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PubMed1981

Pain due to lesions of central nervous system removed by sympathetic block.

Eight patients were studied in whom a lesion within the central nervous system caused constant pain and hyperpathia. Blockade of the sympathetic supply to the periphery was carried out in each patient by stellate ganglion block or intravenous infusion of guanethidine 15 mg in 30 ml saline into a limb on the affected side. On almost every occasion the pain and hypersensitivity were reduced, sometimes completely. Thus chronic pain and hyperpathia arising from a lesion in the central nervous system may be abolished by blocking the sympathetic supply to the periphery; this effect may be achieved when not all the peripheral nerves of the affected region have had their sympathetic nerve supply blocked. Such blockade may be worth repeating in the hope of achieving lasting relief of the intractable pain.

Adult↗
PubMed1979

Chronotropic and dromotropic effects of histamine on the canine heart.

The actions of 2-methylhistamine (H1 agonists), 4-methylhistamine (H2 agonist), and histamine were studied by selective perfusion of the sinus node artery and atrioventricular node artery in 75 dogs anesthetized with pentobarbital sodium. 2-Methylhistamine and histamine had variable and inconsistent effects on the sinus rate. 4-Methylhistamine (100 microgram/ml) produced acceleration of the sinus rate from 158 +/- 4 to 173 +/- 5 beats per minute (P less than 0.05) when perfused via the sinus node artery. The effects of the histamine agonists on atrioventricular junctional rhythms were similar to the effects on sinus rhythm. The response of the sinus node to vagal stimulation was attenuated by selective perfusion with histamine; however, the direct negatively chronotropic action of acetylcholine was not affected by histamine. Neither 2-methylhistamine nor 4-methylhistamine affected the response of the sinus node to vagal stimulations. Both 4-methylhistamine and histamine (but not 2-methylhistamine) attenuated (P less than 0.05) the response of the sinus node to stimulation of the right stellate ganglion. The positively chronotropic effects of directly perfused norepinephrine were unaffected by histamine or 4-methylhistamine. These results suggest a neural depressing action of histamine on autonomic efferent fibers. In the atrioventricular junction, both histamine and 2-methylhistamine (but not 4-methylhistamine) had negatively dromotropic effects. Cimetidine (an H2 antagonist) had no significant direct effects on the sinus rate or atrioventricular conduction and failed to prevent the acceleration of the sinus rate produced by local perfusion with 4-methylhistamine.

Acetylcholine↗
PubMed1998

[Hyperbaric oxygenation therapy in idiopathic sudden sensory neural hearing loss].

We analyzed statistically the prognosis of hearing impairment in patients with idiopathic sudden sensory neural hearing loss. 119 patients (HBO group) were treated with a combination of hyperbaric oxygenation (HBO) and stellate ganglion block (SGB), as well as oral administration of vasodilator and vitamins. Another 107 patients (control group) were treated with various other therapies. Collectively, the therapeutic outcome in the HBO group was better than in the control group. In addition, the recovery rate of hearing in the HBO group was superior to that in the control group for those cases which had severe hearing loss at the first medical examination, had been seen more than two weeks after onset, and had resisted other treatments. As a result of this study, we conclude that HBO is an effective therapeutic tool.

Acute Disease↗
PubMed1975

Neurogenic influence on pulmonary surface tension and cholesterol in cats.

Previous work showed that stress involving the sympathetic nervous system via mechanical head injury and hyperbaric oxygen results in a decreased lung compliance and altered alveolar surfactants. Similar changes were associated with sympathetic nerve stimulation via the stellate ganglion. In view of reports that the minimum surface tension attained by lung wash fluid is increased by very small amounts of cholesterol content of the alveoli. The results show a nearly 200% increase in intra-alveolar cholesterol as well as high minimum surface tensions following sympathetic nerve stimulation. Such changes developed in the absence of any increase in lung wet wt/dry wt ratios. The results from the present study suggest that the previously reported decreased lung compliance and increased minimum surface tension associated with sympathetic stimulation may be due at least in part to contamination of the alveolar surfactants with large amounts of cholesterol.

Animals↗
PubMed1993

Sympathetic stimulation alters left ventricular relaxation and chamber size.

Alterations in left ventricular (LV) contractility, relaxation, and chamber dimensions induced by efferent sympathetic nerve stimulation were investigated in nine anesthetized open-chest dogs in sinus rhythm. Supramaximal stimulation of acutely decentralized left stellate ganglia augmented heart rate, LV systolic pressure, and rate of LV pressure rise (maximum +dP/dt, 1,809 +/- 191 to 6,304 +/- 725 mmHg/s) and fall (maximum -dP/dt, -2,392 +/- 230 to -4,458 +/- 482 mmHg/s). It also reduced the time constant of isovolumic relaxation, tau (36.5 +/- 4.8 to 14.9 +/- 1.1 ms). Simultaneous two-dimensional echocardiography recorded reductions in end-diastolic and end-systolic LV cross-sectional chamber areas (23 and 31%, respectively), an increase in area ejection fraction (32%), and increases in end-diastolic and end-systolic wall thicknesses (14 and 13%, respectively). End-systolic and end-diastolic wall stresses were unchanged by stellate ganglion stimulation (98 +/- 12 to 95 +/- 9 dyn x 10(3)/cm2; 6.4 +/- 2.4 to 2.4 +/- 0.3 dyn x 10(3)/cm2, respectively). Atrial pacing to similar heart rates did not alter monitored indexes of contractility. Dobutamine and isoproterenol induced changes similar to those resulting from sympathetic neuronal stimulation. These data indicate that when the efferent sympathetic nervous system increases left ventricular contractility and relaxation, concomitant reductions in systolic and diastolic dimensions of that chamber occur that are associated with increasing wall thickness such that LV wall stress changes are minimized.

Animals↗
PubMed1988

Delayed myocardial ischemia following the cessation of sympathetic stimulation.

A phenomenon entitled "delayed myocardial ischemia" has been described, in which there is a significant degree of coronary malperfusion following the cessation of behavioral stress. The primary objective of the present study was to develop a model for the delayed ischemic response in anesthetized animals to gain insights into the underlying mechanisms. In 15 morphine and chloralose-anesthetized dogs, a moderate degree of stenosis was applied to the left circumflex coronary artery by means of a toroidal balloon occluder. The pulsed Doppler technique was used to monitor coronary flow. After baseline data were obtained, the left stellate ganglion was stimulated for 30 seconds. Heart rate increased (63%), as did systemic blood pressure (41%) and flow in the left circumflex artery (47%). These parameters rapidly returned to control levels when stimulation was terminated. Forty-five to 90 seconds later, coronary flow decreased by 65% and coronary vascular resistance increased by 45%. These hemodynamic changes were accompanied by ECG abnormalities indicative of regional myocardial ischemia. The delayed ischemic response could be prevented by pretreatment with either nifedipine (20 micrograms/kg) or prazosin (0.3 mg/kg). These data indicate that the primary mechanism for the delayed ischemic response is alpha-adrenergically mediated contraction of the smooth muscle in the coronary artery wall.

Animals↗
PubMed1995

An unusual case of sympathetically maintained facial pain complicated by telangiectasia.

A 32-year-old woman with a history of maxillary sinusitis, multiple surgical interventions in the maxillary sinus, and a hyperalgesic, erythematous skin lesion in her left infraorbital area, had severe burning pain in the left face. The dermal lesion was diagnosed as atypical telangiectasia and the sinus pathoses determined to be unrelated to her symptoms. Two diagnostic stellate ganglion blocks were performed with concurrent bilateral monitoring of blood flow in the infraorbital skin. Blood flow was significantly increased in the painful erythematous patch although no significant change in flow occurred in the unaffected contralateral skin. The changes correlated to patient's relief from pain. The patient's symptoms were subsequently controlled with an oral sympatholytic agent. This article demonstrates the usefulness of laser doppler flowmetry to establish the diagnosis of sympathetically maintained facial pain despite several confounding conditions and supports the theory that sympathetically maintained pain involves altered function of alpha-1 adrenoreceptors.

Adult↗
PubMed1991

Effects of sympathetic and parasympathetic stimulation on the induction of atrial flutter in dogs with aseptic pericarditis.

To study the effects of sympathetic stimulation (SS) and vagal stimulation (VS) on the induction of atrial flutter (AF) and its cycle length, aseptic pericarditis was produced surgically in 17 adult mongrel dogs. Programmed atrial stimulation was used to induce AF and to determine the effective refractory periods (ERP) and maximum conduction delay (maxCD) of the atrium. These tests were performed before and during stimulation of the right cervical vagus nerve and the right stellate ganglion. Results showed: (1) AF could be induced in animals with short ERP and large maxCD before SS; (2) ERP was significantly shortened, maxCD was significantly increased by VS; (3) During SS, ERP was slightly shortened, but there were no changes in maxCD and the induction rate of AF; (4) The cycle length of AF was shortened by SS, however, the cycle length of AF was shortened more notably by VS than by SS. From these findings, a shortening of the ERP and an increase in maxCD appear to be related to an increased AF induction rate by VS.

Animals↗
PubMed1994

Sympathetic nerve influence on alveolar type II cell ultrastructure.

Pulmonary surfactant release from lamellar bodies in alveolar type II cells in response to exogenous and circulating catecholamines is well documented but sympathetic influences from direct nerve stimulation are not as extensively studied. In order to study sympathetic nerve influence on release, ultrastructure of type II cells was examined following one min stimulation of the stellate ganglion (SGS) which sends sympathetic fibers to lung parenchyma. The type II cell secretion was assessed by measuring volume density of lamellar bodies, interpreting decreased volume density to indicate increased secretion according to accepted stereologic principles. The present study showed lamellar body volume density was reduced 20.8% in type II cells of SGS animals. Multivesicular body volume density was increased 150% by SGS, but Golgi bodies were unchanged. These data are consistent with type II cell origin of at least some of the increased saturated phospholipid recovered from airspaces in previous SGS studies, and support the view that sympathetic nerve activity may contribute to surfactant homeostasis under some conditions.

Animals↗
PubMed1976

Central nervous system control of cardiac rhythm.

Stimulation of sites in the midbrain reticular formation and in the posterior hypothalamus of the cat resulted in a large to modest rise of arterial pressure and the induction of cardiac dysrhythmias. Most frequently, these arrhythmias developed upon cessation of brain stem stimulation but also occurred during the stimulus period in 5 of 23 cats studied. The arrhythmias disappeared upon cooling and reappeared upon rewarming the vagus nerves. The ventricular dysrhythmias also were abolished by methylscopolamine, by bilateral vagatomy, or by extirpation of the stellate ganglia. Simultaneous stimulation of both distal end of the cut right vagus nerve and the decentralized right stellate ganglion caused arrhythmias similar to those observed after diencephalic stimulation. These data are interpreted to indicate that the cardiac arrhythmias evoked by brain stem stimulation result from the interplay of both sympathetic and parasympathetic influences on the heart. The response patterns of a population of medullary neurons activated by carotid sinus nerve stimulation were modified by condition stimuli to posterior hypothalamic sites. From studies on unit activity of brain stem areas known to participate in cardiovascular adjustment, a schema is proposed of hypothalamic-medulla interaction as a central mechanism that may account for the development of ventricular arrhythmias.

Animals↗
PubMed1992

Interactive effects of verapamil and sympathetic nerve stimulation on the sinus and AV nodes in the canine hearts.

The interactive effects of verapamil and sympathetic nerve stimulation on the sinus and atrioventricular (AV) nodes were studied in 33 bilaterally stellectomized and vagotomized dogs. Sinus cycle length (SCL) and AV nodal conduction time (AH) at a constant drive cycle length (600 msec) were recorded. Sympathetic nerve stimulation (SNS) was performed for 40 sec by electrical stimulation of the right stellate ganglion. Several doses of verapamil (0.5-2.0 microgram/ml, 1.0 ml) were injected directly into the sinus and AV node arteries at 20 sec of SNS. In addition, SNS was repeated at two different intensities after verapamil administration. Verapamil significantly increased the SCL and the AH in a dose dependent fashion, which was reduced by SNS. The reductions of SCL and AH by the SNS were attenuated in the presence of verapamil when the stimulation intensity was weak, but not when the stimulation intensity was strong. It is concluded that verapamil and sympathetic nerve activity interact antagonistically on the sinus node automaticity and AV nodal conduction.

Animals↗
PubMed1996

[Imbalance of blood flow induced by sympathetic block was corrected by prostaglandin E1].

The purpose of this study was to investigate the effect of prostaglandin E2 (PGE1) on imbalance of blood flow induced by sympathetic block. Seven mongrel dogs were anesthetized with intravenous pentazocine 0.5 mg. kg-1, diazepam 0.1 mg. kg-1 and pancuronium 0.1 mg. kg-1. Bilateral brachial arterial blood flows were measured using an ultrasonic transit time flowmeter (Transonic T201, Advance). After a thoracotomy, left stellate ganglion block (SGB) with 0.5% mepivacaine was performed for sympathetic block. Left brachial arterial blood flow increased significantly by 80% 15 min after SGB, and statistically significant decrease (13%) in right brachial arterial blood flow occurred 15 min after left SGB. After intravenous infusion of PGE1 at a rate of 150 ng. kg-1. min-1 for 10 min, left brachial arterial blood flow increased (127%) still, and right brachial arterial blood flow returned to the pre-value. As to peripheral circulation, a combination of SGB and intravenous infusion of PGE1 was more effective than SGB alone. Moreover, the administration of PGE1 may improve imbalance of blood flow induced by sympathetic block.

Alprostadil↗
PubMed1976

Periaortic denervation in reconstructive surgery of coronary vessels.

Stimulation of sympathetic nervous conductive pathways and ganglia innervating the heart leads to a sudden increase in the cardiac performance and to a qualitative change in the phasic blood flow within the coronary vascular bed. This so-called malignant increase in the blood flow is accompanied by relative coronary insufficiency and increased mechanical stress imposed upon the coronary arteries. A denervation operation according to Arnulf does not prevent the propagation of excitation from the right stellate ganglion to the heart. A complete denervation is obtained by additional cutting of the right-side postganglional fibres. Then in a dog no changes occur in the coronary arterial blood flow measured at rest during the operation. In reconstructive surgery of coronary vessels in man, after denervation the peroperative blood flow in the aortocoronary bypass to the anterior interventicular branch increases. After a surgical denervation operation, the prevention of propagation of sudden neurogenic stimuli via the cervical sympathetic segment to the heart ventricles is the most striking result. Such a "protection" of the heart might retard the development rate of coronary insufficiency accompanying the ischaemic heart disease.

Animals↗
PubMed1984

Distribution of acid protease activity in the squid nervous system.

Acid protease activity was measured in homogenized stellate ganglion, axoplasm extruded from the squid giant axon, homogenized fin nerves, and in lysed synaptosomes prepared from the optic lobe of the squid. At least two different acid protease classes were distinguished on the bases of their inhibitor profiles. Acid protease activity was present in each of the above tissues except extruded axoplasm. This result suggests that the acid protease activity found in our homogenized fin nerves might be located not within the axons but rather in glial cells or extracellular tissue. The absence of acid protease activity in extruded axoplasm indicates that acid proteases are unlikely to play a significant role in the catabolism of intracellular proteins along the length of the axon.

Animals↗
PubMed1993

Amino acid sequence of a putative sodium channel expressed in the giant axon of the squid Loligo opalescens.

A full-length cDNA encoding a putative Na+ channel (GFLN1) has been cloned from a library prepared from the stellate ganglion of Loligo opalescens. The cDNA encodes a predicted protein of 1784 amino acids. Regions of the GFLN1 protein with defined functional importance (membrane span S4, the SS1 and SS2 segments, and interdomain III-IV) are highly conserved among all vertebrate Na+ channel alpha-subunit structures. Northern blot hybridization and RNase protection assays verify that mRNA corresponding to GFLN1 is expressed in neurons of the giant fiber lobe that form the giant axon. We propose that GFLN1 encodes the Na+ channel that has been extensively studied in the squid axon.

Amino Acid Sequence↗
PubMed2001

Sympathetic blockade for the relief of chronic pain.

The sympathetic blocks are useful in many ways for relief of chronic pain. The sympathetic block can be caused at pre- and paravertebral sympathetic ganglia eg, stellate ganglia, coeliac plexus and lumbar sympathetic ganglia. Indications for sympathetic blockade are: Complex regional pain syndrome, phantom limb pain, central pain, acute pancreatitis, pancreatic cancer and cancer pain from upper abdominal viscera. Stellate ganglion blockade is required for the diagnosis, prognosis and therapy for painful and other conditions associated with sympathetic dysfunctions of head, neck and upper extremity. Coeliac plexus block is indicated in pain due to intra-abdominal cancer, stemming from organs innervated by coeliac plexus. Lumbar sympathetic block is indicated for diagnosis, prognosis and therapy for painful and other conditions associated with sympathetic dysfunctions like complex regional pain syndrome I and II, herpes zoster, amputation stump pain and inoperable peripheral vascular vasospastic diseases of the lower limb. Indications for superior hypogastric block are the prognostic and therapeutic purposes of cancer pelvic organs--uterus, cervix, bladder, prostate, urethra, testes and ovaries.

Anesthetics, Local↗
PubMed2000

Reserpine attenuates interstitial adenosine-mediated activation of ecto-5'-nucleotidase in rat hearts in vivo.

We examined whether reserpine-induced norepinephrine (NE) depletion attenuated the products of adenosine in rat heart. A flexibly mounted microdialysis technique was used to measure the concentration of interstitial adenosine and to assess the activity of ecto-5'-nucleotidase in rat hearts in situ. The microdialysis probe was implanted in the left ventricular myocardium of anesthetized rats and perfused with Tyrode solution containing adenosine 5'-monophosphate (AMP) at rate of 1.0 microliter/min. The baseline level of dialysate adenosine was 0.51 +/- 0.09 microM. The introduction of AMP (100 microM) through the probe increased markedly the dialysate adenosine to 8.95 +/- 0.86 microM, and this increase was inhibited by ecto-5'-nucleotidase inhibitor, alpha, beta-methyleneadenosine 5'-diphosphate (AOPCP, 100 microM), to 0.66 +/- 0.38 microM. Thus, the level of dialysate adenosine is a measure of the ecto-5'-nucleotidase activity in the tissue in situ. AMP concentration for the half-maximal effect of adenosine release (EC(50)) was 107.3 microM. The maximum attainable concentration of dialysate adenosine (E(max)) by AMP was 21.1 microM. However, the EC(50) and E(max) values with reserpinized animals were 106.9 and 7.1 microM, respectively. Electrical stimulation of the left stellate ganglion increased significantly dialysate adenosine concentration, from the control level of 8.66 +/- 0.96 microM to 12.38 +/- 1.11 microM. After stimulation, dialysate adenosine returned to near the prestimulation level. When corresponding experiments were performed with reserpinized animals, the effect of electrical stimulation was abolished. Tyramine (endogenous catecholamine trigger) increased the adenosine concentration in a concentration-dependent manner. However, the elevation of adenosine concentration with reserpinized animals was not observed. These results suggest that reserpine attenuates NE-induced adenosine via stimulation of alpha(1)-adrenoceptor and protein kinase C mediated activation of ecto-5'-nucleotidase in rat heart.

5'-Nucleotidase↗
PubMed1979

Pulmonary hemodynamic responses to elevated cerebral spinal fluid pressure in the dog.

To investigate the possibility that a pulmonary vasomotor reflex contributes to the pulmonary hemodynamic response to elevated cerebral spinal fluid pressure (PCSF), we studied 10 chloralose-anesthetized dogs in which the left lower lobe (LLL) perfusion was isolated to eliminate the influence of passive factors and of circulating vasoactive agents. Left lower lobe neural integrity was tested by electrically stimulating the stellate ganglion. This resulted in a 35.5% increase in lobar vascular resistance and a 29.1% increase in systemic vascular resistance. Elevating the PCSF to 137 Torr caused the systemic vascular resistance to increase 33.0%, but resulted in no change in LLL vascular resistance. In the intact right lung, this PCSF elevation resulted in increases in pulmonary artery and left atrial pressures, but no change in right lung vascular resistance. Because the neurally intact LLL did not respond to PCSF elevation and the responses of the right lung could be accounted for by passive mechanisms, we conclude that no pulmonary vascular reflex was elicited by PCSF elevation in this preparation.

Animals↗