myocytes only). Myocyte cultures were used for experiments after three to six weeks. The electrical and contractile properties of cultured myocytes and myocyte-neuronal networks were investigated. RESULTS: The spontaneous beating frequency of ventricular myocytes co-cultured with stellate ganglion neurones increased by approximately 140% (p < 0.001) following superfusion with 10(-5) M ATP. This effect was not modified significantly by tetrodotoxin or by beta adrenoceptor blockade (10(-5) M timolol), but was eliminated following application of the P2 antagonist suramin (10(-5) M). Basal spontaneous contractile rate was reduced by approximately 86% (p < 0.001) in the presence of suramin, indicating the existence of tonically active purinergic synaptic mechanisms in stellate ganglion neurone-myocyte cocultures. Suramin did not significantly affect non-innervated myocyte cultures. ATP increased myocyte contractile rate in intrinsic cardiac neurone-myocyte co-cultures by approximately 40% (p < 0.01) under control conditions, but when beta adrenergic receptors of tetrodotoxin sensitive neural responses were blocked, ATP induced greater augmentation (> 100%). In contrast, ATP induced much smaller effects in non-innervated myocyte cultures (approximately 26%, p < 0.01). Analogues of AT) showed the following order of potency: ATP > UTP > MSATP > beta gamma ATP > alpha beta ATP. Adenosine (10(-4) M) attenuated the beating frequency of myocytes in both types of co-culture, while not significantly affecting non-innervated myocyte cultures. CONCLUSIONS: The experimental model used in this study showed that extrinsic and intrinsic cardiac neurones which possess P2 receptors can greatly enhance cardiac myocyte contractile rate when activated by ATP. Since adenosine reduced contractile rate in both types of co-cultures while not affecting non-innervated myocytes, it is concluded that some of these neurones possess P1 receptors.

Action Potentials↗
PubMed1993

Effect of increases in myocardial epinephrine content on epinephrine release from the dog heart.

The effect of short-term (10 min) and prolonged (180 min) epinephrine (E) infusion (92.5 ng.kg-1.min-1) on E content of the myocardium and on the subsequent release of E from the heart during stimulation of the left stellate ganglion (4 and 10 Hz, 4 V, 2 ms, 1 min) was studied in anesthetized dogs. The E content in the free wall of the left ventricle significantly increased 1.7- and 4.2-fold following short-term and prolonged E infusion, respectively, compared with a control group infused with saline. Tissue norepinephrine (NE) content was not modified by E infusion. The plasma E concentration gradient across the heart indicated a significant release of E during electrical stimulation of the left stellate ganglion, which was related to the amount of E stored in the tissue (e.g., control, 126 +/- 60; 10-min infusion, 279 +/- 105; 180-min infusion, 1487 +/- 287 pg.mL-1; at 10 Hz). NE release from the heart also tended to increase with the amount of E stored in the myocardium and released upon electrical stimulation of the left stellate ganglion, although the difference did not reach statistical significance. These results provide further direct evidence that blood-borne E can be taken up and stored in sympathetic nerve endings and can be released as a cotransmitter with NE. Locally released E could favor NE release.

Anesthesia↗
PubMed1988

Systolic pressure gradients between the wall of the left ventricle, the left ventricular chamber, and the aorta during positive inotropic states: implications for left ventricular efficiency.

To study systolic pressure gradients developed between the left ventricular wall, its chamber, and the aortic root, in one group of dogs left ventricle ventral wall intramyocardial pressure, left ventricular outflow tract pressure, and aorta pressure were compared with aortic flow as well as left ventricular dimension changes during control conditions as well as during positive intropic states induced by isoproterenol, stellate ganglion stimulation, and noradrenaline. In another group of dogs systolic pressures in the ventral wall of the left ventricle, the main portion of the left ventricular chamber, and the aorta were compared with aortic flow during similar interventions, before and after the administration of phentolamine. Pressure gradients between the wall of the left ventricle and the outflow tract of the left ventricle were minimal during control states, but during the three positive inotropic states were increased significantly. In contrast, pressure gradients between the outflow tract of the left ventricle and the aortic root were insignificant during positive inotropic states; those between the wall and main portion of the chamber were only significantly different during left stellate ganglion stimulation. The data derived from these experiments indicate that useful peak power output of the left ventricle (systolic aortic pressure X flow) is unchanged following isoproterenol infusion, but is increased by stellate ganglion stimulation and noradrenaline. The useful peak power output index (an index of left ventricular efficiency derived by dividing useful peak power output by peak intramyocardial pressure) was reduced more by isoproterenol than the other two interventions.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2005

Differential beta-adrenoceptor expression induced by nerve growth factor infusion into the canine right and left stellate ganglia.

BACKGROUND: Nerve growth factor (NGF) infusion into the right stellate ganglion (RSG) is antiarrhythmic, while NGF infusion into the left stellate ganglion (LSG) is proarrhythmic in dogs with myocardial infarction (MI) and complete atrioventricular block (CAVB). This functional asymmetry suggests differential neural remodeling. OBJECTIVES: To test the hypothesis that NGF infusion into the RSG and the LSG can lead to differential beta-adrenoceptor (beta-AR) expression in dogs with MI and CAVB. METHODS AND RESULTS: We performed immunostaining to quantify beta(1)-AR and beta(3)-AR immunoreactivity in six dogs with MI and CAVB, nine dogs with MI, CAVB, and NGF infusion to the LSG, six dogs with MI, CAVB, and NGF infusion to the RSG, and six normal dogs. There was significantly increased beta(3)-AR immunoreactivity in dogs with NGF infusion into the LSG and significantly decreased beta(3)-AR immunoreactivity in dogs with NGF infusion into the RSG compared with controls and with the MI and CAVB group. There were no significant differences in beta(1)-AR immunoreactivity among these four groups. To determine protein and mRNA expression of beta-ARs, we created MI and CAVB and infused NGF into the LSG in six additional dogs. The noninfarcted left ventricle free wall was harvested 1 week later. The protein level and receptor density of beta(3)-AR (but not beta(1)- or beta(2)-AR) significantly increased in these six dogs compared with normal controls. CONCLUSIONS: We conclude that NGF infusion into the RSG and the LSG in dogs with MI and CAVB induced differential beta(3)-AR expression in the left ventricular myocardium.

Animals↗
PubMed1979

Adrenergaically mediated ventricular fibrillation in probucol-treated dogs: roles of alpha and beta adrenergic receptors.

A high incidence of sudden death due to ventricular fibrillation (VF) has been observed in dogs under chronic treatment with probucol, a new hypocholesterolemic agent. The present study describes the cardiac electrophysiologic properties of probucol-treated dogs and characterizes the electrophysiological response of these animals to manipulation of the autonomic nervous system. There was no significant difference in the spontaneous sinus cycle length, the QT interval, refractory period of the atrium, ventricle or A-V junction between normal and probucol-treated dogs. Epinephrine produced VF with few and sometimes no preceding premature ventricular extrasystoles. Electrical stimulation of the stellate ganglion induced VF in 16/19 dogs whereas stimulation of the right stellate ganglion induced VF in 1/19 dogs. Phenylephrine induced VF in 0/19 dogs, isoproterenol in 5/19 dogs, but phenylephrine + isoproterenol induced VF in 9/11 dogs in which isoproterenol did not produce VF. alpha (phentolamine) or beta (propranolol) blockade prevented initiation of VF by epinephrine, phenylephrine + is isoproterenol, and left stellate stimulation but alpha blockade did not prevent induction of VF by isoproterenol when isoproterenol alone produced VF. In this nonischemic model, we conclude that left stellate stimulation is a far more potent initiator of VF than right stellate stimulation and that induction of VF appears to require both alpha and beta adrenergic receptor stimulation.

Angiotensin II↗
PubMed1997

Target-independent cholinergic differentiation in the rat sympathetic nervous system.

Chemical coding in the sympathetic nervous system involves both noradrenergic and, for a minority of neurons, cholinergic neurotransmission. The expression of the cholinergic phenotype in the developing sympathetic nervous system was examined to determine if coding for cholinergic transmission occurs before or after innervation of peripheral target organs. The vesicular acetylcholine transporter (VAChT) and choline acetyltransferase, the products of the "cholinergic gene locus" determining the cholinergic phenotype, were expressed in principal cells of the paravertebral, but only rarely in prevertebral, sympathetic chains as early as embryonic day 14. A subpopulation of VAChT- and choline acetyltransferase-positive sympathetic ganglion cells persisted throughout development of the stellate and more caudal paravertebral ganglia into anatomically distinct cell groups, and into adulthood. The forepaw eccrine sweat glands, innervated exclusively by the stellate ganglion, received VAChT-positive nerve terminals at least as early as postembryonic day 4, coincident with the development of the sweat glands themselves. These terminals, like the VAChT-positive cell bodies of the developing stellate ganglion, have some noradrenergic traits including expression of tyrosine hydroxylase, but did not express the vesicular monoamine transporter, and are therefore not functionally noradrenergic. Development of the cholinergic phenotype in principal cells of the sympathetic paravertebral ganglia apparently occurs via receipt of instructive cues, or selection, within the sympathetic chain itself or perhaps even during migration of the cells of the neural crest from which the paravertebral ganglia arise.

Animals↗
PubMed1995

Pirenzepine-sensitive component of forelimb vascular resistance and heart rate in cats.

In vagotomized, midcollicular decerebrate, non-anesthetized cats, in which the preganglionic input to the stellate ganglion was intact and the right forelimb was autoperfused at constant flow, the muscarinic receptor antagonist pirenzepine (PZP, 50 micrograms/kg i.v.), which does not cross the blood-brain barrier, produced a decrease in forelimb perfusion pressure (FLPP), heart rate (HR) and systemic arterial pressure (SAP). Administration of the nicotinic receptor antagonist hexamethonium (30 mg/kg i.v.) after PZP produced a further, larger drop in FLPP, HR and SAP. The dose of PZP used blocked the increase in FLPP and HR evoked by the muscarinic receptor agonist McN-A-343, but not the increase evoked by the nicotinic receptor agonist DMPP, when these drugs were injected into the arterial supply of the ganglion. Following administration of phentolamine and propranolol (2 mg/kg i.v. of each) which caused bradycardia and forelimb vasodilation, PZP had no effect on FLPP and HR. This finding suggests that PZP decreases sympathetic tone in resistance vessels and in the heart. Pirenzepine did not depress the forelimb vasoconstriction and the cardioacceleration evoked by electrical stimulation of the postganglionic vertebral and inferior cardiac nerves, respectively, suggesting that PZP does not act at the neuro-effector junctions. On the other hand, PZP blocked the forelimb vasoconstriction and the cardioacceleration produced by stimulating the preganglionic input of the stellate ganglion in presence of hexamethonium (30 mg/kg i.v.), indicating the stellate ganglion as the likely site of action of the drug. These findings suggest that the ganglion cell firing that underlies the sympathetic tone of cardiovascular effector cells is generated, in part, by a muscarinic, PZP-sensitive, synaptic mechanism.

Animals↗
PubMed1996

Reduced capacity of cardiac efferent sympathetic neurons to release noradrenaline and modify cardiac function in tachycardia-induced canine heart failure.

To investigate the capacity of efferent sympathetic neurons to modulate the failing heart, stellate ganglion stimulation was performed in dogs with biventricular heart failure induced by rapid ventricular pacing (240 beats/min) for 4-6 weeks. Less noradrenaline was released from cardiac myoneural junctions into coronary sinus blood in response to left stellate ganglion stimulation in anesthetized failing heart preparations (582 pg/mL, lower and upper 95% confidence intervals of 288 and 1174 pg/mL, n = 19) compared with healthy heart preparations (6391 pg/mL, 95% confidence intervals of 4180 and 9770 pg/mL, n = 14; p < 0.001). There was substantial adrenaline extraction by failing hearts (49 +/- 6%), although it was slightly lower than in healthy heart preparations (65 +/- 9%, p = 0.055). In contrast with healthy heart preparations, no net release of adrenaline occurred during stellate ganglion stimulation in any of the failing heart preparations, and ventricular tissue levels of adrenaline fell below the sensitivity limit of the HPLC technique. In failing heart preparations, maximal electrical stimulation of right or left stellate ganglia resulted in minimal augmentation of left ventricular intramyocardial (17%) and chamber (12%) systolic pressures. These indices were augmented by 145 and 97%, respectively, following exogenous noradrenaline administration. Thus, the cardiac efferent sympathetic neurons' reduced capacity to release noradrenaline and modify cardiac function can contribute to reduction of sympathetic support to the failing heart.

Animals↗
PubMed2000

Norepinephrine concentrations in the epicardial transudate reflect early changes in adrenergic activity in the isolated perfused heart.

The aim of this study was to establish whether epicardial transudates could be used to uncover small, but physiologically important changes in interstitial NE concentrations under normal and pathological conditions. Norepinephrine (NE) concentrations measured in epicardial transudate fluid were compared to NE levels in the coronary effluent in normal and pressure overload hypertrophied (POH) rat hearts. Hearts were isolated together with the stellate ganglion and perfused in the inverted position. Epicardial surface transudates, representative fluid of the interstitial myocardial compartment, and coronary effluents were collected for determination of NE levels in the presence and absence of stellate ganglion stimulation. The same protocol was repeated in the presence and absence of nisoxetine, a NE uptake blocker. NE concentrations in epicardial transudates were 16- and 19-fold higher than in the coronary effluent in both sham and POH groups, respectively. NE concentrations in the transudates but not in the coronary effluents were significantly higher (1.6-fold) in hearts with POH when compared to normal hearts. Likewise, nisoxetine (10(-5)m) increased (1.3-fold) NE concentrations in the transudates but not in the effluents of sham animals. As expected, stellate ganglion stimulation increased NE concentrations in both transudates and effluents in sham and POH hearts. In conclusion, determination of NE concentrations in epicardial transudates represents a simple, rapid and sensitive method to detect increases in adrenergic activity in normal and abnormal hearts.

Animals↗
PubMed1984

Glial polypeptides transferred into the squid giant axon.

The proteins synthesized by the glial sheath of an isolated segment of squid giant axon and by the cell bodies of the giant axon in the isolated stellate ganglion were labeled by incubation in the presence of [3H]leucine. The axoplasm, which contained labeled proteins transferred from the glial sheath, was separated from the sheath by mechanical extrusion. The labeled proteins in the axoplasm, the empty sheath and the stellate ganglion were analyzed and compared by one- and two-dimensional polyacrylamide gel electrophoresis. Over 80 glial polypeptides were found to be selectively transferred into the axoplasm and many of these were distinct from stellate ganglion polypeptides which presumably could be supplied to the axon via axonal transport. Three of the more highly labeled transferred glial polypeptides (TGPs) were actin, a fodrin-like polypeptide and a polypeptide we have named traversin. Our observations, considered in the context of other reports, suggest that the squid axon receives a large number of polypeptides from its surrounding glia either by phagocytozing glial cell process that project into it or via cytoplasmic channels between adaxonal glia and the axon. These TGPs may help the axon survive unfavorable conditions.

Animals↗
PubMed1979

Sympathetic control of lower oesophageal sphincter motility in the cat.

1. The action of adrenaline, noradrenaline and efferent sympathetic fibres on the smooth muscle of the lower oesophageal sphincter (l.o.s.) was studied in vivo on the anaesthetized cat and in vitro with the sucrose gap method. 2. Adrenaline and noradrenaline produce a marked depolarization of the circular muscle of the l.o.s. This effect is suppressed by dihydroergotamine or phentolamine, and greatly reduced by atropine; it remains unaltered by hexamethonium. 3. Sympathetic fibres are excitatory for the l.o.s. They come from the stellate ganglion or run along the splanchnic nerve: the fibres arising from the stellate ganglion (mainly by the cardiac branch of the ganglion) join the vagus nerve at the thoracic level; the fibres running along the splanchnic nerve pass through the coeliac ganglion without synapsing; their cellular bodies lie probably in the ganglia of the sympathetic chain. 4. Repetitive stimulation (20--40 Hz) of these fibres induce, with a latency of 5--8 sec, a sustained or rhythmic contraction of the l.o.s. This response is suppressed by dihydroergotamine, and greatly reduced by atropine, while hexamethonium has no effect. 5. Stimulation of sympathetic fibres induces a facilitation of the vagal excitatory responses and an inhibition of the vagal inhibitory responses of the l.o.s. 6. Our data show that the sympathetic response of the l.o.s. results from the stimulation of adrenergic receptors which are located not only on muscular fibres but also, and chiefly, on intrinsic neurones. Thus, the sympathetic control of the l.o.s. is mainly exerted through cholinergic myenteric neurones which could be excited either directly or indirectly by inhibition of inhibitory intrinsic neurones.

Animals↗
PubMed1993

Specificity of pseudorabies virus as a retrograde marker of sympathetic preganglionic neurons: implications for transneuronal labeling studies.

The purpose of the present study was to examine the specificity of the Bartha strain of pseudorabies virus (PRV) as a CNS retrograde marker. This information is critical in assessing whether this virus has potential value as a specific transneuronal marker. The model system chosen for analysis was the intermediolateral cell column (IML)--the principal site of origin of sympathetic preganglionic neurons (SPNs). Two experiments were performed. The first experiment established the usefulness of this model system and the second examined the properties of PRV as a retrograde cell body marker. In the first experiment, injections of two different conventional retrograde cell body markers (cholera toxin-beta subunit (CTb) and Fluoro-Gold) were made in two ipsilateral sympathetic structures (viz., stellate ganglion and adrenal gland) in the same rat. This experiment established that (1) heterogenous SPNs originate in the same cell clusters that form the IML at the T4-T8 levels and 2) SPNs innervate specific sympathetic targets with almost none providing a dual innervation of the stellate ganglion and adrenal gland. This mosaic arrangement of target-specific SPNs makes the IML an excellent CNS site for this type of study. The second experiment followed the same paradigm: PRV was injected into the stellate ganglion and CTb into the adrenal gland (and vice versa). These experiments established that PRV infections of one functional class of SPNs did not produce infections in nearby, functionally unrelated SPNs and did not cause a reduction in the SPN cell population, except under conditions of severe gliosis. These two properties increase the probability that Bartha PRV may be used as a specific retrograde transneuronal marker of central autonomic pathways.

Animals↗
PubMed1991

Dynamics of ventricular repolarisation in the congenital long QT syndromes.

Patients with congenital QT interval prolongation are at risk of ventricular arrhythmias and sudden death. It has been suggested that the susceptibility to arrhythmias in these syndromes may be related to the abnormal dynamics of ventricular repolarisation. The dynamics of ventricular repolarisation, including assessment of the effect of changing heart rate on the QT interval and the duration of the right ventricular monophasic action potential, were studied in eight patients with congenital long QT syndromes. The effects of altered sympathetic tone on these dynamics were investigated with isoprenaline, propranolol, and left stellate ganglion block. The rate adaptation of the QT interval was abnormal in only a few patients and in some patients this feature may be related to the severity of the condition. These abnormalities may be exaggerated by isoprenaline and lessened by propranolol and left stellate ganglion block. Monophasic action potential dynamics were normal in all patients. The hypothesis that impaired QT rate adaptation may play a role in the genesis of ventricular arrhythmias in these syndromes is not, in general, supported by the present data. However, in patients with impaired adaptation the normalisation of QT dynamics after beta blockade and left stellate ganglion block was consistent with the efficacy of these forms of treatment.

Action Potentials↗
PubMed1989

[Modelling of ventricular tachycardia against a background of an elongated Q-T interval].

During the experiments on dogs we've created a mood of stable ventricular tachycardia induced by electrical stimulation of the left stellate ganglion at the elongated Q-T interval. The elongated cardiac systole--Q-T interval on ECG is induced by intravenous cesium chloride (l mmol/kg of dog's weight), which results in the disturbed myocardial electrolyte balance seen as tissue hypokalemia. In the dogs with electrical cardiac instability irritation of the left stellate ganglion resulted in polymorphic ventricular tachyarrhythmia in 83% of the animals. The created model has documented a role played by intracardiac pathology (electrolyte imbalance) in combination with the increased activity of the stellate ganglion in the mechanism of ventricular arrhythmia seen at the elongated Q-T interval.

Animals↗
PubMed1976

Selective activation of nicotinic and muscarinic transmission in cardiac sympathetic ganglion of the dog.

The myocardial contractile responses to electrical stimulation of different segments of the thoracic sympathetic trunk in the pentobarbital-anesthetized dog were studied. Electrical stimulation of the sympathetic trunk between the second and third thoracic ramus and caudal limb of the ansa subclavia elicited myocardial contractile responses which were not completely antagonized by the ganglionic blocking agent chlorisondamine. Atropine in addition to chlone had no effect. When the sympathetic trunk between the third and fourth ramus was electrically stimulated, the response was partially antagonized by atropine as well as by chlorisondamine alone. From these results, it is suggested that impulses travelling via the third thoracic ramus or above it mediate myocardial contractile responses in which the nicotinic type response predominates whereaas impulses travelling via the fourth thoracic ramus or below it mediate myocardial contractile responses in which the muscarinic type predominates. additionally, evidence presented indicates that a major proportion of both nicotinic and muscarinic receptors mediating myocardial contractile changes are located in the caudal cervical ganglion rather than the stellate ganglion of the dog.

Animals↗