Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “STELLATE GANGLION”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 847 records · Page 47Linked to original sources
PubMed1995

[Effects of anticoagulant therapy on retinal vein occlusion].

The combined effect of prostaglandin E1, stellate ganglion block, warfarin potassium and photocoagulation on 66 cases (eyes) of retinal vein occlusion was investigated immediately after, and 3 months and 6 months after final treatment. The time between onset and treatment was 2 months or less. Macular hemorrhage and edema were observed in all cases. The effectiveness rate 6 months after treatment was 35% in hemorrhagic central retinal vein occlusion and 63% in branch retinal vein occlusion. Visual acuity increased gradually with time from immediately after to 6 months after treatment. The effectiveness of treatment including warfarin potassium was lower than that of treatment without warfarin potassium in branch retinal vein occlusion, and many cases showed a marked decrease of visual acuity which might be related to the prolonged hemorrhage. These results suggest that combining prostaglandin E1, stellate ganglion block and photocoagulation in retinal vein occlusion produces better effects on visual acuity than ordinary treatment or spontaneous regression.

Aged↗
PubMed1995

Sympathetic activation, ventricular repolarization and Ikr blockade: implications for the antifibrillatory efficacy of potassium channel blocking agents.

OBJECTIVES: The aim of the present study was to test, in vivo and in vitro, the influence of adrenergic activation on action potential prolongation induced by the potassium channel blocking agent d-sotalol. BACKGROUND: d-Sotalol is not effective against myocardial ischemia-dependent ventricular fibrillation in the presence of elevated sympathetic activity. Most potassium channel blockers, such as d-sotalol, affect only one of the two components of Ik (Ikr) but not the other (Iks). Iks is activated by isoproterenol. An unopposed activation of Iks might account for the loss of anti-fibrillatory effect by d-sotalol in conditions of high sympathetic activity. METHODS: In nine anesthetized dogs we tested at constant heart rate (160 to 220 beats/min) the influences of left stellate ganglion stimulation on the monophasic action potential prolongation induced by d-sotalol. In two groups of isolated guinea pig ventricular myocytes we tested the effect of isoproterenol (10(-9) mol/liter) on the action potential duration at five pacing rates (from 0.5 to 2.5 Hz) in the absence (n = 6) and in the presence (n = 8) of d-sotalol. RESULTS: In control conditions, both in vivo and in vitro, adrenergic stimulation did not significantly change action potential duration. d-Sotalol prolonged both monophasic action potential duration in dogs and action potential duration of guinea pig ventricular myocytes by 19% to 24%. Adrenergic activation, either left stellate ganglion stimulation in vivo or isoproterenol in vitro, reduced by 40% to 60% the prolongation of action potential duration produced by d-sotalol. CONCLUSIONS: Sympathetic activation counteracts the effects of potassium channel blockers on the duration of repolarization and may impair their primary antifibrillatory mechanism. An intriguing clinical implication is that potassium channel blockers may not offer effective protection from malignant ischemic arrhythmias that occur in a setting of elevated sympathetic activity.

Action Potentials↗
PubMed2000

Nerve sprouting and sudden cardiac death.

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

Adrenergic beta-Antagonists↗
PubMed2002

Needlescopic thoracic sympathetic block by clipping for craniofacial hyperhidrosis: an analysis of 28 cases.

BACKGROUND: Endoscopic thoracic sympathectomy or sympathicotomy of the lower part of the stellate ganglion is an efficient method for the treatment of craniofacial hyperhidrosis, but postoperative compensatory sweating may be troublesome in some patients. Needlescopic thoracic sympathetic block by clipping may achieve a similar effect as well as providing a possible reverse operation for patients who suffer from intolerable postoperative compensatory sweating. METHODS: Between January 1998 and June 2000, we collected a total of 28 patients with craniofacial hyperhidrosis. There were 15 men and 13 women with a mean age of 39.2 years (ranges, 19-50). All patients were placed under single-lumen intubated anesthesia in a semisitting position. Two ports were needed. We used a 2-mm 0 degrees thoracoscope and endo clips to perform a sympathetic block by clipping the lower third of the stellate ganglion at the second intercostal space. RESULTS: The operation was usually accomplished within 20 min (ranges, 15-30). All patients were discharged within 4 h after the operation. There were no surgical complications or surgical mortality cases. All patients achieved improvement of craniofacial hyperhidrosis without recurrent symptoms after a mean of 25.3 months (range, 12-41) of follow-up. Twenty-five patients (85.7%) developed compensatory sweating of the trunk and lower limbs. One of these patients could not tolerate this postoperative sweating; he therefore underwent a reverse operation and obtained improvement of the compensatory sweating 18 days after removal of the endo clips. CONCLUSION: Needlescopic thoracic sympathetic block by clipping is a safe and effective method for the treatment of craniofacial hyperhidrosis; compensatory sweating may be improved after a reverse operation and removal of the endo clips.

Adult↗
PubMed1992

Cardiac responses elicited by stimulation of loci within stellate ganglia of developing swine.

Stimulation with bipolar electrodes of specific loci in stellate ganglia elicited in anesthetized piglets, 1-4 weeks of age, alterations in cardiac function and aortic pressure. Responses were also elicited by chemical stimulation in specific loci of these ganglia. The probability of eliciting a cardiovascular response by stimulating loci in a stellate ganglion increased with increasing postnatal age. For instance, no responses were elicited when loci in the left stellate ganglia of 1-week-old piglets were stimulated. Significant heart rate responses were obtained only when loci in right stellate ganglia were stimulated. The number of ganglionic loci from which cardiovascular responses were obtained increased with increasing postnatal age. It is concluded that the capacity of stellate ganglion neurons to modulate the cardiovascular system matures during the first four weeks of life, heart rate being modulated primarily by neurons in the right stellate ganglion and inotropism by neurons in both stellate ganglia.

Aging↗
PubMed1966

The action of calcium on neuronal synapses in the squid.

1. The isolated stellate ganglion of the squid (L. pealii) was studied with intracellular and extracellular micro-electrodes. Three or four nerve fibres in the preganglionic nerve establish synaptic relations with the giant axon in the last stellar nerve. Accordingly, 1-3 small presynaptic spikes (< 1 mV) could be recorded from within the post-synaptic axon.2. A micro-electrode was inserted in the presynaptic fibre and used to polarize and record simultaneously. In the distal (giant) synapse, hyperpolarization of the ending produced an increase in the size of the presynaptic action potential and post-synaptic potential (PSP). Depolarization had the opposite effect. These effects of polarization took more than 10 sec to develop fully, and declined with a similar time course at the end of polarization. Analogous results were obtained with two other preganglionic fibres, which make contacts in the proximal synaptic region.3. The second of a pair of preganglionic impulses evoked a PSP larger than the first. This facilitation of PSP was sometimes accompanied by a small increase in the size of the second action potential in the presynaptic axon. At some shorter intervals, the second presynaptic action potential was reduced in amplitude, but the PSP was still increased. Hyperpolarization of the presynaptic terminal increased the size of both PSPs in a pair and abolished the facilitation. With stronger hyperpolarization the second PSP was even smaller than the first.4. Removing or reducing the Ca in the bathing fluid reversibly abolished the post-synaptic response. The small presynaptic spikes remained practically unaffected. In these conditions a nerve impulse still invaded the ending and normal action potentials could be recorded from the pre-synaptic terminal. This shows that electrical coupling between pre- and post-synaptic axons is insufficient to account for synaptic transmission.5. In low-Ca solution synaptic transmission could be restored locally by extracellular ionophoretic application of Ca to a small portion of the synapse. At sensitive spots a post-synaptic current (recorded with the Ca pipette) and PSP could be detected earlier than 1 sec after commencing the application of Ca.6. Ca was ineffective when injected intracellularly into the presynaptic fibre at a spot where extracellular ionophoresis of Ca restored the PSP.7. The results indicate that synaptic transmission in the squid stellate ganglion is not electrical but due to the release of an unidentified transmitter. Release of this transmitter by the presynaptic nerve impulse requires the presence of Ca in the external medium. During the impulse Ca would combine with a ;Ca-receptor' in the membrane and initiate the reactions which lead to transmitter release. It appears that the ;Ca-receptor' is only accessible from the outside of the membrane.

Animals↗
PubMed1982

Physiological studies of canine sympathetic ganglia and cardiac nerves.

Anatomical studies have indicated that the middle cervical ganglion is the primary locus of sympathetic postganglionic neurons which have axons projecting in canine cardiac nerves. Small regions of thoracic sympathetic ganglia were stimulated electrically with bipolar electrodes and the generated compound action potentials were recorded from ipsilateral cardiac nerves. Several procedures were used to distinguish the effects of stimulating preganglionic axons, ganglionic sites and postganglionic axons. Following hexamethonium it was found that only low frequency stimulation (e.g. 1 Hz) of ganglionic sites resulted in the generation of compound action potentials in cardiac nerves. These ganglionic sites were located throughout the middle cervical ganglion, but only in the cranial medial pole of the stellate ganglion. Stimulation of a single locus in a stellate or middle cervical ganglion generated compound action potentials in all major ipsilateral sympathetic cardiac nerves. A ganglion was also identified at the junction of the thoracic vagus and the cranial vagal nerve which may be as important as the right stellate ganglion in cardiac regulation. These results demonstrate that there are discrete loci in thoracic ganglia which contain neurons projecting in several ipsilateral cardiac nerves. Low frequency stimulation of these loci was found to be optimal for generation of compound action potentials.

Animals↗
PubMed1985

Changes in ventricular fibrillation threshold with stimulation of cardiac sympathetic nerves of the developing dog.

The effect of stimulation of the developing cardiac sympathetic nerves on the vulnerability to ventricular fibrillation was investigated in 50 puppies 1 to 6 weeks of age. Ventricular fibrillation thresholds were obtained before and during sympathetic nerve stimulation. Stimulation of either stellate ganglion increased ventricular fibrillation threshold, possibly due to diffuse functional innervation in pups. The effect of the left stellate increased progressively with age, whereas the effect of the right, although initially greater than that of the left, did not increase further with age. In contrast, stimulation of the left ventrolateral cardiac nerve, which is locally distributed, resulted in decreased ventricular fibrillation threshold. This decrease was progressively greater with age. The fact that activation of the left stellate ganglion and the left ventrolateral cardiac nerve affects ventricular fibrillation threshold in opposite directions suggests different sympathetically mediated changes on ventricular vulnerability in early life. The differing temporal patterns of maturation and the localized nature of the major distal branch distributions could provide a mechanism for promotion of arrhythmiogenesis under some conditions in early life.

Animals↗
PubMed1979

Altered adrenergic activity in coronary arterial spasm: insight into mechanism based on study of coronary hemodynamics and the electrocardiogram.

To elucidate the pathophysiologic mechanism of coronary arterial spasm, the hypothesis was examined that underlying alterations in sympathetic activity may account for this syndrome in some patients. Observations were directed to alterations in coronary arterial hemodynamics and the electrocardiogram. Spasm of the left anterior descending coronary artery produced a mean increase in coronary vascular resistance of 107 percent (P less than 0.05) in four patients in whom coronary sinus blood flow was measured with the thermodilution technique. The alpha adrenergic blocking agent phentolamine, given intravenously, acutely reversed coronary spasm and its clinical manifestations in eight patients and reduced coronary resistance. In four patients, administration of the long-acting oral alpha blocking agent phenoxybenzamine (20 to 80 mg/day) caused disappearance of symptoms during a follow-up period of 3 to 12 months. Transient prolongation of the corrected Q-T interval preceded spontaneous or ergonovine maleate-provoked coronary spasm in 11 patients with variant angina pectoris, whereas no significant change in the Q-T interval followed ergonovine administration in 27 control patients with atypical chest pain who did not have coronary spasm. T wave inversions in the resting electrocardiogram were normalized by isoproterenol infusion in one patient and by long-term phenoxybenzamine treatment in four patients with variant angina pectoris. These Q-T and T wave changes are analogous to those described with unilateral or asymmetric stellate ganglion stimulation in animals. These observations suggest that alterations in the sympathetic nervous system that are consistent with asymmetric stellate ganglion activity and transient alpha adrenergic receptor stimulation can presage the development of coronary arterial spasm in some patients with variant angina pectoris.

Adult↗
PubMedDate not supplied

Cardiac arrhythmias elicited by interaction between acute myocardial ischemia and sympathetic hyperactivity: a new experimental model for the study of antiarrhythmic drugs.

The choice of an adequate model for the study of antiarrhythmic drugs, relevant to the clinical problem of life-threatening arrhythmia, is a difficult and important task for contemporary cardiovascular pharmacology. Guided by pathophysiological considerations, we have designed an arrhythmia model in which ventricular tachyarrhythmias can be reproducibly elicited by combining the two clinically relevant stimuli of acute myocardial ischemia and augmented sympathetic activity. In anesthetized cats, following ablation of the right stellate ganglion, the left anterior descending coronary artery is occluded for 2 min. After 1 min of occlusion the left stellate ganglion is electrically stimulated for 30 s. In most experiments ventricular tachyarrhythmias, usually ventricular tachycardia or fibrillation, can be regularly elicited for six to eight trials. The consistency of the arrhythmic response allows an internally controlled study, since a drug may be administered after three trials under control conditions. This avoids the limitations due to individual variability of comparisons between groups. This model seems to be particularly well suited for preliminary evaluation, before final study in conscious animals, of drugs thought to have a protective effect against malignant arrhythmias associated with acute myocardial ischemia.

Animals↗
PubMed1979

Sympathetic control of major coronary artery diameter in the dog.

The diameter of a major coronary artery, the ramus interventricularis ventralis (RIV), was measured in dogs with arrested hearts perfused by an extracorporeal circulation. The resting diastolic diameter was 1.78 +/- 0.07 mm (mean +/- SE) at a diastolic pressure of 74.2 +/- 3.4 mm Hg. Bilateral supramaximal stimulation of fibers leaving the cranial pole of the stellate ganglion decreased the diameter by 71.2 +/- 8.9 micrometer, i.e., 4.0 +/- 0.5% of the resting diameter. Stimulation of the left stellate ganglion contributed 59.8 +/- 5.7% of the maximum response; that of the right contributed 40.3 +/- 5.5%. Stimulation of the thoracic ganglia (T2-4) resulted in a 1.2 +/- 0.4% decrease in coronary vessel diameter. RIV failed to respond to bilateral caudal cervical ganglion stimulation. After iv administration of phentolamine, 1-2 mg/kg, no response to sympathetic stimulation could be elicited. Therefore, it appears that alpha-receptors are activated by the release of the sympathetic neurotransmitter to sympathetic stimulation and that beta-receptors are not involved in the response of RIV to sympathetic stimulation.

Animals↗
PubMed1999

Neurofilament phosphorylation and axon diameter in the squid giant fibre system.

Electron energy loss spectroscopic analysis of squid giant axons in a phosphorus energy window yielded bright signals, which were shown to originate from highly phosphorylated neurofilaments. The frequency and distribution of these signals were analysed at defined intervals in cross-sections of the giant axon, starting from its origin in the stellate ganglion and extending distally along the stellar nerve. The analysis revealed a proximodistal gradient of increasing neurofilament phosphorylation. Within the stellate ganglion and for some distance beyond, the increase in frequency of signals correlated with the widening of the neurofilament meshwork and the radial growth of the axon. This agrees with the hypothesis that neurofilament phosphorylation regulates axon calibre by affecting interfilament spacing. In distal axon domains where the axon diameter diminished, contrary to expectations, the spacing of signals increased and the signals were significantly larger. Hyperphosphorylation apparently compensated for a diminishing supply of neurofilament protein. Contrary to predictions, the presynaptic terminal of the giant synapse contained a distinct and highly phosphorylated neurofilament meshwork. We conclude that the growth of the axon diameter is a function of neurofilament phosphorylation, interfilament spacing and neurofilament density. A mature and highly phosphorylated neurofilament cytoskeleton completely filled the presynaptic terminal of the giant synapse.

Animals↗
PubMed1982

Electrocardiographic alterations in subarachnoid haemorrhage. Correlation between spasm of the arteries of the left side on the brain and T inversion and QT prolongation.

In a retrospective study of 89 patients with subarachnoid haemorrhage (SAH), the frequency and specificity of changes in the electrocardiogram (ECG) were determined, as well as electrocardiographically established arrhythmias. The ECG changes were correlated with neurological as well as angiographic findings (localization of the aneurysm and vascular spasm). Abnormal ECGs were found in about 80% of the patients. The following abnormalities were found with decreasing frequency: depression and elevation of the ST segment, prolongation of the QT interval, flattening and inversion of the T wave, U waves and TU fusion waves, and arrhythmias (sinus tachycardia and bradycardia, extrasystole). A verified correlation (chi-square test) was shown between angiographically demonstrated spasm of the brain arteries of the left side and negative T waves as well as a prolongation of the QT interval. These results are related to the causal role of the left stellate ganglion in the generation of ECG changes and arrhythmias (animal experiments, and the success by blockade or surgical removal of the stellate ganglion in hereditary QT prolongation.

Adolescent↗
PubMed1984

Clonidine inhibits nicotinic effects in ganglia of the cholinergic-sympathetic system.

The electrodermal potential (EDP) recorded with surface electrodes between the palm and the shaven back of the forepaws of anaesthetized cats was taken as a measure of sudomotor activity in response to submaximal activation of cholinergic-sympathetic efferents with the nicotinic ganglionic stimulant DMPP. The intravenous injection of 30 micrograms/kg clonidine inhibited EDPs in despinalized cats and in vagotomized cats with chronic denervation of the stellate ganglion. In vagotomized cats clonidine (30 micrograms/kg i.v.) shifted the dose-response curve of DMPP (4-256 micrograms/kg i.v.) to the right. An inhibitory effect was also observed in despinalized cats upon topical application of 0.1 and 1 microgram clonidine to the stellate ganglion. In all preparations the inhibitory effect of clonidine could be antagonized by intravenous injection of 200 micrograms/kg yohimbine. As all substances used were also active when injected during arrest of blood flow to the foreleg by means of a tourniquet, actions at the level of the sweat gland could be excluded. The results lead to the conclusion that the activation of postsynaptic somadendritic alpha 2-adrenoceptors in sudomotor ganglia of the cholinergic-sympathetic nervous system inhibits the effects of nicotinic ganglionic stimulation. It is assumed that this action is due to the known ganglionic hyperpolarization induced by alpha 2-adrenoceptor stimulants.

Animals↗
PubMed1976

A histochemical investigation on mucopolysaccharides in the dog sympathetic ganglia.

A histochemical study in the dog Superior Cervical ganglion and in the Cervicothoracic or Stellate ganglion is reported. The mucopolysaccharide composition of these ganglia are studied by means of five histochemical techniques. The different histochemical composition between the neurons of these ganglia is investigated. In the sections stained with the PAS technique some neurons appeared more intensely stained than the others. With Thionin or Toluidine blue some neurones appeared more metachromatic than others. A peculiar distribution of the Nissl bodies, related with metachromasia, is reported. In sections stained with the Colloidal Iron method yellow neurons like those presented in the dorsal root ganglia were not found in the sympathetic ganglia. This fact suggests that the yellow neurons might be a different type of neuron. The possibility that the staining variations associated to the distribution of the Nissl bodies perhaps correspond to different functional states of the same type of neurons is also suggested.

Animals↗
PubMed1982

Interactions of catecholamine uptake inhibitors and norepinephrine on autonomic ganglia.

The effect of catecholamine uptake inhibitors on blockade by norepinephrine was observed in the isolated stellate ganglion of the hamster. The preganglionic nerve was stimulated, supramaximally, at 0.2 Hz and compound action potentials were recorded from the postganglionic nerve. Norepinephrine blocked ganglionic transmission. The sensitivity of the ganglion to norepinephrine was increased by the catecholamine uptake inhibitors, desipramine (3 X 10(-7) M), d-amphetamine (10(-6) and 10(-5) M) and tyramine (10(-4) M). Ouabain (10(-5) and 3 X 10(-5) M) did not change the sensitivity of the ganglion to norepinephrine. All the drugs reduced the uptake by the [3H]norepinephrine into the ganglion. The inhibition of [3H]norepinephrine uptake by the drugs could be correlated with the increase in sensitivity of the ganglion to norepinephrine. These results support the hypothesis that catecholamine uptake is important in terminating the actions of exogenously applied norepinephrine, and that inhibition of the catecholamine uptake increases the sensitivity of the ganglion to norepinephrine.

Animals↗
PubMed1990

Cardiac effects induced by chemically activated neurons in canine intrathoracic ganglia.

Regional or global cardiac responses were elicited when various chemicals were injected into discrete loci within acutely decentralized stellate and middle cervical ganglia. Nicotine (100 micrograms), acetylcholine (100 micrograms), or isoproterenol (1, 2, or 5 micrograms) in 1 microliters of normal saline was administered individually into 30 discrete loci within each stellate ganglion and 25 within each middle cervical ganglion. Cardiac augmentation was elicited when approximately 1 site per ganglion was injected with nicotine or acetylcholine. Similar injections into sites approximately 1-2 mm away from an active site usually failed to elicit cardiac responses. Isoproterenol elicited cardiac augmentations when injected into, on average, 3 different loci per ganglion. The responses elicited by isoproterenol injections were eliminated when the efferent sympathetic nerves arising from an injected ganglion were divided or when timolol maleate (0.1 mg/microliters normal saline) was previously injected into the same locus. These data indicate that the effects elicited by injecting isoproterenol into an intrathoracic ganglion locus were not due to leakage of this agent into the blood in sufficient quantities to directly activate cardiac myocytes. When L-glutamic acid (100 microliters of 1 M solution in normal saline) or L-aspartic acid (100 microliters of 1 M solution in normal saline) was injected into a stellate ganglion or middle cervical ganglion, positive chronotropic and/or inotropic responses were elicited. When DL-homocysteic acid (100 microliters of 1 M solution in normal saline) was administered no augmentation occurred. It is concluded that intrathoracic ganglion cardiac neurons can be activated by nicotinic or beta-adrenergic agonists, as well as by specific amino acids. These neurons are located throughout the stellate and middle cervical ganglia, cardiac neurons in one ganglionic locus being capable of activation by more than one of these chemicals.

Acetylcholine↗
PubMed1987

Reflex sympathetic dystrophy in a patient with pre-existing torsade de pointes.

A case is presented of a patient with pre-existing torsade de pointes who developed reflex sympathetic dystrophy. A trial of stellate ganglion blocks with ECG monitoring was instituted and the patient obtained relief. The pathophysiology of torsade de pointes is discussed with emphasis on the role of the stellate ganglion. Recommendations for management of similar patients are made.

Autonomic Nerve Block↗