Effects Of Stellate Ganglion Stimulation Research Articles

Effects of extrinsic cardiac nerve stimulation on atrial fibrillation inducibility: The regulatory role of the spinal cord.

To investigate the effect of the mutual regulation of the extrinsic cardiac nerves on atrial electrophysiology and atrial fibrillation (AF) vulnerability. Fourteen dogs were randomly divided into two groups: spinal cord stimulation (SCS) group (n = 7) and spinal cord block (SCB) group (n = 7). SCS was performed with 90% of the threshold voltage stimulating the T1 -T2 spinal level, while SCB was performed by injecting 2% lidocaine into the epidural space at the T2-3 level. The effective refractory period (ERP), ERP dispersion, and AF inducibility were measured during atrial pacing combined with different extrinsic cardiac nerve stimulation. ERPs were decreased in the atrium and pulmonary veins and ERP dispersion was increased from baseline during left cervical vagus nerve stimulation (VNS) or left stellate ganglion stimulation (SGS) in the two groups. When combined with SCS, VNS resulted in diminished ERPs at all recording sites, longer ERP dispersion and more episodes of AF than were observed during VNS, whereas ERPs were greater and correspondingly fewer episodes of AF occurred during SCS combined with SGS than SGS. In the SCB group, ERPs were shortened, ERP dispersion was lengthened, and episodes of AF were increased during SGS after SCB. SCS enhanced the activity of the left vagus nerve but attenuated the left stellate ganglion and superior left ganglionated plexus. SCS modulates extrinsic and intrinsic cardiac nerve activity among the vagus nerve, stellate ganglion, and ganglionated plexus. SCS facilitates the effect of VNS and attenuates the effect of SGS on atrial electrophysiology.

Effects of Stellate Ganglion Stimulation on Bilateral Cochlear Blood Flow

The effect of intraneural electrical stimulation of the stellate ganglion (SG) on bilateral cochlear blood flow (CBF) was investigated with laser-Doppler flowmetry. The SG of 15 anesthetized guinea pigs was exposed by a novel surgical approach and stimulated with a specially designed intraneural bipolar platinum-iridium electrode. Bilateral CBF was continuously monitored. Stimulation of 0.25 mA caused a detectable increase of the systemic blood pressure (BP) and a bilateral decrease of the cochlear vascular conductance (R, defined as the ratio CBF/BP). A stimulus of 0.5 mA elicited a statistically significant ipsilateral CBF (CBFi) decrease of 3.6% +/- 5.1% from the baseline and a contralateral CBF (CBFc) decrease of 3.1% +/- 5.5%. That no statistical difference was found between CBFi and CBFc indicates that a unilateral sympathetic stimulation of the SG can cause equal bilateral responses. These responses were accompanied by a significantly increased BP (8.7% +/- 5.2% of baseline) and consequently a greatly decreased R (12.2% +/- 6.5%) of the ipsilateral cochlea. Bilateral sections of the cervical sympathetic trunk below the level of the superior cervical ganglion did not alter the evoked changes in CBF, BP, and R. It is concluded that SG stimulation can decrease the conductivity of the cochlear vessels or the supplying vessels of the cochlea. Additionally, the SG nerve fibers that cause these effects do not pass through the superior cervical ganglion.

Stellate ganglion influence on static compliance and surface layer lipids in cat lungs

In order to determine the effects of stellate ganglion stimulation (SGS) on static lung compliance, pressure-volume relationships were measured on lungs in situ in cats anesthetized with ketamine. The lungs were inflated with 100% oxygen to 100, 93.75, 87.5, 81.25, 75, 50, and 25% TLC as determined at 20 cm H 2O transpulmonary pressure. After a maximal filling, lungs were inflated twice to each volume alternating unstimulated and SGS conditions. Static lung compliance was decreased by SGS at 93.75 (5.7 ± 0.4 (SE) vs. 5.4 ± 0.4 ml/cm H 2O; P < 0.05) and 87.5% TLC (6.6 ± 0.6 vs. 6.0 ± 0.5 ml/cm H 2O; P < 0.05). In order to assess possible effects of SGS on surfactant that might be related to the loss of compliance, lung lipids and proteins obtained during SGS were quantitated. Total phospholipid (TPL) increased form 3.2 ± 0.33 to 4.16 ± 0.23 mg/g lung after 1 min 7V SGS ( P < 0.05) and to 4.8 ± 0.61 mg/g lung after 4 min 20V ( P < 0.05). The ratio of cholesterol (chol) to disaturated phosphatidylcholine (DSPC) decreased after 4 and 6 min, and may have resulted in increased surface tension forces at high lung volumes. The data from this study lend support to previous findings which showed that the compliance decrease during SGS may be related to increased surface tension forces.

The Effects of Stellate Ganglion Stimulation and Stellate Ganglion Block for Tinnitus

The Effects of Stellate Ganglion Stimulation and Stellate Ganglion Block for Tinnitus

Absence of stellate ganglion influence on alveolar-duct constriction.

Previous work has shown decreased lung compliance with high wash fluid surface tensions, but normal ratios of lung weight to body weight during stellate ganglion stimulation (SGS) in cats and monkeys. In the present study, effects of SGS on diameters of alveolar ducts were determined in spontaneously breathing cats under ketamine anesthesia. Compliance and pulmonary resistance were also measured. A fluorocarbon cooled to - 100 degrees C was poured onto an exposed lung lobe after rapidly opening the chest after sham operation and during SGS. Examination of the outer 2 mm of the lungs by light microscopy revealed no alveolar-duct constriction by SGS, although compliance decreased by 15%. Pulmonary resistance was unchanged. Alveolar-duct diameters were 157 +/- 4.3 micron (mean +/- SEM) in control animals and 163 +/- 4.6 micron in SGS cats. Absence of alveolar-duct constriction suggests that peripheral airway constriction did not contribute to the decrease in compliance during SGS.

星状神経節刺激による血行動態および心電図の変化(実験的研究)

星状神経節刺激による血行動態および心電図の変化(実験的研究)

Effect of stellate ganglion stimulation on myocardial blood flow, oxygen consumption, and cardiac efficiency during beta-adrenoceptor blockade.

The β-adrenoceptor antagonists LB46, oxprenolol, K01366, propranolol, and practolol all decrease the myocardial demand for oxygen and increase efficiency; with the exception of practolol, they reduce coronary blood flow. Stellate ganglion stimulation causes coronary vasoconstriction after β-adrenoceptor blockade has been established with propranolol, LB46, oxprenolol, or K01366; in the presence of practolol it causes coronary vasodilatation.

Pharmacology of Dl-5-Methyl-8-(2-Hydroxy-3-t-Butylaminopropoxy) Coumarin Hydrochloride (CS-359), A New β-Adrenergic Blocking Agent

β-Adrenergic blocking activity and other pharmacological properties of CS-359, 5-methyl-8-(2-hydroxy-3-t-butylaminopropoxy) coumarin were compared with those of propranolol. CS-359 inhibited the positive chronotropic and the smooth muscle relaxing responses to isoproterenol. The cardiac effect of stellate ganglion stimulation in anesthetized dogs was also abolished. CS-359 given orally to conscious dogs inhibited the positive chronotropic response to isoproterenol given i.v. The β-adrenergic blocking activity of this compound was 2 to 3 times more potent than that of propranolol, both of which were devoid of any intrinsic stimulant activity. Aconitine- and ouabain-induced arrhythmias in anesthetized dogs were protected by CS-359. As to local anesthetic action on frog sciatic nerve and guinea-pig cornea, CS-359 had one-tenth the activity of propranolol. Concerning percent reduction of the maximum rate of rise of action potential recorded intracellularly from the ventricular muscle fiber, CS-359 was 3 times less potent than propranolol. It reduced heart rate but had only minor effects on the blood pressure and respiration in anesthetized dogs. These data suggest that CS-359 is a more specific β-adrenergic blocking agent with a greater potency and a less cardiac depression than propranolol.

On the sympathetic control of ventricular automaticity. The effects of stellate ganglion stimulation.

The effects of stellate ganglion stimulation on idioventricular automaticity were studied in anesthetized dogs. An idioventricular rhythm was obtained in one series of animals by ligating the His bundle and in the other by stimulating the vagus. On isolation of the left stellate ganglion, the idioventricular rate fell by 5 beats/min which is compatible with a rate of "tonic" discharge of about 3 impulses/sec. On stimulation of the stellate ganglia at increasingly higher frequencies, the idioventricular rate accelerated progressively and the frequency-response curve was sigmoid. When the stimulation frequency was increased above 10 to 15 pulses/sec, there was no further enhancement of ventricular automaticity. The ventricular rates attained during sympathetic stimulation rarely exceeded 70/min. The interval between the initiation of sympathetic stimulation and the maximal ventricular acceleration was shorter at higher stimulation frequencies. The effects of right and left stellate stimulation on the rate of idioventricular pacemakers were comparable. Reflex vagal inhibition had little influence on the acceleratory action of the sympathetic nerves on the idioventricular pacemakers since in dogs with atrioventricular block the results before and after vagotomy were similar. Furthermore, the idioventricular rhythm during vagally induced block increased on sympathetic stimulation to values comparable to those obtained in dogs with surgically induced block.