Cervical Sympathetic Stimulation Research Articles

Differences in the regulatory mechanism of blood flow in the orofacial area mediated by neural and humoral systems.

Marked blood flow (BF) changes mediated by the autonomic neural and humoral systems may be important for orofacial hemodynamics and functions. However, it remains questionable whether differences in the autonomic vasomotor responses mediated by neural and humoral systems exist in the orofacial area. This study examined whether there are differences in changes in the BF and vascular conductance (VC) between the masseter muscle and lower lip mediated by autonomic neural and humoral systems in urethane-anesthetized rats. Electrical stimulation of the central cut end of the lingual nerve elicited BF increases in the masseter (mainly cholinergic) and lower lip (mainly non-cholinergic), accompanied by an increase in arterial blood pressure (ABP), while cervical sympathetic trunk stimulation consistently decreased BF at both sites. The lingual nerve stimulation induced a biphasic change in the VC in the masseter, consisting of an initial decrease and a successive increase. This decrease in VC was positively correlated with changes in ABP and diminished by guanethidine. Cervical vagus nerve stimulation also induced BF increases at both sites; the increases were greater in the masseter than in the lower lip. Adrenal nerve stimulation and isoproterenol administration induced BF increases in the masseter but not in the lower lip. These results indicate that cholinergic parasympathetic-mediated hemodynamics evoked by trigeminal somatosensory inputs are closely related to ABP changes. The sympathetic nervous system, including the sympathoadrenal system and visceral inputs, may be more involved in hemodynamics in the muscles than in epithelial tissues in the orofacial area.

Effect of Cervical Sympathetic Chain Stimulation on Upper Airway Pressure is Dependent on Direct Post‐Ganglionic Innervation from the Superior Cervical Ganglion

BACKGROUNDWe have previously demonstrated that cervical sympathetic chain (CSC) stimulation improves airway patency in Zucker Fat rats (model of concentric airway collapse). Anatomical studies reveal the presence of two major post‐ganglionic projections to the head and neck arising from the superior cervical ganglion (External Carotid Nerve (ECN) and Internal Carotid Nerve (ICN)), however, their functional contribution to improve upper airway patency is unclear.AIMWe sought to investigate the contribution of the CSC‐SCG‐ECN and CSC‐SCG‐ICN pathways on lowering upper airway pressure (UAP) and cardiorespiratory systems.METHODSUrethane‐anaesthetized healthy male Sprague‐Dawley (SD) rats and pathological Zucker Fat (ZF) rats were used to measure UAP, ECG, blood pressure and diaphragmatic EMG while the intact CSC was stimulated (bilaterally and unilaterally). CSC stimulation mediated effects on UAP and cardiorespiratory parameters were then assessed following systematic transection of ECN and ICN branches.RESULTSWe present two novel findings. Firstly, in all cases of CSC stimulation (SD control UAP (mmHg): −27% bilateral, −20% right, −6% left; ZF control UAP (mmHg): −34% bilateral, −19% right, −22% left), ECN denervation had no significant effect on UAP reductions or hemodynamics in both healthy and disease rats. Secondly, bilateral denervation of the ICN abolished CSC mediated UAP reductions, while leaving hemodynamic effects intact. UAP mediated effects via unilateral CSC stimulation were of ipsilateral origin, as contralateral ICN denervation prior to ipsilateral denervation had no effect. Little to no impact of laterality of CSC stimulation and ICN transection was seen in hemodynamics or diaphragmatic EMG.CONCLUSIONFor the first time, we have demonstrated that CSC stimulation reductions on upper airway pressure are dependent on ipsilateral post‐ganglionic innervation via the ICN. However, the lack of effect on hemodynamics remains to be defined.Support or Funding InformationNIH1OT2OD023860‐01, Galvani BioelectronicsThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Stimulated release of tissue plasminogen activator from artery wall sympathetic nerves: Implications for stress-associated wall damage

Recurrent stress is clinically associated with early onset hypertension and coronary artery disease. A mechanism linking emotion to pathogenic remodeling of the artery wall has not been identified. Stress stimulates acute regulated release of tissue plasminogen activator (t-PA) into the circulation, which is presently attributed to the vascular endothelium. Sympathetic neurons also synthesize t-PA and axonally transport it to the arterial smooth muscle. Unlike release by the endothelium, a stress-stimulated sympathetic discharge would potentially accelerate degradation of the wall matrix by plasmin. To assess whether sympathetic axons are the principal source of acute stress-induced arterial release of t-PA, we compared the output from small densely innervated and large sparsely innervated isolated artery segments before and after sympathetic stimulation, and after ablations. Following phenylephrine infusion densely-innervated microvessels in uveal eyecups were released over 60-fold greater amounts of active t-PA per milligram than the sparsely innervated aorta; and ten-fold more than carotid artery segments. Mesenteric artery release was 4.8-fold greater than release by the carotid artery. In vivo, uveal release of t-PA increased more than three-fold within one minute following superior cervical sympathetic ganglion electrical stimulation, and after phenylephrine, or nicotine infusions of the anterior chamber. Circulating levels of t-PA fell 70% following chemical sympathectomy. We propose that sympathetic nerves are the primary source of stress-induced release of t-PA into and from the densely innervated resistance arteries and arterioles, where dysregulated plasmin-induced proteolysis could damage the wall matrix.

J.L. Corning and vagal nerve stimulation for seizures in the 1880s.

Beginning in the late 18th century, facial flushing and bounding carotid artery pulses during seizures were seen as evidence that seizures resulted from "venous hyperaemia" of the CNS. Consequently, physicians used digital compression of the carotid artery, and later carotid ligation, to abort seizures. In the early 1880s, New York neurologist James Leonard Corning (1855--1923) developed several instruments for carotid artery compression in the treatment of seizures. These devices included a two-pronged, fork-like instrument (the "carotid fork") for temporary compression as an abortive treatment and an adjustable belt-like instrument to encircle the neck (the "carotid truss") for chronic compression as a prophylactic treatment. Corning's uncontrolled observations suggested that the abortive treatment decreased the duration of seizures and that the prophylactic treatment decreased the frequency of seizures. Corning later combined instrumented carotid artery compression with other devices to decrease cerebral blood flow, including transcutaneous electrical vagal nerve and cervical sympathetic stimulation. Observed side effects of treatment included bradycardia, dizziness, and syncope. Corning's use of instrumented carotid compression and his precocious application of transcutaneous electrical vagal nerve stimulation were not widely adopted by neurologists, and these techniques and devices ultimately were abandoned in the late 19th century.

Regional regulation of choroidal blood flow by autonomic innervation in the rat.

Regional influences of parasympathetic and sympathetic innervation on choroidal blood flow were investigated in anesthetized rats. Parasympathetic pterygopalatine neurons were activated by electrically stimulating the superior salivatory nucleus, whereas sympathetic neurons were activated by cervical sympathetic trunk stimulation and uveal blood flow was measured by laser Doppler flowmetry. Parasympathetic stimulation increased flux in the anterior choroid and nasal vortex veins but not in the posterior choroid. Vasodilation was blocked completely by the neuronal nitric oxide synthase inhibitor 1-(2-trifluoromethylphenyl)imidazole but was unaffected by atropine. Sympathetic stimulation decreased flux in all regions, and this was blocked by prazosin. Parasympathetic stimulation did not affect vasoconstrictor responses to sympathetic stimulation in the posterior choroid but attenuated the decrease in blood flow through the anterior choroid and vortex veins via a nitrergic mechanism. We conclude that sympathetic alpha-noradrenergic vasoconstriction occurs throughout the choroid, whereas parasympathetic nitrergic vasodilation plays a selective role in modulating blood flow in anterior tissues of the eye.

Long-term depression of a sympathetic ganglionic response to opioids by prolonged synaptic activity and by phorbol esters

We studied the effect of the adenylate cyclase activator forskolin, of protein kinase C-activating phorbol esters and of prolonged preganglionic input activation on the inhibitory response of the perfused superior cervical ganglion of the cat to exogenous met-enkephalin (Met-ENK). Met-ENK inhibited, in a concentration-dependent manner, the postganglionic compound action potential evoked by cervical sympathetic trunk stimulation. The inhibition was reversible, was blocked by naloxone as well as by pertussis toxin and showed no homologous desensitization in the concentration range 0.01–10 μM. Pretreatment of the ganglion with 4β-phorbol 12,13-dibutyrate or 4β-phorbol 12,13-diacetate depressed the Met-ENK response for several hours, while pretreatment with forskolin had no effect. This action of phorbol esters was prevented by the protein kinase inhibitor H-7 but not by the calmodulin antagonist W-7 or the protein kinase A inhibitor HA 1004 and was calcium-dependent. Recovery of the response from the depression produced by phorbol esters was not affected by a protein synthesis inhibitor. A 40 Hz 20 min stimulus train to the cervical sympathetic trunk mimicked the effect of phorbol esters, depressing for several hours the inhibition produced by Met-ENK. Stimulus trains of duration shorter than 5 min or frequency lower than 5 Hz were ineffective. This effect of prolonged preganglionic stimulation occurred even when the stimulus train was delivered during complete block of nicotinic and muscarinic ganglionic transmission but was lost when the stimulus train was delivered during perfusion with calcium-free Krebs. The protein kinase inhibitor H-7 prevented the depression of the Met-ENK response by the train, while W-7 and HA 1004 had no effect. These findings suggest that, in the superior cervical ganglion of the cat, a kinase, activated by phorbol esters and inhibited by H-7, exerts a long-term control of the ganglion cell responsiveness to opiate receptor activation. A similar mechanism can be synaptically activated by a non-cholinergic transmitter, released by the preganglionic axons during prolonged, high frequency, activity.

Sympathetic stimulation and raised intraocular pressure

Oculosympathetic spasm is a rare condition caused by cervical sympathetic chain stimulation. We describe a patient with an apical lung tumour presenting with ipsilateral facial flushing and raised intraocular pressure which subsided following radiotherapy. This is an unusual mode of presentation for a thoracic tumour and our case highlights the clinical significance of oculosympathetic spasm.

Sympathetic thyroidal vasoconstriction is not blocked by a neuropeptide Y antagonist or antiserum

Sympathetic nerve fibers to thyroid blood vessels contain both norepinephrine (NE) and neuropeptide Y (NPY). To assess the involvement of endogenous NPY in the sympathetic neural control of thyroid blood flow, appropriate doses of a selective NPY antagonist, α-trinositol, and an NPY antiserum (NPY-AS) were used during cervical sympathetic trunk stimulation in anesthetized rats. During all experiments, thyroid blood flow was continuously monitored by laser Doppler blood flowmetry. Neither α-trinositol nor NPY-AS blocked the thyroidal vasoconstriction evoked by either the first or second stimulation of the cervical sympathetic trunks. Our results suggest that NPY is not involved either directly or indirectly during acute sympathetic vasoconstriction in the rat thyroid gland.

Release of vasoactive intestinal peptide and neuropeptide Y from canine heart

The effects of right cervical vagal and left sympathetic stimulation on release of immunoreactive vasoactive intestinal peptide (VIP) and neuropeptide Y (NPY) into cardiac venous and lymphatic effluent was tested in 11 anesthetized adult mongrel dogs. After stimulation of the right cervical vagus (1 ms, 20 Hz, 5 V) for 3 min, VIP output in lymphatic effluent was significantly increased at 1.90 +/- 0.56 pg/min compared with control of 0.90 +/- 0.42 pg/min. NPY output in lymphatic effluent and VIP and NPY release into coronary venous effluent, as measured by the arterial-coronary sinus concentration difference, were not changed. After stimulation of the ansae of the left sympathetic ganglion (1 ms, 10 Hz, 5 V) for 3 min, NPY output in lymphatic effluent was significantly increased at 4.72 +/- 1.58 pg/min compared with a control of 0.73 +/- 0.66 pg/min. VIP output in lymphatic effluent was not changed. VIP arterial-coronary sinus concentration difference decreased slightly but significantly, and NPY arterial-coronary sinus concentration difference decreased markedly after left sympathetic stimulation. In three additional dogs in which coronary sinus blood flow was measured, NPY overflow during left sympathetic stimulation increased from 28.2 +/- 23.5 to 129.6 +/- 212.7 pg/min. Thus VIP and NPY release from the canine heart can be evoked by right cervical vagal and left sympathetic stimulation, respectively. VIP and NPY may play a role as cardiac noncholinergic-nonadrenergic neurotransmitters.

An AF-DX 116 sensitive inhibitory mechanism modulates nicotinic and muscarinic transmission in cat superior cervical ganglion in the presence of anticholinesterase.

The effect of the muscarinic receptor antagonist AF-DX 116 on the inhibitory action of muscarinic agonists and on responses mediated by nicotinic or muscarinic ganglionic transmission was studied in the superior cervical ganglion of the anesthetized cat. The postganglionic compound action potential evoked by cervical sympathetic trunk stimulation was depressed by methacholine or acetylcholine (ACh) injected into the ganglionic arterial supply. The depression was blocked by AF-DX 116. The compound action potentials evoked by preganglionic stimulus trains were also depressed when the intratrain frequency was 2 Hz or greater. This intratrain depression was, however, insensitive to AF-DX 116. The anticholinesterase drug physostigmine markedly enhanced the intratrain depression of the compound action potential. This effect was reversed by AF-DX 116. During nicotinic receptor block with hexamethonium, preganglionic stimulus trains with intratrain frequencies of 5 Hz or greater produced nicitating membrane contractions that could be blocked by the M1 muscarinic receptor antagonist pirenzepine. The amplitude of the contractions increased with frequency and reached a maximum at 20-40 Hz. AF-DX 116 had no effect on these responses. After administration of physostigmine, the amplitude of the nictitating membrane responses decreased with increasing intratrain frequency. AF-DX 116 reversed this effect. The data suggest that, in the superior cervical ganglion, AF-DX 116 sensitive muscarinic receptors which depress synaptic transmission are activated by exogenous agonists but not by the ACh released by the preganglionic axon terminals unless cholinesterase activity is inhibited.(ABSTRACT TRUNCATED AT 250 WORDS)

Vasomotor responses in the isolated perfused external and internal carotid vascular beds of the rat

1. 1. The external (ECB) or the internal (ICB) carotid vascular beds of the rat were isolated and perfused with Krebs-Henseleit solution at constant flow (1 ml/min). Changes in perfusion pressure (PP) were recorded after cervical sympathetic stimulation and after the administration of norepinephrine (NE) and serotonin (5-HT). 2. 2. Sympathetic stimulation induced an increase in PP (vasoconstriction) in both vascular beds, however, this effect was significantly higher in the ECB than in the ICB. 3. 3. Exogenous NE also induced a significantly higher contractile response in the ECB. 4. 4. Prazosin (10 −8 M) significantly inhibited the response to sympathetic stimulation and to NE both in the ECB and in the ICB, but yohimbine (10 −7 M) had no effect, suggesting that the vasoconstriction was mainly due to the activation of α 1-adrenoceptors. 5. 5. 5-HT induced a contractile response both in the ECB and the ICB. In contrast with the response to NE, the contraction induced by 5-HT in the ICB was significantly higher than in the ECB. 6. 6. Ketanserine (10 −8 M) antagonised both responses, indicating the involvement of 5-HT 2 receptors. 7. 7. The contractile effect of 5-HT in the ECB was significantly enhanced by a subthreshold sympathetic stimulation that did not modify the PP by itself. This effect was not seen in the ICB. 8. 8. The differential perfusions of the ECB or the ICB demonstrated a different reactivity of ECB and ICB, both to sympathetic stimulation and to the administration of exogenous NE or 5-HT. 9. 9. Furthermore, the response to 5-HT in the ECB was modulated by a subthreshold sympathetic stimulation. 10. 10. The results suggest that the different reactivity of the ECB and the ICB may be due to differences in the characteristics and/or density of adrenoceptors and 5-HT receptors in both vascular beds.

Blood Pressure and Heart Rate Changes in Streptozotocin Diabetic Rats, with Special Reference to Postural Hypotension.

Blood pressure and heart rate changes were recorded on supine or prone head-up tilt and on carotid artery occlusion in normal and streptozotocin diabetic rats (65 mg/kg). In general supine tilt induced a larger blood pressure fall, slower blood pressure recovery from the fall and larger heart rate fall than prone tilt, both in normal and diabetic rats. Heart rate recovery from the fall was slightly larger in prone than in supine tilt in normal rats. The blood pressure fall and heart rate fall accompanying the tilt were statistically larger in diabetic than in normal rats. Furthermore, blood pressure recovery from the fall was statistically more rapid and larger in normal than in diabetic rats. The exaggerated blood pressure fall with the tilt of diabetic rats might correspond to postural hypotension. Blood pressure rise and heart rate rise with carotid artery occlusion were smaller in diabetic than in normal rats. Blood pressure changes with cervical sympathetic or vagus stimulation were almost the same in normal and diabetic rats. However, in diabetic rats such cervical autonomic nerve stimulation produced larger heart rate changes than in normal rats.

Pial vascular behavior during bilateral and contralateral cervical sympathetic stimulation.

The present study in cats investigates the effect of cervical sympathetic stimulation on changes of diameter of pial arteries and veins, CBF, and intracranial pressure (ICP) using the cranial window and hydrogen clearance techniques. During 20 min of bilateral stimulation, pial arteries maximally constricted by 12%, veins by 13-15%. While the constriction of the large arteries remained stable during the whole 20-min period of bilateral stimulation, small arteries escaped after some 2 min. A similar though weaker trend was noted for the veins. CBF was reduced at 2 min by 31%, and was not different from resting at 18 min. Contralateral stimulation for 20 min induced early constriction only in small arteries, while all other vessels remained more or less unreactive. This phenomenon is explained by interhemispheric arterial collaterals that bring sympathetic fibers mainly to small arteries contralaterally. ICP was lowered initially by 47 +/- 12% during bilateral and by 23 +/- 5% during contralateral stimulation. ICP escaped after 2 and 5 min during bilateral and contralateral stimulation, respectively, and even started to rise after some 10 min. From these data, it is concluded that the sympathoadrenergic system exerts a short-lasting protective effect upon cerebral vascular volume. Small arteries escape from constriction as a consequence of primarily myogenic counteraction of pial and intraparenchymal vessels, and probably additional metabolic dilatation of intraparenchymal vessels.

The effect of glycerol-induced acute renal failure upon cardiac reactivity in the rat: influence of indomethacin treatment and renal pedicle ligation

Cardiac chronotropic responses to isoprenaline, carbachol and electrical stimulation of the cervical sympathetic and vagal nerves were recorded in rats with glycerol-induced acute renal failure (ARF) and control rats. The experiments involving electrical stimulation of cardiac nerves were performed in rats which either had been pretreated with indomethacin (1 mg kg-1 twice daily for 2 days) or had undergone acute bilateral renal pedicle ligation. The findings from this investigation indicate that the reduced chronotropic responses to vagal stimulation in rats with glycerol-induced ARF are due to a reduction in acetylcholine release mediated by prostaglandins possibly originating from the damaged kidneys. The diminished response to cervical sympathetic stimulation results from a decreased postsynaptic response to beta-adrenoceptor stimulation.

Sympathetic modulation of cold-receptive neurones in the trigeminal system of the rat.

The effects of cervical sympathetic electrical stimulation on the activity of cold-receptive neurones in the trigeminal system of the rat have been studied. Sympathetic stimulation caused excitation and/or suppression of cold-receptive cells in the trigeminal nucleus caudalis. The responses were complex but within any one cell low-frequency stimulation (below 5 Hz) usually (81% of cells) caused excitation, while high-frequency stimulation (above 10 Hz) caused excitation and suppression. The temperature of the cutaneous receptive fields was 'clamped' with a thermode. Measurements of surface and intradermal temperatures suggested that the temperature fall caused by sympathetic stimulation was not sufficient to account for the increased firing rate observed. The suppression was blocked by a low dose of phentolamine; it was mimicked by carotid occlusion and may be a consequence of vasoconstriction. The excitation was resistant to beta-blockade; it was best mimicked by the alpha-agonist phenylephrine. Similar frequency-dependent excitations and suppressions, and responses to pharmacological agonists, were obtained in recordings from cold-receptive primary afferent neurones in the trigeminal ganglion. The excitation may be a complex secondary effect, or there may be a direct alpha-receptor-mediated excitation of cold-receptive primary afferent fibres by the sympathetic system.

Cardiac reactivity in rats with acute renal failure.

Cardiac reactivity has been determined in rats with acute renal failure (ARF) induced by either bilateral nephrectomy or intramuscular glycerol injection. Rats with bilateral nephrectomy showed reduced chronotropic responses to cervical sympathetic stimulation but no appreciable alteration in the chronotropic responses to vagal stimulation. By contrast, we have previously noted that rats with glycerol-induced ARF show diminished chronotropic responses to stimulation of both nerves. The negative chronotropic and inotropic responses to carbachol in isolated atria from both nephrectomized and glycerol-injected rats were not significantly different from their respective controls. In both models of ARF the atrial positive chronotropic responses to isoprenaline were significantly decreased whilst positive inotropic responses were not significantly different from controls. The results indicate that the cause of the reduced chronotropic response to vagal stimulation observed in glycerol-injected rats is of presynaptic origin whilst the reduced chronotropic response to cervical sympathetic stimulation noted in both models of ARF may be due to an impaired postsynaptic response.

Effects of Scopoletin on Autonomic Transmissions

AbstractThe effects of scopoletin, a coumarin isolated from the fruit of Tetrapleura tetraptera Taub (Mimosaceae), have been investigated on the electrically-induced contractions, relaxations and twitches of some cholinergically- and adrenergically-innervated muscle preparations in vitro and in vivo. Scopoletin depressed or abolished electrically-evoked contractions of the chick oesophagus, rabbit duodenum and guinea-pig vas deferens in vitro. The coumarin also reduced or abolished the indirect electrically-evoked twitches of the rat isolated hemidiaphragm muscle preparation, or the contractions of the cat nictitating membrane induced by pre-ganglionic cervical sympathetic nerve electrical stimulation in vivo. Furthermore, scopoletin prevented or reversed the high frequency electrical stimulation-evoked relaxations of the rabbit isolated duodenum. These results were taken to imply blockade of neurotransmitters by scopoletin at the cholinergic and adrenergic neuro-effector junctions, neuromuscular junction...

Cardiovascular responses in rats with glycerol-induced acute renal failure.

Autonomic and cardiovascular function were assessed in rats with glycerol-induced acute renal failure (ARF). Rats with ARF had significantly lower mean arterial blood pressure and heart rates and significantly elevated plasma noradrenaline concentrations. The chronotropic responses to right cervical sympathetic and vagal stimulation were diminished in rats with ARF. The pressor and depressor responses to noradrenaline and nitroprusside respectively when expressed as a change in mmHg pressure were significantly reduced in rats with ARF when compared to controls. However, when the depressor responses to nitroprusside were expressed as a percentage fall in basal mean arterial pressure, with the exception of the response to a dose of 10 micrograms kg-1, there were no significant differences between control and uraemic rats. The present findings show that in the rat, changes in cardiovascular responsiveness occur after a brief period of uraemia which are similar to those observed in patients and rats with chronic renal failure.

The role of sympathetic efferent activity in the regulation of brain temperature.

The role of nasal heat exchange in the control of brain temperature has been studied in cats, pigs, ducks and rabbits during acute experiments under general anaesthesia. Nasal air flow at physiological rates caused hypothalamic temperature to fall at between 0.2 and 0.5 degrees C/min in cats, pigs and ducks, which all have arterial rete systems that can cool blood flowing to the brain, but not in rabbits, which lack an arterial rete. Bilateral stimulation of cervical sympathetic trunks reduced or abolished the brain cooling effect of nasal air flow in cats, pigs and ducks. After a period of airflow during which brain cooling was reduced by sympathetic stimulation, the end of stimulation was sometimes followed by marked and rapid brain cooling, indicating re-perfusion through ischaemic cooled tissues. Cervical sympathetic stimulation caused a reduction in resistance to nasal airflow in all species studied, by inducing vasoconstriction and shrinkage of the nasal mucosa. In species with well-developed arterial retia, the effect of cervical sympathetic stimulation in regulating nasal cooling of the brain is probably mediated by controlling blood flow through the nasal mucosa. Although this vascular control also occurs in rabbits, they cannot selectively cool the brain and sympathetic stimulation has no effect on rabbit brain temperature.

Effects of Cervical Sympathetic Stimulation on Vestibulo-Ocular Reflex of Rabbits with Normal, Low and High Blood Pressure

The effect of an unilateral cervical sympathetic stimulation on per-rotational nystagmus was investigated in alert rabbits with low, normal and high blood pressure. The cervical sympathetic chain and vagus nerve on one side were cut and the distal part of the cervical sympathetic ganglion (CSG) was stimulated electrically. When a CSG was stimulated, nystagmus towards the stimulated side was suppressed predominantly. As a result, directional preponderance which was directed away from the stimulated side appeared. This effect became obvious when the animal's blood pressure was low. Oxygen partial pressure was recorded in the perilymph of inner ear and cerebellum. Unilateral CSG stimulation predominantly suppressed oxygen tension of stimulated side. This results suggested that the influence of CSG stimulation on the vestibuloocular reflex is considered to be due to aregional ischemia induced by vasoconstriction.