OBJECTIVE: To investigate the expression and localization of metabotropic glutamate receptors 7 and 8 (mGluR7/8) in rat superior cervical ganglion (SCG) and their changes in response to chronic intermittent hypoxia (CIH). METHODS: We detected the expressions of mGluR7 and mGluR8 in the SCG of 8-week-old male SD rats using immunohistochemistry and characterized their distribution with immunofluorescence staining. The expression of mGluR7 and mGluR8 in the cytoplasm and nucleus was detected using Western blotting. A 6-week CIH rat model was established by exposure to intermittent hypoxia (6% oxygen for 30 s followed by normoxia for 4 min) for 8 h daily, and the changes in systolic blood pressure, diastolic blood pressure and mean arterial pressure were measured. The effect of CIH on expression levels of mGluR7 and mGluR8 in the SCG was analyzed using Western blotting. RESULTS: Positive expressions of mGluR7 and mGluR8 were detected in rat SCG. mGluR7 was distributed in the neurons and small fluorescent (SIF) cells with positive staining in both the cytoplasm and nuclei, but not expressed in satellite glial cells (SGCs), nerve fibers or blood vessels; mGluR8 was localized in the cytoplasm of neurons and SIF cells, but not expressed in SGCs, nerve fibers, or blood vessels. Western blotting of the nuclear and cytoplasmic fractions of rat SCG further confirmed that mGluR7 was expressed in both the cytoplasm and the nucleus, while mGluR8 exists only in the cytoplasm. Exposure to CIH significantly increased systolic blood pressure, diastolic blood pressure and mean arterial pressure of the rats (all P < 0.001) and augmented the protein expressions of mGluR7 and mGluR8 in the SCG (P < 0.05). CONCLUSION mGluR7 and mGluR8 are present in rat SCG but with different localization patterns. CIH increases blood pressure of rats and enhanced protein expressions of mGluR7 and mGluR8 in rat SCG.
Male ; Animals ; Rats ; Rats, Sprague-Dawley ; Superior Cervical Ganglion ; Receptors, Metabotropic Glutamate ; Hypoxia

BACKGROUND: A stellate ganglion block (SGB) causes increased blood flow in the maxillofacial region, exhibiting the potential for regenerative effects in damaged tissue. The focus of this study was to understand the efficacy of SGB for regenerative effects against nerve damage. A rat model of the superior cervical ganglion block (SCGB) was created instead of SGB, and facial blood flow, as well as sympathetic nervous system function, were measured. METHODS: A vertical incision was made on the left side of the neck of a Wistar rat, and a 5-mm resection of the superior cervical ganglion was performed at the back of the bifurcation of the internal and external branches of the left common carotid artery. Blood flow in the skin at the mandibular angle and mean facial temperature were measured using a laser-Doppler blood flow meter and a thermographic camera, respectively, over a 5-week period after the block. In addition, the degree of ptosis and miosis were assessed over a period of 6 months. RESULTS: The SCGB rat showed significantly higher blood flow at the mandibular angle on the block side (P < 0.05) for 3 weeks, and significantly higher skin temperature (P < 0.05) for 1 week after the block. In the SCGB rat, ptosis and miosis occurred immediately after the block, and persisted even 6 months later. CONCLUSIONS: SCGB in rats can cause an increase in the blood flow that persists over 3 weeks.
Animals ; Carotid Artery, Common ; Horner Syndrome ; Miosis ; Models, Animal ; Neck ; Rats ; Regional Blood Flow ; Skin ; Skin Temperature ; Stellate Ganglion ; Superior Cervical Ganglion ; Sympathetic Nervous System ; Thermography

BACKGROUND: Cerebral blood vessels are innervated by sympathetic nerves from the superior cervical ganglion (SCG). The purpose of the present study was to evaluate the neuroprotective effect of superior cervical sympathetic ganglion block in rats subjected to permanent focal cerebral ischemia. METHODS: Thirty male Sprague-Dawley rats (270-320 g) were randomly assigned to one of three groups (control, lidocaine and ropivacaine). A brain injury was induced in all rats by middle cerebral artery occlusion with a nylon thread. The animals of the local anesthetic group received 30 microl of 2% lidocaine or 0.75% ropivacaine in the SCG. Neurologic scores were assessed 24 hours after brain injury. Brain samples were then collected. The infarct and edema ratios were measured by 2.3.5-triphenyltetrazolium chloride staining. RESULTS: There were no differences in the death rates, neurologic scores, or infarction and edema ratios between the three groups. CONCLUSIONS: These findings suggest that superior cervical sympathetic ganglion block may not influence the brain damage induced by permanent focal cerebral ischemia in rats.
Amides ; Animals ; Blood Vessels ; Brain ; Brain Injuries ; Brain Ischemia ; Edema ; Ganglia, Sympathetic ; Humans ; Infarction ; Infarction, Middle Cerebral Artery ; Lidocaine ; Male ; Neuroprotective Agents ; Nylons ; Rats ; Rats, Sprague-Dawley ; Superior Cervical Ganglion

BACKGROUND: Cerebral blood vessels are innervated by sympathetic nerves from the superior cervical ganglia (SCG), and these nerves may influence the cerebral blood flow. The purpose of the present study was to evaluate the neuroprotective effect of superior cervical sympathetic ganglion block in rats that were subjected to focal cerebral ischemia/reperfusion injury. METHODS: Eighty male Sprague-Dawley rats (270-320 g) were randomly assigned to one of two groups (the ropivacaine group and a control group). In all the animals, brain injury was induced by middle cerebral artery (MCA) reperfusion that followed MCA occlusion for 2 hours. The animals of the ropivacaine group received 30microl of 0.75% ropivacaine, and their SCG. Neurologic score was assessed at 1, 3, 7 and 14 days after brain injury. Brain tissue samples were then collected. The infarct ratio was measured by 2.3.5-triphenyltetrazolium chloride staining. The terminal deoxynucleotidyl transferase mediated dUTP-biotin nick-end labeled (TUNEL) reactive cells and the cells showing caspase-3 activity were counted as markers of apoptosis at the caudoputamen and frontoparietal cortex. RESULTS: The death rate, the neurologic score and the infarction ratio were significantly less in the ropivacaine group 24 hr after ischemia/reperfusion injury. The number of TUNEL positive cells in the ropivacaine group was significantly lower than those values of the control group in the frontoparietal cortex at 3 days after injury, but the caspase-3 activity was higher in the ropivacaine group than that in the control group at 1 day after injury. CONCLUSIONS: The study data indicated that a superior cervical sympathetic ganglion block may reduce the neuronal injury caused by focal cerebral ischemia/reperfusion, but it may not prevent the delayed damage.
Amides ; Animals ; Apoptosis ; Blood Vessels ; Brain ; Brain Injuries ; Caspase 3 ; DNA Nucleotidylexotransferase ; Ganglia, Sympathetic ; Humans ; In Situ Nick-End Labeling ; Infarction ; Male ; Middle Cerebral Artery ; Neurons ; Neuroprotective Agents ; Rats ; Rats, Sprague-Dawley ; Reperfusion ; Superior Cervical Ganglion

BACKGROUND: Cerebral blood vessels are innervated by sympathetic nerves that originate in the superior cervical ganglia (SCG). This study was conducted to determine the effect of an SCG block on brain injury caused by focal cerebral ischemia/reperfusion in a rat model. METHODS: Male Sprague-Dawley rats (270-320 g) were randomly assigned to one of three groups (lidocaine, ropivacaine, and control). After brain injury induced by middle cerebral artery (MCA) occlusion/reperfusion, the animals were administered an SCG bloc that consisted of 30 microliter of 2% lidocaine or 0.75% ropivacaine, with the exception of animals in the control group, which received no treatment. Twenty four hours after brain injury was induced, neurologic scores were assessed and brain samples were collected. The infarct and edema ratios were measured, and DNA fragmented cells were counted in the frontoparietal cortex and the caudoputamen. RESULTS: No significant differences in neurologic scores or edema ratios were observed among the three groups. However, the infarct ratio was significantly lower in the ropivacaine group than in the control group (P<0.05), and the number of necrotic cells in the caudoputamen of the ropivacaine group was significantly lower than in the control group (P<0.01). Additionally, the number of necrotic and apoptotic cells in theropivacaine group were significantly lower than inthe control group in both the caudoputamen and the frontoparietal cortex (P<0.05). CONCLUSIONS: Brain injury induced by focal cerebral ischemia/reperfusion was reduced by an SCG block using local anesthetics. This finding suggests that a cervical sympathetic block could be considered as another treatment option for the treatment of cerebral vascular diseases.
Anesthetics, Local ; Animals ; Blood Vessels ; Brain Injuries* ; Brain* ; DNA ; Edema ; Ganglia, Sympathetic* ; Humans ; Lidocaine ; Male ; Middle Cerebral Artery ; Models, Animal* ; Rats* ; Rats, Sprague-Dawley ; Superior Cervical Ganglion ; Vascular Diseases

OBJECTIVETo investigate the influence of cervical sympathetic nerve block (SB) on blood flow volume and barrier function of intestinal mucosa after combined radiation and burn injury in rat.

METHODSSD rats were divided into three groups: control (n = 18), combined injury group (n = 100, rats with Co gamma ray body irradiation with a dose of 5 Gy plus 15% TBSA full-thickness burn injury), and combined injury with SB treatment (n = 100, with the same dose of gamma-ray irradiation and burn injury, treated with SB). Twenty rats were sacrificed on 0, 1, 5, 7 days after combined injuries for various observations. SB was conducted with injection of ropivhydrochloride into the neck bilaterally for the SB group, and same amount of normal saline was injected instead in the combined injury group. Blood flow volume, changes in villus height and crypt depth in jejunum, Na(+)-K+ ATPase activity, permeability of small intestine were measured at different time-points.

RESULTSThe blood flow volume in small intestinal mucosal on 1 post-injury days (PID) [(0.29 +/- 0.07) ml x min(-1) x g(-1)] were obviously decreased than that in normal controls [(1.26 +/- 0.23) ml x min(-1) x g(-1), P < 0.01 ], with serious destruction of pit cells, decrease in intestinal mucosal Na(+)-K+ ATPase activity, and increase in intestinal mucosal permeability. Compared with combined injury group, the blood flow volume was [(0.82 +/- 0.11) ml x min(-1) x g(-1) 1 day after combined injury, P < 0.01], and the Na(+)-K+ ATPase activity was obviously increased, and the permeability of small intestine was ameliorated.

CONCLUSIONSB can increase blood flow volume of rat small intestine after combined radiation and burn injury, promote the repair of intestinal epithelium and improve the barrier function of the intestinal wall.

Animals ; Autonomic Nerve Block ; Blood Volume ; physiology ; Burns ; physiopathology ; Intestinal Mucosa ; blood supply ; metabolism ; physiopathology ; Intestine, Small ; Radiation Injuries, Experimental ; physiopathology ; Rats ; Rats, Sprague-Dawley ; Superior Cervical Ganglion

To compare the difference in action sites between mecamylamine (MEC) and hexamethonium (HEX) on nicotinic receptors of sympathetic neurons, we investigated the effects of MEC and HEX on the nicotine-induced currents in cultured superior cervical ganglion neurons by whole-cell patch clamp technique. The IC(50) of MEC and HEX for antagonizing the effect of 0.08 mmol/L nicotine was 0.0012 and 0.0095 mmol/L, respectively. Both MEC and HEX accelerated the desensitization of nicotinic receptors. Furthermore, by comparing their effects at holding potentials 30, 70 and 110 mV, it was indicated that their suppressing effect on the nicotine-induced currents was voltage-dependent. However, different from that of HEX, the inhibitory effect of MEC increased with administering the mixture of MEC and nicotine at intervals of 3 min, indicating a use-dependent effect of MEC. It is concluded that the action site of MEC on nicotinic receptors of sympathetic neurons is different from that of HEX.
Animals ; Animals, Newborn ; Cells, Cultured ; Hexamethonium ; pharmacology ; Mecamylamine ; pharmacology ; Neurons ; drug effects ; physiology ; Nicotinic Antagonists ; pharmacology ; Patch-Clamp Techniques ; Rats ; Rats, Wistar ; Receptors, Nicotinic ; drug effects ; physiology ; Superior Cervical Ganglion ; cytology ; physiology

The origin of sympathetic and sensory nerves innervating heart in the cat was investigated using HRP (Horseradish peroxidase) and WGA-HRP (Wheat germ agglutinin-horseradish peroxidase) as neuronal tracers. The neural tracers were injected into subepicardial layer and myocardium of the right atrium, left atrium, right ventricle and left ventricle, respectively. Labeled sympathetic neuronal cell bodies were found in superior cervical ganglia, middle cervical ganglia, stellate ganglia and 4th and 5th thoracic ganglia, mainly in middle cervical ganglia and stellate ganglia. Heavier labeled neuronal cell bodies were found in the middle cervical ganglia and stellate ganglia when the neural tracers were injected into left atrium, right ventricle and left ventricle. Labeled sensory neuronal cell bodies were found in nodose ganglia and T1-T6 spinal ganglia, mainly in T1-T5 spinal ganglia. Heavier labeled neuronal cell bodies were found in the nodose ganglia when the neural tracers were injected into left atrium and right ventricle. These results may provide a neuroanatomical data on origin of sensory nerves innervating the heart of the cat.
Animals ; Cats* ; Ganglia ; Ganglia, Sensory ; Ganglia, Spinal ; Ganglia, Sympathetic ; Heart Atria ; Heart Ventricles ; Heart* ; Horseradish Peroxidase ; Myocardium ; Neurons* ; Nodose Ganglion ; Sensory Receptor Cells ; Stellate Ganglion ; Superior Cervical Ganglion ; Wheat Germ Agglutinin-Horseradish Peroxidase Conjugate*

BACKGROUND: Stellate ganglion block (SGB) has been used to treat over 150 diseases which include diabetes mellitus and gout. This study was planned to investigate whether stellate ganglion block (SGB) could lower the levels of blood glucose, uric acid, epinephrine, and norepinephrine. METHODS: Sixty Sprague-Dawley rats within the weight of 250-350 gm were randomly devided into four groups. CS group was normal group with sham SGB with normal saline, CL group was normal group with SGB with lidocaine, DS group was diabetic group with SGB with normal saline, DL group was diabetic group with SGB with lidocaine. The diabetes was induced by intraperitoneal injection of 40 mg/kg of streptozotocin in citrate buffer (0.01 M, pH 4.5). Nondiabetic groups were given same amount of the citrate buffer. Seven days after the last injection of the streptozotocin blood glucose level was checked and more than 300 mg/dl was considered diabetic. The SGB was performed three times at right superior cervical ganglion two days apart from two days after the conformation of diabetes. Successful SGB was conformed by the ipsilateral ptosis or conjunctival congestion. Blood samplings from tail vein for the check of glucose, uric acid, and catecholamines were done before the injection of streptozotocin, seven days after the last injection of streptozotocin, and two days after the last SGB. RESULTS: The SGB with lidocaine reduced the blood glucose level only in the diabetic rats while SGB with the saline did not. The epinephrine levels were increased in the diabetics and decreased by the SGB with lidocaine without any statistical significance. Norepinephrine and uric acid levels had not been effected by the SGB and both of them had no correlationship with the glucose level. CONCLUSIONS: SGB in the diabetic rats decreases the blood glucose level. But for the effects of the SGB on the level of epinephrine further study would be needed.
Animals ; Blood Glucose* ; Catecholamines* ; Citric Acid ; Diabetes Mellitus ; Epinephrine ; Estrogens, Conjugated (USP) ; Glucose ; Gout ; Hydrogen-Ion Concentration ; Injections, Intraperitoneal ; Lidocaine ; Norepinephrine ; Rats* ; Rats, Sprague-Dawley ; Stellate Ganglion* ; Streptozocin ; Superior Cervical Ganglion ; Uric Acid* ; Veins

BACKGROUND AND OBJECTIVES: Recently, nitric oxide (NO) has been considered to be a neurotransmitter or a signaling molecule in a number of distinct subpopulation of neurons in the central and peripheral nervous systems. This study attempted to define the distribution patterns and quantitative participation according to the origin of nitrergic innervation in the canine laryngeal ventricles of eight adult dogs. MATERIALS AND METHODS: The nitrergic innervation in the intralaryngeal, superior cervical and nodose ganglion to the laryngeal ventricle were investigated by using double labelled neuronal NO synthase (nNOS) immunocytochemistry combined with a retrograde tracer, cholera toxin subunit B-conjugated horseradish peroxidase (CTB-HRP). RESULTS: NO is suggested to participate in parasympathetic, sympathetic and sensory innervation. Intralaryngeal ganglion is the main source of nitrergic innervation in the canine laryngeal ventricle. The proportions of the nitrergic innervation in the intralaryngeal ganglion, superior cervical ganglion, and nodose ganglion to the canine laryngeal ventricle were 63.1%, 37.7%, 4.9% respectively. CONCLUSION: NO originating from the intralaryngeal ganglion in a canine laryngeal ventricle may play an important role in controlling the laryngeal gland secretion and in regulating the blood flow by modulating the classical parasympathetic cholinergic neurotransmitter as like a neuronal messenger or comediator. NO also may participate in the same role through the sympathetic innervation of superior cervical ganglion: however, NO originating from intralaryngeal ganglion may play more important role than that from superior cervical ganglion. Many neurons of nodose ganglion have demonstrated to have nNOS, but might be less involved in the ventricular sensory innervation.
Adult ; Animals ; Cholera Toxin ; Dogs ; Ganglion Cysts ; Horseradish Peroxidase ; Humans ; Immunohistochemistry ; Neurons ; Neurotransmitter Agents ; Nitric Oxide ; Nitric Oxide Synthase ; Nitric Oxide Synthase Type I ; Nodose Ganglion ; Peripheral Nervous System ; Superior Cervical Ganglion