Stimulation Of Superior Cervical Ganglion Research Articles

Novel endovascular transmural technique for pharmacological block of superior cervical ganglion prevents sympathetic-mediated cerebral vasospasm

BackgroundSympathetic-mediated vasoconstriction from the superior cervical ganglion (SCG) is a significant contributor to cerebral vasospasm. Inhibition of the SCG has been shown to improve cerebral blood flow and reverse cerebral...

Sympathetic nervous system hyperactivity results in potent cerebral hypoperfusion in swine.

Cerebral vasospasm is a complex disease resulting in reversible narrowing of blood vessels, stroke, and poor patient outcomes. Sympathetic perivascular nerve fibers originate from the superior cervical ganglion (SCG) to innervate the cerebral vasculature, with activation resulting in vasoconstriction. Sympathetic pathways are thought to be a significant contributor to cerebral vasospasm. We sought to demonstrate that stimulation of SCG in swine can cause ipsilateral cerebral perfusion deficit similar to that of significant human cerebral vasospasm. Furthermore, we aimed to show that inhibition of SCG can block the effects of sympathetic-mediated cerebral hypoperfusion. SCG were surgically identified in 15 swine and were electrically stimulated to achieve sympathetic activation. CT perfusion scans were performed to assess for changes in cerebral blood flow (CBF), cerebral blood volume (CBV), mean transit time (MTT) and time-to-maximum (TMax). Syngo.via software was used to determine regions of interest and quantify perfusion measures. SCG stimulation resulted in 20-30% reduction in mean ipsilateral CBF compared to its contralateral unaffected side (p<0.001). Similar results of hypoperfusion were seen with CBV, MTT and TMax with SCG stimulation. Prior injection of lidocaine to SCG inhibited the effects of SCG stimulation and restored perfusion comparable to baseline (p>0.05). In swine, SCG stimulation resulted in significant cerebral perfusion deficit, and this was inhibited by prior local anesthetic injection into the SCG. Inhibiting sympathetic activation by targeting the SCG may be an effective treatment for sympathetic mediated cerebral hypoperfusion.

Selective Peripheral Chemoreceptor Hyperreflexia Evoked after Sympathetic Stimulation

Previous studies have demonstrated that the integrity of the carotid bodies is essential for the development and maintenance of hypertension. In this condition, both increased tonicity and hyperreflexia are displayed by chemosensitive neurons in the petrosal ganglia of spontaneous hypertensive rats (SHR). However, what drives carotid body hyper‐excitability is not known. We hypothesised this was triggered by the sympathetic nerves innervating the carotid body, which originate from the superior cervical ganglion (SCG). The aim of our study was test if activation of the SCG could modulate carotid body activity. Experiments were carried out in 6 juvenile Wistar rats (60–80g) using the decerebrated in situ working heart‐brainstem preparation (WHBP). Simultaneous recordings of phrenic (PN) and thoracic sympathetic nerves (tSNA) were obtained using glass suction electrodes. Heart rate (HR) was derived from the electrocardiogram (ECG). Chemoreflex was activated using NaCN (50μL, 0.04%, i.a.) and the SCG was stimulated electrically (ES; 30Hz, 2 ms, 10V) using a Grass SD9 stimulator via a bipolar microelectrode. The chemoreflex was evoked before and immediately after ES of the SCG. Changes in sympathetic activity, perfusion pressure, phrenic and heart rate were analysed quantitatively. Data are displayed as mean ± SEM with a level of significance set at P&lt;0.05; differences were tested using paired student‐t test.The only component of the chemoreflex augmented by SCG stimulation was the evoked increase in sympathetic activity. In Wistars, the control response of 29.3 ± 3.2% from baseline was augmented to 46.04 ± 3.58% after ES (P=0.006). Within 10 min of the stimulation, the sympatho hyperreflexia had returned to control (20.24 ± 5.96%). SHR also presented sympatho hyperreflexia (43.0 ± 6.3 vs 62.9 ± 9.2 %, P= 0.015) but the change of sensitization was of similar magnitude between rat strains. The SCG induced carotid body hyperreflexia was prevented by application of lignocaine into the SCG. We conclude that stimulation of the efferent sympathetic nerves innervating the carotid body can increase the gain of the chemoreflex symathoexcitatory response. We are currently assessing whether chemoreflex hyperreflexia observed in neurogenic hypertension is mediated by sympathetic nerves innervating the carotid body.Support or Funding InformationHealth Research Council of New Zealand

(192) The Impact of Stress and Sex on Sympathetic Regulation of Dural Vessel Tone

Migraine is a common, disruptive, and often debilitating neurological disorder that the World Health Organization classifies in the highest disability category. Migraine is up to three times more common in women than men. Attacks are commonly triggered by stress, and many migraineurs show signs of sympathetic dysregulation. While the vascular hypothesis for migraine has largely fallen from favor, there are still several lines of evidence to suggest that dysregulation of the dural vasculature may contribute to the initiation of a migraine attack. These include the evidence that migraine pain arises from dural nociceptors, that the dural vasculature is heavily innervated by both nociceptors and sympathetic post-ganglionic neurons, that vascular endothelial cells may be a source of inflammatory mediators contributing to the sensitization and activation of dural nociceptors, and that the vasculature is a primary target for CGRP, a peptide that appears to play a central role in both the initiation and maintenance of pain associated with a migraine attack. We hypothesized that stress would result in a sex-dependent loss of sympathetic control over dural vasculature. Male and female rats were randomized to one of three groups: naive, acute stress (studied right after stress) or recovery (studied 24 hrs after stress). Stress consisted of a 30-minute immobilization restraint. A bipolar electrode was placed in the superior cervical ganglion (SCG) and the skull was thinned over the middle meningeal artery. FITC-dextran was used to visualize dural blood vessels while the SCG was stimulated at differing frequencies. Vasopressin and nitroprusside were used to establish the minimum and maximum vessel diameters, respectively, per rat. Preliminary results suggest that the SCG stimulation frequency range of vessel regulation is sex-dependent and may be shifted in stressed animals. A stress-induced loss of sympathetic regulation of dural vessels could contribute to migraine initiation.

Sympathetic nerve‐mediated nitrergic dilation of basilar arteries of the rat in vivo

Brain arteries receive sympathetic nerves originating in superior cervical ganglion (SCG), and norepinephrine (NE) is thought the transmitter for vasoconstriction. The exact role of the sympathetic nerve in regulating brain circulation, however, remains unclear. Results of studies in isolated cerebral arteries indicate that activation by nicotine of cerebral perivascular sympathetic nerves induces NE release. NE then diffuses to act on β2‐adrenoceptors located on nitrergic nerve terminals to release nitric oxide (NO) that relaxes the smooth muscle. This axo‐axonal interaction in regulating cerebral blood flow, therefore, was examined in the rat in vivo. Electrical stimulation of SCG caused dilation of basilar arteries in anesthetized normotensive Wistar‐Kyoto rats (WKY). The vasodilation was blocked by inhibitors for NO synthesis and beta2‐adrenoceptors. In spontaneously hypertensive rats (SHRs), electrical stimulation‐of‐SCG‐induced nitrergic dilation of basilar arteries, however, was diminished. This is consistent with reported findings of decreased parasympathetic nerve terminals in cerebral arteries of SHR. These findings indicate that activation of cerebral perivascular sympathetic nerves does not cause significant vasoconstriction, but predominant nitrergic dilation of the basilar arteries in normotensive animals. This effect of sympathetic nerves may change in hypertension.

Increased Acetylcholine Content Induced by Antidromic Stimulation of a Sympathetic Ganglion: A Possible Retrograde Action of Adenosine

Prolonged high-frequency orthodromic stimulation of superior cervical ganglia is known to result in increased acetylcholine (ACh) synthesis and ACh content after the period of stimulation. In a previous study, we provided evidence to suggest that adenosine acts as an extracellular signal to activate this increased ACh synthesis and we proposed that the source of that adenosine might be postsynaptic. Thus, the purpose of the present study was to test whether direct stimulation of the post-ganglionic nerves could affect ganglionic ACh content. Antidromic conditioning of ganglia (15 Hz, 45 min) did not affect significantly their ACh content. However, if ganglia were allowed a 15-min rest period after this antidromic conditioning, their ACh stores were increased by 20%; a similar increase was induced by 4-Hz stimulation before the rest period. During the 15-Hz antidromic stimulation, ACh release was not clearly increased above the basal level, suggesting that preganglionic nerve endings were not stimulated to an extent that could explain the increased ACh content. Orthodromic stimulation (5 Hz) of ganglia 15 min after they had been subjected to antidromic conditioning (15 Hz, 45 min) showed increased ACh release in comparison with that from control unconditioned ganglia. Moreover, the extra ACh released by the conditioned ganglia was quantitatively similar to the increase in the ACh stores, as if most, or all, of the additional ACh was released by preganglionic stimulation. If the antidromic conditioning and the rest period were done during perfusion with Ca(2+)-free medium, the ganglia did not accumulate extra ACh.(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of superior cervical ganglion stimulation of vestibular function

The sympathetic nervous system, which originates in the superior cervical ganglion (SCG) and is distributed in vestibular end organs, has been proposed to have some influence on vestibular function. The present investigation was conducted to assess the effects of unilateral electrical stimulation of the SCG, administration of a vasopressor drug, and introduction of KCl (0.7 M/ml) into the tympanic cavity on vestibular function in alert guinea pigs. Nystagmus was not observed as result of electrical irritation of the SCG (22 test animals), infusion of the KCl solution into the middle ear cavity (5 test animals), or the combination of SCG stimulation and vasopressor drug administration (7 test animals). However, when the SCG was stimulated electrically after introduction of the KCl solution into the ipsilateral cavity, nystagmus and postural deviation were observed (5 out of 12 animals). Furthermore, after the administration of a vasopressor drug to these 12 animals, irrespective of the manifestation of nystagmus, the same changes took place in response to the electrical stimulation (7 animals). These results suggest that SCB stimulation is a provocative factor for nystagmus, that infusion of KCl solution into the tympanic cavity induces a hypersensitive state in the inner ear, and that high blood pressure increases this hypersensitivity.

Cardiodepressant activity in the medium incubating in situ the posterior pituitary lobe during vagal afferent or superior cervical ganglion stimulation.

Cardiodepressant activity in the medium incubating in situ the posterior pituitary lobe during vagal afferent or superior cervical ganglion stimulation.

Effects of electrical stimulation of the superior cervical ganglion on cochlear blood flow in guinea pig.

It has been proposed that cochlear blood flow (CBF) is controlled in part by the sympathetic nervous system. In the present study the effect of electrical stimulation of the superior cervical ganglion (SCG) on CBF in guinea pigs was investigated using laser Doppler flowmetry (LDF). Animals were anesthetized with diazepam and fentanyl and the SCG was exposed. A custom-designed bipolar cuff electrode was fixed around the ganglion and 1 ms biphasic current pulses were injected at 0.15 mA to 1.5 mA, 6 Hz. Bilateral CBF was monitored, while the ganglion was stimulated for 3 or 5 min before and after the ascending sympathetic trunk and nerve branches from SCG were sectioned. Electrical stimulation of 0.5 mA caused the ipsilateral CBF (CBFi) to decrease 11.7% +/- 1.3 from the baseline (BL), while the contralateral CBF (CBFc) increased slightly due to the change in systemic blood pressure (BP). A linear relation was observed between the level of current stimulation and evoked reduction in CBF. Cervical sympathetic trunk section (between the SCG and the middle cervical ganglion) did not influence the pattern or the amplitude of CBF change in response to electrical stimulation of SCG. Sectioning the efferent fibers of the medial inferior and medial superior branch of the SCG only minimally reduced the amplitude of the CBF decrease evoked by electrical stimulation. However, sectioning the superior lateral branch abolished this decrease.(ABSTRACT TRUNCATED AT 250 WORDS)

Rat pineal exhibits two electrophysiological patterns of response to microiontophoretic norepinephrine application.

The spontaneous activity of 117 pineal units was recorded in urethane-anesthetized rats. The pineal units exhibited a wide range of firing rates of which 50% were on average slower than 14 spikes per second. Superior cervical ganglion (SCG) stimulation was studied in 76 pineal units; this stimulation caused excitation in 55% of the units. Microiontophoretic application of norepinephrine (NE) induced changes of firing rates in 61% of the pineal units tested. Two patterns of activity following NE microiontophoresis was observed: increase in firing rate (64%) and decrease in firing rate (36%). NE-induced excitation was observed only in those units excited by SCG stimulation. When NE and SCG stimulation were applied together, partial summation of the excitation induced by each one alone was observed. None of the units in which NE depressed the firing rate responded to SCG stimulation. Local application of propranolol blocked the excitation initiated by SCG stimulation as well as the excitation and the depression induced by NE microiontophoresis.

Sustained elevation of hippocampal cyclic 3'-5' adenosine monophosphate levels after medial septal lesions.

The cyclic 3'-5' adenosine monophosphate (cyclic AMP) content of the rat hippocampal formation doubles during the week following a medial septal lesion and remains elevated for at least 1 month, the longest time period studied. This elevation in cyclic AMP does not result from sympathetic ingrowth, as neither superior cervical ganglion stimulation nor ganglionectomy influences hippocampal cyclic AMP content after lesions. Interruption of the cholinergic septohippocampal pathway in the fornix did not elevate hippocampal cyclic AMP content. Further, treatment of septal-lesioned animals with oxotremorine or of normal animals with atropine did not influence hippocampal cyclic AMP content. Finally, neither locus ceruleus lesions nor treatment with propranolol affected hippocampal cyclic AMP content. We believe this to be the first report of a sustained elevation in hippocampal cyclic AMP content. Like other long-term events, it is likely to have profound effects on hippocampal function and represents a remarkable brain adaptation to remote injury.

Effects of synaptic and antidromic stimulation on tyrosine hydroxylase activity in the rat superior cervical ganglion.

1. The effects of orthodromic and antidromic stimulation of the rat superior cervical ganglion on the specific activity of the enzyme tyrosine hydroxylase have been studied. 2. Orthodromic stimulation of the ganglion via the sympathetic trunk produced an increase in the activity of tyrosine hydroxylase when measured 3 days later while causing no change in the protein content of the ganglion. This increase in the specific activity of tyrosine hydroxylase was blocked by administration of the nicotinic antagonist, hexamethonium. 3. Antidromic stimulation of the superior cervical ganglion by stimulating the internal carotid nerve, the external carotid nerve or both nerves simultaneously produced no change in the specific activity of tyrosine hydroxylase. 4. Parallel increases in tyrosine hydroxylase activity and protein content per ganglion were seen when the internal carotid nerve was stimulated but similar changes were seen in "sham-stimulated" animals. These "non-specific" changes were apparently produced by the trauma involved in the extensive dissection necessary to position electrodes on this nerve trunk. 5. We conclude that an increase frequency of firing in post-ganglionic neurones is not a sufficient stimulus to elevate the specific activity of tyrosine hydroxylase. Rather some other aspect of nicotinic receptor stimulation seems to be required.

Role of the cervical sympathetic ganglia on neurogenic control and autoregulation of basilar arterial flow (authors transl)

In recent years the presence of adrenergic nerve fibers on cerebral arteries as small as 10 to 15 μ both on the pial and within the brain substance has been confirmed morphologically. Although possible roles of the adrenergic fibers in control of cerebral circulation are fairly well clarified, there are few studies as to neural factors in the territory of the basilar artery. In the present study, electrical stimulation of the superior cervical ganglion (SCG) was performed to define the contribution of neural mechanism to control of basilar arterial flow. Studies were also made to determine the effects of hexamethonium(C6)and chronic bilateral superior cervical ganglionectomy on autoregulation mechanism and CO2 reactivity in the territory of the basilar artery. Fifty-two mongrel adult dogs weighing 8 to 26 kg were anesthetized with pentobarbital and mechanically ventilated. The basilar artery was exposed through the transcervical-transclival approach and the flow was measured with an electromagnetic flowmeter. The unilateral and bilateral SCG were stimulated by square-wave direct current impulses (3-5 v, 2.0 msec duration, 20 Hz). Autoregulation of basilar flow was studied under acute hypertension, which was induced by an intraaortic balloon inflation before and after intravenous administration of C6. The same study was performed in the animals, in which both SCG were removed 2 weeks to 2 months prior to the experiment. Also changes in basilar flow following 7 % CO2 inhalation were studied in the respective experiments. The mean percentage reduction of basilar flow was 11.7% on unilateral SCG stimulation and 20.4% on bilateral, associated with a slight rise of systemic blood pressure. The effects of bilateral stimulation were greater than those of unilateral (p<0.01). Inflation of the balloon produced an increase in basilar flow. However, it returned rapidly to the resting level and remained unchanged during 3 minutes period of induced hypertension. After the administration of C6, basilar flow increased along with the rise of blood pressure. CO2 reactivity was well maintained under this condition. Two to four weeks after bilateral SCG-ectomy, fluorescence of the adrenergic fibers disappeared completely from the trunk and main superficial branches of the basilar artery. Studies using chronically bilaterally sympathectomized dogs revealed an impairment of autoregulation in response to rise of blood pressure. Adrenergic fibers observed in abundance on the basilar artery may have an important functional role in conveying vasoconstrictive impulses via the SCG. It is assumed that the bilateral SCG contribute to neurogenic control of blood flow in the territory of the basilar artery and the neurogenic control plays an important role in autoregulation of cerebral blood flow in response to rise of blood pressure.

Sympathetic control of the mechanical properties of the canine carotid sinus.

ARTICLESSympathetic control of the mechanical properties of the canine carotid sinusRJ Bagshaw, and LH PetersonRJ Bagshaw, and LH PetersonPublished Online:01 Jun 1972https://doi.org/10.1152/ajplegacy.1972.222.6.1462MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByCardiac dysautonomia and arterial distensibility in essential hypertensivesAutonomic Neuroscience, Vol. 146, No. 1-2Effects of Exercise Training on Baroreflex Control of the Cardiovascular System25 January 2006 | Annals of the New York Academy of Sciences, Vol. 940, No. 1Exercise Training Increases Baroreceptor Gain Sensitivity in Normal and Hypertensive RatsHypertension, Vol. 36, No. 6Effects of norepinephrine on the mechanical properties of the human radial artery in vitroAmerican Heart Journal, Vol. 136, No. 4Comparative reactivity and mechanical properties of human isolated internal mammary and radial arteries1 March 1998 | Cardiovascular Research, Vol. 37, No. 3Carotid Sinus Hypersensitivity in Patients Undergoing Coronary Arteriography:.Journal of Cardiovascular Electrophysiology, Vol. 8, No. 11Sympathetic Modulation of Radial Artery Compliance in Congestive Heart FailureHypertension, Vol. 26, No. 2An anterograde-retrograde labeling study of the carotid sinus nerve of the Japanese monkey (Macaca fuscata)Neuroscience Research, Vol. 22, No. 4Autonomic nervous system and large conduit arteriesEffects of epinephrine on firing characteristics of two functionally different types of carotid baroreceptors.Circulation Research, Vol. 69, No. 4Baroreceptor Discharge Behavior and ResettingInfluence of substance P on carotid sinus nerve baro- and chemoreceptor activity in rabbitsPeptides, Vol. 11, No. 5The carotid sinus connections: a WGA-HRP study in the catBrain Research, Vol. 455, No. 1Dual effects of norepinephrine and mechanisms of baroreceptor stimulation.Circulation Research, Vol. 61, No. 3EVOLUTION OF CARDIOVASCULAR BARORECEPTOR CONTROLBiological Reviews, Vol. 60, No. 2Effect of norepinephrine and vasopressin on carotid sinus baroreceptor activity in the anesthetized rabbitExperientia, Vol. 40, No. 8Vascular Mechanics1 January 2011Baroreflex Control of Systemic Arterial Pressure and Vascular Bed1 January 2011Cerebral infarction due to carotid occlusion and carbon monoxide exposure. II. Influence of preganglionic cervical sympathectomy.Journal of Neurology, Neurosurgery & Psychiatry, Vol. 46, No. 8Attenuation of Baroreflexes During Operant Cardiac ConditioningPsychophysiology, Vol. 19, No. 6Modification of carotid baroreceptor function by electrical stimulation of the ganglioglomerular nerveJournal of the Autonomic Nervous System, Vol. 4, No. 1Enhanced depressor reflex by stimulation of superior cervical ganglion and by propranololExperientia, Vol. 37, No. 1Coincidental relationship of activity in the sympathetic ganglioglomerular nerve innervating the carotid bifurcation with the intracarotid systolic pulsesBrain Research, Vol. 204, No. 1Circulatory Correlates: Vascular Impedance, Resistance, and Capacity1 January 2011Influence of cervical sympathetic nerve stimulation on carotid sinus baroreceptor afferentsExperientia, Vol. 36, No. 11Baroreceptor function changed by breathingExperientia, Vol. 35, No. 4Control of Vasomotor Function and the Hemodynamic Consequences of the Contractile Behavior of ArteriesAdaptation of controlled range of the carotissinus baroreceptorsIFAC Proceedings Volumes, Vol. 10, No. 15Baroreceptors in NormotensionEffect of thoracotomy upon the carotid sinus control of regional hemodynamics in the dogThe Journal of Thoracic and Cardiovascular Surgery, Vol. 72, No. 4Vegetative Component of InteroceptorsResetting as a General Functional Property of Cardiovascular Mechanoreceptors (Experimental Study of Mechanoreceptors in the Aorta and Auricles)Baroreceptor reflex control of arterial hemodynamics in the dog.Circulation Research, Vol. 37, No. 6Dispersion of Blood Pressure and Heart Rate in Essential HypertensionIEEE Transactions on Biomedical Engineering, Vol. BME-22, No. 6Evidence for an Indirect Sympathetic Control of Atrial Stretch Receptor Discharge in the DogCirculation Research, Vol. 34, No. 4Neurohumoral Control of the Vascular System More from this issue > Volume 222Issue 6June 1972Pages 1462-1468 Copyright & PermissionsCopyright © 1972 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1972.222.6.1462PubMed5030203History Published online 1 June 1972 Published in print 1 June 1972 Metrics

Observations on a rabbit for thirty months after the removal of the superior cervical ganglion

Langendorff1 reported that in one experiment on a cat one hundred and five days after the removal of the superior cervical ganglion, the paralytic symptoms of the eye disappeared, and stimulation of the cervical sympathetic nerve caused the typical effects. Microscopically no nerve cells could be detected, and Langendorff assumed that there was a union between the preganglionic and postganglionic nerve fibers. Langley,2 on the other hand, reported, about one year before Langendorff, an experiment on a cat in which twenty-three months after the removal of the superior cervical ganglion stimulation of the cervical sympathetic did not produce the usual effects, and on microscopical examination some postganglionic nerve fibers were found to have been regenerated; but there were neither nerve cells nor any union between the postganglionic and preganglionic nerve fibers. Later Langley and Anderson1 repeated the experiment on eight cats.In six of the animals, which lived between one hundred and eighty-three and ...