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Antinociceptive effect of linear polarized 0.6 to 1.6 microm irradiation of lumbar sympathetic ganglia in chronic constriction injury rats.

Linear polarized near-infrared light created with linear polarized near-infrared light therapy equipment (Super Lizer HA-550, Tokyo Iken Co, Ltd, Tokyo, Japan) has been used for the treatment of various painful disorders in Japan. Irradiation near the stellate ganglion with a Super Lizer (ISGL) is an especially notable therapeutic method used with stellate ganglion block (SGB) or substitutes for SGB. ISGL is a safe, simple, well-tolerated, and effective treatment. We examined the effects of irradiation with a Super Lizer applied to an area near the lumbar sympathetic ganglia on the ligated side in a chronic constriction injury (CCI) model, which is believed to be an animal model of complex regional pain syndrome (CRPS). Rats showing thermal hyperalgesia in a radiant heat test 1 wk postoperatively were used in Experiments 1 and 2: (1) Thermal hyperalgesia of irradiation group (n = 11) was less than that of the control or nonirradiation (n = 11) group at 1, 3, and 8 h after irradiation; however, the effect disappeared 12 h after irradiation. (2) Daily irradiation (n = 16) and 1 wk (n = 14) from 7 days after nerve ligation significantly shortened the interval from thermal hyperalgesia until recovery. Rats showing mechanical hyperalgesia in the von Frey hair test 1 wk postoperatively were used in Experiment 3: 1 wk irradiation beginning 7 days after nerve ligation (n = 9) did not promote the recovery from mechanical hyperalgesia. We speculate that repeated ISGL may be more effective than a single ISGL in alleviating pain in CRPS patients. We cannot explain the discrepancy between the results obtained in Experiments 2 and 3. We believe the results of this study are relevant to the effect of ISGL for patients with upper-limb CRPS: irradiation near the lumbar sympathetic ganglia of the rat is effective for thermal but not mechanical pain in CCI.

Animals↗

Responses of medullary raphespinal neurons to electrical stimulation of thoracic sympathetic afferents, vagal afferents, and to other sensory inputs in cats.

1. Medullary raphespinal neurons antidromically activated from the T2-T5 segments were tested for responses to electrical stimulation of cervical vagal and thoracic sympathetic afferents (by stimulating the left stellate ganglion), somatic probing, auditory stimuli, and visual stimuli in cats anesthetized with alpha-chloralose. A total of 99 neurons in the raphe nuclei were studied; the locations of 76 cells were histologically confirmed. Neurons were located in raphe magnus (RM, 65%), raphe obscurus (RO, 32%), and raphe pallidus (RPa, 4%). The mean conduction velocity of these neurons was 62 +/- 2.9 (SE) m/s with a range of 1.1-121 m/s. 2. A total of 60/99 tested neurons responded to electrical stimulation of sympathetic afferents. Quantitation of responses was obtained for 55 neurons. With one exception, all responsive neurons were excited and exhibited an early burst of spikes with a mean latency of 16 +/- 1.2 ms. From a spontaneous discharge rate of 5.2 +/- 1.2 spikes/s, neuronal activity increased by 2.9 +/- 0.3 spikes/stimulus. In addition to an early peak, 15 neurons (25%) exhibited a late burst of spikes with a latency of 182 +/- 12.9 ms; neuronal activity increased by 5.0 +/- 1.3 spikes/stimulus. Duration of the late peak (130 +/- 18.5 ms) was longer than for the early peak (18 +/- 0.7 ms), but threshold voltages for eliciting each peak were comparable. Sixteen of 29 spontaneously active neurons exhibited a postexcitatory depression of activity that lasted for 163 +/- 19.1 ms. All but one tested neuron in RO responded to stimulation of sympathetic afferents, but 65% of neurons in RM responded to this stimulus. 3. In response to vagal afferent stimulation, 19% of 57 neurons exhibited inhibition only, 11% were only excited, and 9% were either excited or inhibited, depending on the stimulus paradigm used; the remaining 61% of neurons were unresponsive. From a spontaneous rate of 7.9 +/- 3.8 spikes/s, excited cells increased their discharge rate by 1.6 +/- 0.3 spikes/stimulus. Activity of inhibited cells was reduced from 21.3 +/- 5.8 to 7.8 +/- 3.1 spikes/s. The conditioning-test (CT) technique was used to assess 11 neurons' responses. Stellate ganglion stimulation was the test stimulus, and vagal stimulation the conditioning stimulus. Vagal stimulation reduced the neuronal responses to stellate ganglion stimulation by an average of 50% with a CT interval of 60-100 ms, and cell responses returned to control after 300 ms. With spontaneous cell activity, low frequencies of vagal stimulation were generally excitatory, and high frequencies (10-20 Hz) inhibitory.(ABSTRACT TRUNCATED AT 400 WORDS)

Acoustic Stimulation↗

Localization of the reflex pathway responsible for the vasodepressor reaction induced by inferior vena caval occlusion and isoproterenol.

Vasodepressor reactions were induced in 27 rats by a combination of inferior vena caval occlusion and an infusion of isoproterenol. A vasodepressor reaction was defined as paradoxical heart rate slowing during inferior vena caval occlusion. The R-R intervals were measured at 5-s intervals before, during, and after 60 s of inferior vena caval occlusion. The purpose of this study was to examine the role of the right and left vagus nerve and the right and left stellate ganglia in this reflex. Under control conditions inferior vena caval occlusion accelerated the rate (R-R, -15.9 +/- 0.9 ms). During an infusion of isoproterenol (0.5-1.0 micrograms.min-1), inferior vena caval occlusion produced paradoxical rate slowing, i.e., a vasodepressor reaction (R-R, +75.0 +/- 2.2 ms). The vasodepressor reaction was examined during inferior vena caval occlusion and isoproterenol under the following additional states: atropine methyl bromide or right vagotomy did not alter the reaction; left vagotomy eliminated the reaction; and right or left stellectomy greatly reduced the vasodepressor reaction. We conclude the following: (1) left vagal afferents mediate the vasodepressor reaction; (2) cardiac sympathetic fibers participate in the vasodepressor reaction by withdrawing efferent tone through the right stellate ganglion, and by generating the afferent signal, which triggers the vasodepressor reaction through the left stellate ganglion.

Animals↗

Ulnar artery thrombosis: a 6-year experience.

Thrombosis of the ulnar artery can be a cause of significant morbidity. Most often a consequence of blunt trauma to the hypothenar eminence of the hand, it may be attributable to one traumatic event or to repetitive insults. Surgery is often required. We reviewed the presentation and diagnosis of ulnar artery thrombosis and evaluated the effectiveness of treatment by ulnar artery excision with interposition vein grafting. Retrospective chart analysis from 1989 to 1995 at the Medical Center of Central Georgia showed that nine patients (eight male, one female) were treated for ulnar artery thrombosis. Three had associated ulnar artery aneurysms. Eight of the nine were treated with artery excision and interposition vein grafting. Four also received stellate ganglion blocks before surgery. One was treated with stellate ganglion blocks alone. All patients had symptomatic relief and resolution of physical findings. We conclude that ulnar artery thrombosis can be managed with ulnar artery excision and interposition vein grafting when conservative measures fail.

Adolescent↗

[Sympathetic regulation of heart rhythm under the effect of delta sleep peptide and its deficiency].

In acute experiments on 16 rabbits we've studied effects of delta-sleep peptide and its deficiency on the irritation of the stellate ganglion. It has been revealed, that peptide injection (60 nM/kg) produces lowered positive chronotropic effect and elongated response development during irritation of this ganglion. Administration of antiserum to delta-sleep peptide (T = 1:3000) causes opposite effect: enhances sympathetic response during irritation of the stellate ganglion. Thus, delta-sleep peptide promoted lowered sympathetic influences on the heart.

Animals↗

Sympathetic innervation of the young canine heart using antero- and retrograde axonal tracer methods.

The present study was performed to determine the origin of cardiac sympathetic postganglionic fibers and to demonstrate their distribution in the heart. Young dogs were used in this study. Wheat germ agglutinin-horseradish peroxidase (WGA-HRP) was injected into various regions of the heart, and cholera toxin B subunit (CTB) and WGA-HRP were injected into the middle cervical ganglion or the stellate ganglion. In our retrograde axonal transport study, a large number of WGA-HRP-labeled cells were observed in the middle cervical and stellate ganglia bilaterally. Only a small number of the labeled cells were observed in the superior cervical ganglia bilaterally. In the anterograde axonal transport study, CTB and WGA-HRP labels showed terminal-like structures in the intrinsic ganglia located in the sinoatrial node, left atrium, and the origin of the ascending aorta. The labeled fibers were also observed around the coronary arteries.

Animals↗

Complications of quinine poisoning.

Of 165 patients admitted to hospital with acute quinine poisoning 70 (42%) had visual symptoms. 19 were left with a permanent visual deficit, though none was left completely blind. 5 patients died. Bilateral stellate ganglion block was carried out on 34 patients with impaired visual acuity or blindness, but an improvement of symptoms was reported in only 4 cases. It is concluded that stellate ganglion blockade is not effective enough to justify its regular use in quinine-induced amblyopia. Quinine overdose can have serious consequences, and the drug should not be prescribed indiscriminately.

Acute Disease↗

[The long Q-T syndrome without Q-T prolongation (author's transl)].

Case description of a 30 year-old woman with recurrent attacks of symptomatic ventricular tachyarrhythmias but without Q-T prolongation in the electrocardiogram. All conventional antiarrhythmic agents failed to suppress the arrhythmia and electrical defibrillation had to be carried out 99 times. Blockade of the left stellate ganglion with lidocaine followed by stellectomy led to successful control of the dangerous rhythm disturbance for a follow-up period of 1.5 years. As in patients with the classical long Q-T syndrome stellate ganglion blockade and stellectomy might be indicated in cases with the so called latent Q-T syndrome and life threatening ventricular arrhythmias resistant to antiarrhythmic agents.

Adult↗

Treatment of sudden sensorineural hearing loss with a continuous epidural block.

The efficacy of a continuous epidural block was evaluated in the treatment of 20 patients with sudden sensorineural hearing loss (SNHL). Ten patients were treated with continuous cervicothoracic epidural block (group A) and the other 10 were treated with stellate ganglion block (group B). No significant difference in factors affecting prognosis was noted between the groups. In the epidural block group 70% achieved substantial hearing improvement, while this occurred in only 30% of patients undergoing stellate ganglion block. These findings suggest that continuous epidural block can be effective in the treatment of sudden SNHL.

Adult↗

Influence of reduced presynaptic myocardial norepinephrine stores on left ventricular contractility.

Many investigators have reported that myocardial norepinephrine content is decreased in congestive heart failure. However there have been no studies of how decrease in myocardial norepinephrine might influence myocardial contraction. To clarify whether decreased myocardial norepinephrine per se affects myocardial contraction, we observed the change in left ventricular contractility during 30 min of left stellate ganglion stimulation in control and acutely reserpinized dogs. We obtained left ventricular max dp/dt and left ventricular end-systolic pressure-segment length relationships as indicators of left ventricular contractility. Both parameters decreased after left stellate ganglion stimulation in reserpinized dogs (left ventricular max dp/dt: 2064 +/- 200 to 1608 +/- 168 mmHg/s, left ventricular end-systolic pressure-segment length slope 117 +/- 22 to 79 +/- 14 mmHg/mm, n = 8, P less than 0.05), while they did not change in controls. In reserpinized dogs, left ventricular norepinephrine content decreased to one-third that of controls before the stimulation, and further decreased after stimulation. These data indicate that lowered myocardial norepinephrine itself may be responsible for the negative effect on left ventricular contractility in congestive heart failure.

Animals↗

Stellate block for trigeminal zoster.

Stellate ganglion block for relief of pain and prevention of ophthalmic complications in trigeminal herpes zoster has been advised for many years. In a series of 27 patients, control of pain was dramatic after local anesthetic block of the stellate ganglion. This report is presented to stimulate renewed interest in this old form of therapy. Because of the retrospective nature of this investigation, the lack of adequate numbers and the absence of controls, no conclusions on efficacy of treatment can be made. However, enough hope of success is presented to justify a controlled series in a large metropolitan area where adequate numbers of patients can be accumulated for a double-blind protocol.

Bupivacaine↗

Ganglionic blockade by d-amphetamine.

The actions of d-amphetamine on ganglionic transmission in the isolated stellate ganglion of the hamster were observed. Blockade of the compound action potential by d-amphetamine had a slow onset with an onset half-time of 2-5 min. The concentration-blockade relationship for d-amphetamine was not shifted by phentolamine (10(-5) M) or propranolol (10(-6) M). The blockade was frequency-dependent, and the frequency-dependence was suppressed by atropine (10(-6) M). It was suggested that the frequency-dependence of d-amphetamine involved a muscarinic mechanism. In support of this suggestion, the afterdischarges from repetitive stimulation in hexamethonium were relatively insensitive to d-amphetamine. Also afterdischarges could be recorded after repetitive stimulation in 10(-4) M d-amphetamine, without hexamethonium. High concentrations of d-amphetamine (10(-3) M) induced discharges in the postganglionic nerve and potentiated the discharges from the cholinergic agonists, DMPP and McN-A-343. Tolerance rapidly developed to these stimulatory effects. These results indicate that ganglionic blockade by d-amphetamine is produced by a different mechanism than ganglionic blockade by the catecholamines.

Action Potentials↗

Autonomic innervations in the middle ear and pharynx.

Autonomic innervations of the mucosa in the middle ear and pharynx were investigated by retrograde labelling of the autonomic ganglia with horseradish peroxidase (HRP). Of the sympathetic ganglia, the superior cervical ganglion (SCG), middle cervical ganglion (MCG) and stellate ganglion (StG) were examined, and of the parasympathetic ganglia, the pterygopalatine ganglion (PpG) and the otic ganglion (OtG) were examined. Sympathetic innervation of the middle ear mucosa was accomplished by fibers originating in the ipsilateral SCG, but not by those originating in the MSG or StG. Parasympathetic innervation was by fibers originating in the ipsilateral PpG, but not by those originating in the OtG. The epipharynx received sympathetic innervation from the ipsilateral SCG, but not from the MCG or StG. Its parasympathetic innervation was from the PpG bilaterally, but not from the OtG. Sympathetic innervation of the mesopharynx was supplied by the SCG, MCG and StG, but no parasympathetic supply came from the PpG or the OtG. Sympathetic innervation was bilateral, but predominantly from the ipsilateral side. The hypopharynx resembled the mesopharynx, but had more innervation from the MCG and StG.

Animals↗

[Sympathetic innervation in the larynx of cats].

The site of origins, peripheral courses and intramucosal distribution of the sympathetic post-ganglionic nerve fibers supplying to the larynx were investigated by means of wheat germ agglutinin-horseradish peroxidase (WGA-HRP) and Falck-Hillarp method in 51 cats. The cervical sympathetic ganglia which send the postganglionic fibers to the larynx were the superior cervical ganglion (SCG), middle cervical ganglion (MCG), and stellate ganglion (SG). Location of MCG was at the bifurcation of the cervical sympathetic trunk, rostrally to the point of its crossing with the subclavian artery. After WGA-HRP injection, labeled sympathetic nerve fibers were observed mainly in the wall of the blood vessels and around the laryngeal glands of the posterior and caudal parts of the larynx. Labeled fibers originated from SCG were seen in the mucosa of the arytenoid region and posterior glottis ipsilaterally. Both the internal and external branches of the superior and inferior laryngeal nerves contained the postganglionic fibers from SCG. Labeled nerve fibers from MCG were recognized in the ipsilateral mucosa of the glottis and subglottis and were also contained in the internal and external branches of the superior and the inferior laryngeal nerves. Labeled sympathetic nerve fibers from SG appeared in the mucosa caudal to the first tracheal ring. The pattern of distribution of labeled sympathetic nerve fibers revealed by WGA-HRP technique coincided with that of the noradrenergic fibers stained by Falck-Hillarp method.

Adrenergic Fibers↗

Subpopulations of sympathetic neurons project to specific vascular targets in the pinna of the rabbit ear.

We have characterised sympathetic neurons projecting to a range of cutaneous and striated muscle vascular targets in the pinna of the rabbit ear by examining neurotransmitter-related enzymes and peptides in perivascular axons and in somata identified by retrograde axonal tracing. Fast Blue was injected into one of seven sites in each pinna (n = 21 pinnae). The soma cross-sectional area and immunoreactivity (IR) for tyrosine hydroxylase (TH) and neuropeptide Y (NPY) were determined for each of 2,041 retrogradely labelled neurons in the ipsilateral superior cervical ganglion (SCG) or stellate ganglion (StG). Larger neurons in the SCG with TH-IR but not NPY-IR projected predominantly to veins along the medial edge of the pinna. Larger neurons in the StG with TH-IR but not NPY-IR projected predominantly to arteries and veins in the tip and lateral edge of the pinna. Smaller neurons in the SCG with IR to both TH and NPY projected predominantly to arteries in the striated muscles at the base of the ear. The smallest retrogradely labelled neurons in the SCG or StG lacked TH-IR but contained NPY-IR and projected almost exclusively to arterial vessels in the lateral muscle at the base of the ear. Thus, somata of sympathetic neurons projecting to cutaneous versus striated muscle vessels or to different regions of the cutaneous bed could be distinguished by a combination of location, size, and immunohistochemical profile. Consequently, regulation of blood flow within the rabbit ear is likely to involve coordination between neuronal pathways containing neurochemically and morphologically distinct populations of sympathetic neurons.

Animals↗

[Presynaptic regulation of co-release of neuropeptide Y and noradrenaline induced by electrical stimulation of the sympathetic nerve in guinea pig heart].

In the present study, co-release of noradrenaline and neuropeptide y (NPY) evoked by electrical stimulation of the left stellate ganglion, was investigated in the in situ perfused guinea pig heart with intact sympathetic innervation, a model modified from Legendorff technique. Endogenous noradrenaline was measured by HPLC and endogenous NPY was determined by RIA. Electrical stimulation of the left stellate ganglion (4, 8, 12 and 50 Hz) evoked a calcium-dependent and frequency-related overflow of noradrenaline and NPY. The release of both transmitters was positively correlated (r = 0.83, p less than 0.001). When two subsequent stimulations were performed in the same heart, adding exogenous noradrenaline before the second stimulation reduced NPY overflow on the contrary, and NPY decreased the overflow of noradrenaline. The stimulated release of noradrenaline and NPY was increased by the alpha 2-adrenergic receptor antagonist yohimbine, and attenuated by the alpha 2-adrenergic receptor agonist B-HT 920, respectively. The adenosine analogue cyclohexyladenosine significantly reduced co-release of noradrenaline and NPY. Blocking the uptake of NA with despramine or Nisoxetine significantly increased noradrenaline overflow, however, NPY release was markedly reduced. We concluded that electrical stimulation can induce calcium-dependent co-release of noradrenaline and NPY, and this co-release of both transmitters is modulated by presynaptic alpha 2-adrenoceptors.

Animals↗

Modulation of QT interval by cardiac sympathetic nerve sprouting and the mechanisms of ventricular arrhythmia in a canine model of sudden cardiac death.

INTRODUCTION: We previously reported that there is a high incidence of sudden cardiac death (SCD) in dogs with myocardial infarction (MI), complete AV block (CAVB), and nerve growth factor (NGF) infusion to the left stellate ganglion (LSG). Whether or not QT interval prolongation underlines the mechanism of SCD was unclear. METHODS AND RESULTS: We analyzed QT intervals in three groups of dogs. All dogs had CAVB and MI. The LSG group (n = 9) and right stellate ganglion (RSG) group (n = 6) received NGF infusion via the osmotic pumps over a 5-week period to LSG and RSG, respectively. The control group (n = 6) received no NGF. The dogs either died suddenly or were sacrificed within 2 to 3 months after MI. Heart rhythm and QT and RR intervals were monitored using implantable cardioverter defibrillator ECG recordings. There was a time-dependent increase of QTc intervals in the LSG group and a time-dependent decrease of QTc intervals in the RSG group. At the end of NGF infusion, QTc intervals in the LSG group (408 +/- 41 msec) were significantly longer than those in the control (350 +/- 41 msec; P < 0.05) and RSG groups (294 +/- 23 msec; P < 0.01). In the LSG group, 4 of 9 dogs died of SCD. There was no SCD in either the RSG or control group. Immunocytochemical staining showed NGF infusion to LSG and RSG resulted in left and right ventricular sympathetic nerve sprouting and hyperinnervation, respectively. CONCLUSION: NGF infusion to the LSG in dogs with MI and CAVB resulted in increased QT interval and incidence of ventricular tachycardia, ventricular fibrillation, and SCD, whereas NGF infusion to the RSG shortened QT interval and reduced the incidence of ventricular tachycardia. These findings indicate that QT interval prolongation is causally related to the occurrence of ventricular arrhythmia in dogs with nerve sprouting, MI, and CAVB.

Animals↗

[The role of humoral factors in the pathogenesis of the postoperative syndrome].

Blood plasma levels of "pain substances" (serotonin, histamine, prostaglandin F2 alpha, adrenaline /A/) and neuropeptides (beta-endorphin, somatostatin) have been evaluated in 39 patients during the early postoperative period after lung and mediastinum surgery. The studies have shown that the content of these biologically active substances increases considerably. Following stellate ganglion blockade A concentration decreased significantly, the uptake of narcotic analgesics used for postoperative analgesia reduced 1.7-fold, however the levels of "pain substances" and neuropeptides remained unchanged. It is believed that postoperative pain syndrome develops due to the elevation of the levels of the substances under study. Stellate ganglion blockade produces only sympatholytic effect, which shows the necessity of the elaboration of drug therapeutic techniques blocking "pain" receptors and using "pain substance" antagonists.

Adolescent↗