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PubMed1987

Effects of captopril on sympathetic control of the heart and vasculature in dogs.

Experiments were conducted in pentobarbital anesthetized dogs to investigate the effects of captopril on sympathetic neuronal control of the heart and hindlimb vasculature. Captopril, 3.1 mg/kg, i.v. produced marked reductions in blood pressure and hindlimb perfusion pressure, an observation consistent with the high plasma renin activity in the test animals. Increments in hindlimb perfusion pressure elicited by electrical stimulation of the lumbar sympathetic chain were also significantly reduced following captopril administration (p less than .002). The subsequent administration of a ten fold higher dose of captopril, 31.0 mg/kg, produced no further attenuation of the neurally mediated responses. In contrast to the decreased vascular responses to nerve stimulation after captopril, the tachycardia produced by stimulation of pre- or post-ganglionic neurons to the stellate ganglion were not altered. The results of the present study suggest that captopril acts by inhibiting vascular sympathetic neuronal function when the activity of the renin-angiotensin system is elevated. The attenuation of neurally mediated vasoconstriction may be due to the interruption of angiotensin II formation, thereby, preventing the facilitatory effects of angiotensin on sympathetic neurons.

Animals↗
PubMedDate not supplied

A comparative and quantitative study of small intensely fluorescent (SIF) cells in the sympathetic ganglia of some small mammals.

This comparative study of the number of SIF cells in the ganglions of the rat, cat, rabbit, mouse and hamster has confirmed that the mean number of SIF cells in the same ganglion of different species varies greatly, for instance in the superior cervical ganglion (SCG) of the rat and the cat, in the stellate ganglion of the cat and the mouse, or in the inferior mesenteric ganglion of the hamster and the other species. There is also considerable variability among individuals of the same animal species. In the SCG, the only ganglion for which there are data on the number of neurons, the ratio of SIF cells to neurons is around 1% in the rat, 0.2% in the rabbit, 0.3% in the mouse and 0.05% in the cat, i.e. a twenty-fold difference between the cat and the rat. Williams et al. (1975) distinguished type 1 SIF cells, corresponding to interneurons, from type 2, which are purely endocrine cells. Type 2 appears to be predominant in all ganglia, except the rabbit SCG where type 1 is highly predominant, and in all species, except the rat, in which this distinction is not applicable. The possible implications of these data on ganglionic functioning are discussed.

Animals↗
PubMed1984

Localization of sympathetic postganglionic and parasympathetic preganglionic neurons which innervate different regions of the dog heart.

The locations of sympathetic postganglionic and parasympathetic preganglionic neurons projecting to the heart have not yet been clearly established. Therefore, aliquots of horseradish peroxidase (HRP) were injected into specific regions of the heart, intraventricular cavity, pericardial sac, aortic arch, and the skin in 27 dogs. Following injections into the heart, aorta, or pericardial sac, retrogradely labeled neurons were present in the greatest numbers in the middle cervical ganglia bilaterally. Labeled neurons were located in the cranial poles of the stellate ganglia bilaterally and occasionally in the superior cervical ganglia. Labeled cells were also found in small ganglia located along cardiopulmonary nerves. Injections of HRP into specific areas of the heart did not result in labeling of cells in specific loci of the thoracic or cervical sympathetic ganglia. When the ansae were cut on one side, no labeled cells were found in the ipsilateral stellate ganglion or upper thoracic chain. Following injections into the skin of the left elbow or left cranial nipple, labeled cells were found in the stellate ganglia and the sympathetic chain and in one case in the middle cervical ganglion as well. These data suggest that postganglionic sympathetic neurons which project efferent axons to a specific cardiac region are not located in a specific region of a sympathetic ganglion or a specific sympathetic ganglion. Rather, neurons in one region of a sympathetic ganglion project axons to widespread areas of the myocardium. Sympathetic postganglionic neurons in the stellate ganglion or sympathetic chain project their axons to the heart via the subclavian ansae or interganglionic nerves, not via nerves arising directly from the sympathetic chain. Small numbers of labeled neurons were found in the medulla oblongata, thus indicating that in comparison to sympathetic postganglionic neurons relatively few preganglionic parasympathetic neurons project directly to the heart. When labeled cells were present in the medulla, the majority were located in the ventrolateral nucleus ambiguus.

Animals↗
PubMed1982

Potentiation of the ganglionic blocking action of norepinephrine by cocaine.

Concentration-response curves for the blocking action of norepinephrine were determined in the isolated stellate ganglion of the hamster. The blocking effect of norepinephrine on the postganglionic compound action potential from preganglionic nerve stimulation at 0.2 Hz was reduced by phentolamine (10(-5) M), but was not altered by propranolol (10(-6) M). Cocaine (10(-6) and 10(-5) M) increased the sensitivity of the ganglion to norepinephrine. These concentrations of cocaine produced less than 25% blockade when applied alone. The local anesthetic, procaine, did not change the sensitivity of the ganglion to norepinephrine. The blockade by norepinephrine in the presence of cocaine was antagonized by phentolamine and unaffected by propranolol. The time course of the blockade by norepinephrine was more rapid in onset and slower in recovery in the presence of cocaine. If it is assumed that cocaine is blocking norepinephrine uptake into cells within the ganglion, these results indicate that the catecholamine uptake mechanism is involved in terminating the blocking action of exogenously applied norepinephrine.

Animals↗
PubMed2001

Upregulation of immunoreactive angiotensin II release and angiotensinogen mRNA expression by high-frequency preganglionic stimulation at the canine cardiac sympathetic ganglia.

The possible involvement of the local angiotensin system in ganglionic functions was investigated in the canine cardiac sympathetic ganglia. Positive chronotropic responses to preganglionic stellate stimulation at high frequencies, after intravenous administration of pentolinium plus atropine, were inhibited by the nonpeptide angiotensin AT(1) receptor antagonist forasartan or the angiotensin I-converting enzyme inhibitor captopril, whereas the rate increases elicited by the postganglionic stellate stimulation and norepinephrine given intravenously failed to be inhibited by these antagonists. The levels of endogenous immunoreactive angiotensin II, as determined by radioimmunoassay in the incubation medium of the stellate and inferior cervical ganglia, were increased after the high-frequency preganglionic stimulation of the isolated ganglia. The increment of the peptide was also antagonized by the pretreatment with captopril but not by a chymase inhibitor, chymostatin. The expression of angiotensinogen mRNA was observed in the stellate ganglion, adrenal, liver, and lung but not in the ovary and spleen. The expression of the mRNA in the stellate and inferior cervical ganglia increased after high-frequency preganglionic stimulation of the in vivo dogs for a period of 1 hour. These results indicate that an intrinsic angiotensin I-converting enzyme-dependent angiotensin system exists in the cardiac sympathetic ganglia, which is activated by high-frequency preganglionic stimulation.

Angiotensin II↗
PubMed2001

[Migraine and nerve block].

Migraine is essentially an episodic headache usually accompanied by neurological disorder, vomiting, photo- and phonophobia and malaise. The sensory nerves in the cerebral blood vessels are activated during migraine attack. The trigeminal systems is the sensory system that innervation cranial vessels and dura mater via its first ophthalamic division. Pain fibers from the trigeminal nerve descends to the second cervical cord segment where fibers from the occipital region transverse the dorsal root ganglion to converge on second order neurons. C2 root ganglion block therapy is the most efficacious treatment of the acute attack of migraine. Stellate ganglion block is a usefulness of amelioration of the sensory nerves of the intracranial vessels and prevention of migraine headache.

Ganglia, Spinal↗
PubMed1979

The orthograde labeling of postganglionic sympathetic cardiac nerves in the dog and cat as demonstrated by autoradiography.

Previous functional and anatomical techniques have characterized the cardiac nerves and plexuses. They cannot, however, determine the course of fibers arising from a specific ganglion. This study has found that the intraaxonal orthograde labeling of axons can be used to determine the course of postganglionic sympathetic cardiac fibers in the dog and cat. The canine left caudal cervical ganglion and the feline right stellate ganglion were exposed through appropriate thoracotomies. Each ganglion received multiple injections of tritiated leucine (500 muCi/animal). Following a 3--14-day survival period the anesthetized animals were sacrificed by vascular perfusion. The injected ganglia, extracardiac nerves and selected portions of the heart were processed for autoradiography. Autoradiographs from the dog demonstrated labeled postganglionic sympathetic nerves in the extracardiac plexus, left atrial epicardium and the epicardium beneath the coronary sulcus. Labeled nerves in the cat heart were found within the epicardial layers and associated with blood vessels in the left ventricular myocardium. Neither myelinated fibers traveling through the injection site nor intrinsic cardiac ganglion cells were labeled, although the latter were often closely approximated to heavily labeled fibers.

Animals↗
PubMed1992

Effects of a coronary alpha 1-constriction on transmural left ventricular flow and contractile function.

Modulation of myocardial contractile function and perfusion by alpha 1-adrenergic receptors were examined in anesthetized dogs during left stellate ganglion stimulation. In 11 dogs, stellate stimulation significantly increased heart rate, mean arterial pressure, left ventricular systolic pressure, maximal rate of left ventricular pressure generation, segmental shortening and rate of shortening in anterior and posterior ventricular regions, and myocardial oxygen extraction. Myocardial lactate extraction decreased. The selective alpha 1-adrenergic antagonist prazosin (0.5 mg) injected into the circumflex artery during stellate stimulation caused significant additional increases in maximal rate of left ventricular pressure generation by 19 +/- 5% and in rate of shortening in posterior subendocardium by 20 +/- 6%. No changes were observed in posterior subepicardial or anterior subendocardial segmental contractile function. Myocardial oxygen and lactate extractions returned to their control values following prazosin injection. Regional left ventricular perfusion was measured using tracer microspheres in five additional dogs. Stellate stimulation increased subepicardial and subendocardial perfusion by 30%. Prazosin increased both subepicardial and subendocardial perfusion by an additional 36%. Stellate stimulation increased norepinephrine concentration in the coronary sinus, but no further increase was noted after blockage of alpha 1-receptors by prazosin. Thus, during sympathetic stimulation, an alpha 1-vasoconstriction existed uniformly across the left ventricular wall. However, blockade of this vasoconstriction was associated with an increase in contractile function only in the deeper muscle layers.

Adrenergic alpha-Antagonists↗
PubMed2001

Thoracic origin of a sympathetic supply to the upper limb: the 'nerve of Kuntz' revisited.

An understanding of the origin of the sympathetic innervation of the upper limb is important in surgical sympathectomy procedures. An inconstant intrathoracic ramus which joined the 2nd intercostal nerve to the ventral ramus of the 1st thoracic nerve, proximal to the point where the latter gave a large branch to the brachial plexus, has become known as the 'nerve of Kuntz' (Kuntz, 1927). Subsequently a variety of sympathetic interneuronal connections down to the 5th intercostal space were reported and also described as the nerve of Kuntz. The aim of this study was to determine: (1) the incidence, location and course of the nerve of Kuntz; (2) the relationship of the nerve of Kuntz to the 2nd thoracic ganglion; (3) the variations of the nerve of Kuntz in the absence of a stellate ganglion; (4) to compare the original intrathoracic ramus with sympathetic variations at other intercostal levels; and (5) to devise an appropriate anatomical classification of the nerves of Kuntz. Bilateral microdissection of the sympathetic chain and somatic nerves of the upper 5 intercostal spaces was undertaken in 32 fetuses (gestational age, 18 wk to full term) and 18 adult cadavers. The total sample size comprised 99 sides. Sympathetic contributions to the first thoracic nerve were found in 60 of 99 sides (left 32, right 28). Of these, 46 were confined to the 1st intercostal space only. The nerve of Kuntz (the original intrathoracic ramus) of the 1st intercostal space had a demonstrable sympathetic connection in 34 cases, and an absence of macroscopic sympathetic connections in 12. In the remaining intercostal spaces, intrathoracic rami uniting intercostal nerves were not observed. Additional sympathetic contributions (exclusive of rami communicantes) were noted between ganglia, interganglionic segments and intercostal nerves as additional rami communicantes. The eponym nerve of Kuntz should be restricted to descriptions of the intrathoracic ramus of the 1st intercostal space. Any of these variant sympathetic pathways may be responsible for the recurrence of symptoms after sympathectomy surgery.

Adult↗
PubMed1987

Cardiac alpha-1 adrenoceptors are not involved in heart rate control of the anaesthetized dog.

To study the possible role of cardiac postsynaptic alpha-1 adrenoceptors in heart rate control of the anaesthetized open-chest dog we injected a specific alpha-1 agonist (amidephrine) into the right coronary artery or stimulated electrically the right stellate ganglion. Reflex influences were minimized by bilateral cervical vagotomy and de-afferentiation of both stellate ganglia. Activation of alpha-2, beta- and muscarinic receptors was prevented by intravenous administration of yohimbine, propranolol and atropine, respectively. Since alpha-1 receptor stimulation could affect heart rate indirectly via coronary constriction, a continuous intracoronary infusion of adenosine (0.25 mg/kg/h) was given. Amidephrine did not affect heart rate at the lower dose (1-10 microgram). After the highest dose (100 micrograms) the maximum variation in heart rate was an increase of 2.2 +/- 1.1 bpm at 3 min after injection (mean +/- SEM; P less than 0.05). This slight cardioacceleration was simultaneous with an aortic pressure rise of 13.8 +/- 3.4 mm Hg and it was abolished by alpha-1 blockade with prazosin (1 mg/kg i.v.). After propranolol (1 mg/kg +0.5 mg/kg/h) the residual positive chronotropic effect of sympathetic stimulation (12.2 +/- 4.0 bpm) was not significantly altered (13.8 +/- 5.7 bpm) by prazosin administration. Similar results were recorded without adenosine infusion. We conclude that in the anaesthetized dog chronotropic effects directly mediated by alpha-1 adrenoceptors either do not exist or lack physiological significance.

Adenosine↗
PubMed1992

Immunohistochemical study of the sympathetic and sensory innervation to the blood vessels of the dog forepaw.

Immunohistochemical staining of arteries supplying the dog forepaw showed a dense distribution of nerve fibers which were immunoreactive to tyrosine hydroxylase (TH), neuropeptide Y (NPY), vasoactive intestinal peptide (VIP), substance P (SP), and calcitonin gene-related peptide (CGRP) around the vascular walls. The density of each immunoreactive fiber tended to increase in the peripheral branch of the vascular tree. Retrograde axonal tracing with Fast Blue from the artery revealed that these immunoreactive fibers originated from NPY-containing catecholaminergic as well as VIP/SP/CGRP-containing non-catecholaminergic neurons in the stellate ganglion and SP/CGRP-containing neurons in the dorsal root ganglia of segments C7 to Th1. After stellate ganglionectomy, TH-, NPY-, and, VIP-immunoreactive fibers disappeared completely from the arterial walls while approximately 40% of SP- and CGRP-immunoreactive fibers remained. The present results indicate that the artery of the dog forepaw receive triple innervation of adrenergic sympathetic, non-adrenergic sympathetic, and sensory fibers, and suggest that about 40% of SP- and CGRP-immunoreactive fibers are of sensory origin.

Animals↗
PubMed1977

Effects of halothane on ganglionic discharges.

The effects of halothane on ganglionic transmission were studied by recording extracellular potentials from the postganglionic nerve of the isolated hamster stellate ganglion. Halothane, at concentrations greater than 0.1 mM, decreased the potentials evoked by preganglionic stimuli at 0.2 Hz. Halothane also blocked discharges elicited by 1,1-dimethyl-4-phenylpiperazinium, a selective nicotinic agonist, and discharges elicited by the nicotinic actions of exogenous acetylcholine. Repetitive preganglionic stimulation (30 Hz, 5 seconds) in the presence of nicotine (10(-3) M), or hexamethonium (10(-3) M), evoked asynchronous discharges in the postganglionic nerve. These discharges were suppressed by low concentrations of atropine, and were probably due to the muscarinic actions of neurotransmitter. Halothane depressed these discharges at approximately the same concentration that it depressed the compound action potential elicited by low frequency preganglionic stimulation in the untreated ganglion. Halothane had no effect on the discharges elicited by 4-(m-chlorophenylcarbamoyloxy)-2-butynyltrimethylammonium chloride (McN-A-343), a selective muscarinic agonist, or the discharges elicited by the muscarinic actions of acetylcholine. These results are most readily explained by hypothesizing that halothane acts at two sites in the ganglion. It appears to depress the postsynaptic response to the nicotinic actions of the neurotransmitter, acetylcholine. Also, it probably depresses transmitter release from the presynaptic nerve endings during repetitive stimulation.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMedDate not supplied

Post-train depression of ganglionic transmission in the presence of d-amphetamine.

Repetitive stimulation (30 Hz, 20 sec) of the preganglionic nerve to the hamster isolated stellate ganglion in a control solution had only small effects on the compound action potentials of the postganglionic nerve (0.2 Hz) after the train. When 10(-5) M d-amphetamine was added to the superfusing solution, the repetitive stimulation induced a post-train depression of the postganglionic compound action potential. The mean reduction of the compound action potential during the post-train depression in d-amphetamine was 37 +/- 15% and the duration was from 60 to 120 sec. Post-train depression only occurred after long conditioning trains and was never observed with less than 100 stimuli in the conditioning train. A post-train depression (45 +/- 8%) was also observed in the presence of 10(-5) M cocaine. The post-train depression in d-amphetamine was significantly reduced by the alpha-adrenoceptor antagonist, phentolamine (10(-5) M) and by the alpha 2-adrenoceptor antagonist, yohimbine (10(-6) M), but not by the alpha 1-adrenoceptor antagonist, prazosin (10(-5) M). There was no post-train depression in the presence of d-amphetamine in ganglia from five hamsters that were pretreated with reserpine (6 mg/kg, i.p., 4 hr). Atropine (10(-6) M) increased and prolonged the post-train depression in the presence of d-amphetamine. These results indicate that repetitive stimulation in the presence of d-amphetamine leads to a post-train depression of the postganglionic compound action potential that is mediated by an action of endogenous catecholamines at alpha 2-adrenoceptors. Muscarinic cholinoceptors do not appear to be involved in the generation of the post-train depression.

Action Potentials↗
PubMed1984

Blockade of ganglionic afterdischarges by tyramine may be mediated by endogenous catecholamines.

Tyramine reduced the compound postganglionic action potential from preganglionic stimulation of the golden hamster isolated stellate ganglion at 0.2 Hz. This action of tyramine was only slightly reduced by phentolamine (10(-5)M), an alpha adrenoceptor antagonist. Tyramine also reduced the postganglionic discharges after preganglionic stimulation at 30 Hz for 2 sec in the presence of hexamethonium. The blockade of afterdischarges by tyramine was markedly reduced by phentolamine. Furthermore, tyramine was much less effective in blocking ganglia from reserpine-pretreated hamsters (6 mg/kg, 4 hr before isolation). Blockade of afterdischarges by norepinephrine was reduced by phentolamine, but not by reserpine. These results indicate that the blockade of afterdischarges with tyramine is mediated by endogenous catecholamines. The blocking action of tyramine was not reduced by cocaine (10(-5)M). Cocaine did reduce the afterdischarges, and this action of cocaine was partially antagonized by phentolamine and reserpine. These results suggest that the blockade of afterdischarges by tyramine and cocaine is due to inhibition of catecholamine uptake which potentiates the actions of endogenous catecholamines.

Action Potentials↗
PubMed1980

Innervation of sympathetic neurones in the guinea-pig thoracic chain.

We have investigated the organization of the guinea-pig thoracic chain by studying the innervation of the stellate and fifth thoracic sympathetic ganglia with intracellular recording. 1. These ganglia receive preganglionic innervation from different but overlapping sets of spinal cord segments: the stellate ganglion is innervated by preganglionic axons from spinal segments more rostral than those supplying the fifth thoracic ganglion, but somewhat more caudal than those innervating the superior cervical ganglion. 2. Individual thoracic ganglion cells are innervated by only some of the spinal segments that supply each ganglion as a whole. In general, the subset of spinal segments innervating a ganglion cell is contiguous; one of these segments provides the strongest innervation, with progressively weaker innervation arising from spinal levels adjacent to the dominant one. This selective pattern of innervation is similar to that in the superior cervical ganglion (Njå & Purves, 1977 a). 3. Preganglionic axons frequently innervate neurones in more than one ganglion. 4. Although neurones innervated by the same spinal cord segments are found in both the stellate and the fifth thoracic ganglion, as well as in the superior cervical, the number of ganglion cells receiving innervation from particular spinal segments is different in each ganglion. Moreover, neurones dominated by the same segment but located in different ganglia receive somewhat different average innervation from adjacent segments as a function of the ganglion in which they reside. 5. These results indicate that neurones in the thoracic chain ganglia, as those in the superior cervical ganglion, are selectively innervated by particular spinal cord segments. We suggest that the different average innervation of sympathetic ganglia reflects at least two related factors: the selective qualities of their constituent neurones, and the availability of different preganglionic axons to each ganglion.

Animals↗
PubMed1993

Chemical blockage of cervical sympathetic trunks for facial palsy.

Impairment of microcirculation of the facial nerves is considered to play an important role in etiology of facial palsy, and the main emphasis of the conservative treatment is aimed at circulatory improvement. Therefore, at the pain clinic, improved blood flow to the facial nerve by chemical blockage of cervical sympathetic trunks (stellate ganglion block; SGB) is employed in treating patients with facial palsy. The circulatory effects of SGB were clinically determined in 20 patients with acute Bell's palsy, and the effects of chemical blockage of cervical sympathetic trunks on the tissue circulation of facial nerve were also experimentally evaluated in dogs. In the clinical study, the blood flow volume of the common carotid artery increased significantly in 5 minutes after SGB, and has reached its peak of 176.4% in 20 minutes. This significant increase continued up to 75 minutes. In the animal model experiments, the common carotid arterial blood flow volume increased immediately after performing experimental SGB with a peak rise of 143.5% in 15 minutes, and the significant increase continued up to 45 minutes. The blood flow volume in the facial nerve tissue also increased for 5 minutes with a peak rise of 115.2% in 20 minutes after SGB, and this significant increase persisted for up to 60 minutes. A marked increase was observed in the blood flow volume in the facial nerve tissue as well as through the common carotid artery. The circulatory improvement performed by SGB extended as far as the facial nerve itself. From the facts above mentioned, SGB is considered to be an extremely effective treatment for the Bell's palsy.

Adolescent↗
PubMed1987

Lipid metabolism in various regions of squid giant nerve fiber.

The purpose of this investigation was to compare the incorporation of radioactivity from various precursors into lipids of different regions of squid giant nerve fiber systems including axoplasm, axon sheath, giant fiber lobes which contain stellate ganglion cell bodies, and the remaining ganglion including giant synapses. To identify the labeled lipids, stellate ganglia including giant fiber lobes and the remaining tissue were first incubated separately with [14C]glucose, [32P]phosphate, [14C]serine, [14C]acetate and [3H]myristate. The radioactivity from glucose, after conversion to glycerol and fatty acids, was incorporated into most lipids, including triacylglycerol, free fatty acids, cardiolipin, phosphatidylethanolamine, phosphatidylglycerol, phosphatidylcholine, phosphatidylinositol, phosphatidylserine, sphingomyelin and ceramide 2-aminoethylphosphanate [corrected]. The radioactivity from serine was largely incorporated into phosphatidylserine and, to a lesser extent, into other phospholipids, mainly as the base component. The sphingoid bases of ceramide and sphingomyelin were also significantly labeled. Saturated and monounsaturated and, to a lesser extent, polyunsaturated fatty acids of these lipids were synthesized from acetate, glucose and myristate. Among the major lipids, cholesterol was not labeled by any of the radioactive compounds used. Ganglion residues incorporated the most radioactivity in total lipids from either [14C]glucose or [14C]serine, followed by giant fiber lobes and then sheath. Axoplasm incorporated the least. Among various lipids, phosphatidylethanolamine with shorter saturated fatty acids and phosphatidylglycerol contained the most radioactivity from glucose in all regions. Axoplasm was characterized by a higher proportion of glucose radioactivity in ceramide, sphingomyelin and phosphatidylglycerol. Axoplasm and sheath contained a higher proportion of serine radioactivity than did the other two regions in ceramide. Essentially no radioactivity from [14C]galactose was incorporated in any region.

Acetates↗
PubMed1997

Developmental changes in modulation of cardiac repolarization by sympathetic stimulation: the role of beta- and alpha-adrenergic receptors.

INTRODUCTION: Our goals were to study the role of development in determining the cardiac effects of sympathetic neural activation, and to identify the roles of alpha- and beta-adrenergic receptor-mediated pathways in modulating the effects of sympathetic stimulation. METHODS AND RESULTS: We compared responses of young and adult canine hearts in situ to right, left, and bilateral stellate ganglion stimulation. We focused on changes in heart rate, rhythm, QT interval, rate-corrected QT interval (QTc), and T wave amplitude. Right stellate stimulation (RSS) induced more pronounced sinus tachycardia in adult than young animals. Left stellate stimulation (LSS) induced junctional tachycardia in adult more than young animals. In adults, LSS and RSS prolonged QTc (LSS > RSS), whereas 1-week-olds manifested QTc shortening with RSS. LSS also increased T wave amplitude, most markedly in adults. In all studies, bilateral stellate stimulation induced responses intermediate between those seen with RSS and LSS. beta-Adrenergic blockade (propranolol) abolished all responses to LSS in adult hearts, but alpha-blockade (prazosin) attenuated only the LSS-induced prolongation in QTc. CONCLUSION: In the postnatal modulation of cardiac rhythm, rate, and repolarization by the sympathetic nervous system, beta-adrenergic receptors play a major role at all ages, whereas alpha-adrenergic receptors play a lesser role, which is manifested only in adults. Moreover, expression of junctional tachycardias, which are beta-adrenergically modulated, is seen only in the adults.

Animals↗