scholarly journals Noninvasive low-frequency electromagnetic stimulation of the left stellate ganglion reduces myocardial infarction-induced ventricular arrhythmia

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Songyun Wang ◽  
Xiaoya Zhou ◽  
Bing Huang ◽  
Zhuo Wang ◽  
Liping Zhou ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Ventricular Arrhythmia ◽  
Stellate Ganglion ◽  
Low Frequency ◽  
Electromagnetic Stimulation ◽  
Left Stellate Ganglion ◽  
Stimulation Of

Effect of changes in myocardial epinephrine stores on plasma norepinephrine gradient across the dog heart

1994 ◽  
Vol 266 (6) ◽  
pp. H2404-H2409 ◽  
Author(s):  
F. Peronnet ◽  
G. Boudreau ◽  
J. de Champlain ◽  
R. Nadeau
Keyword(s):  
Electrical Stimulation ◽  
Adrenal Medulla ◽  
Pulse Width ◽  
Stellate Ganglion ◽  
Plasma Norepinephrine ◽  
Direct Support ◽  
Left Stellate Ganglion ◽  
Ici 118,551 ◽  
Beta 2 ◽  
Stimulation Of

Plasma norepinephrine (NE) concentration ([NE]) gradient across the heart was measured under electrical stimulation of the left stellate ganglion (LSG; 4 Hz, 4 V, 2 ms pulse width, 1 min) in control (Ctrl) and in adrenalectomized (Adrx) dogs, without and with a 10-min epinephrine (Epi) infusion (92 ng.kg-1.min-1), which partly restored myocardial Epi stores in Adrx dogs (2.9 +/- 0.7 ng/g vs. 6.4 +/- 0.7 ng/g in Ctrl dogs) and slightly increased tissue Epi stores in Ctrl dogs (10.5 +/- 1.3 pg/g). Compared with Ctrl dogs (1,069 +/- 172 pg/ml), the [NE] gradient across the heart under stimulation of the LSG was not modified 1 wk after bilateral adrenalectomy (1,190 +/- 122 pg/ml) or after Epi infusion in Ctrl (1,134 +/- 276 pg/ml) and Adrx (1,259 +/- 279 pg/ml) dogs. The beta 2-antagonist ICI-118,551 significantly reduced the stimulation-induced [NE] gradient across the heart in Ctrl dogs (621 +/- 190 and 603 +/- 86 pg/ml without and with a 10-min Epi infusion, respectively) but not in Adrx dogs deprived of tissue Epi (1,345 +/- 345 pg/ml). Partial repletion of myocardial Epi stores in Adrx dogs restored the effect of ICI-118,551 on the stimulation-induced [NE] gradient (776 +/- 121 pg/ml). These results provide direct support of the hypothesis that tissue Epi, which originates from the adrenal medulla and which is released locally along with NE, is the endogenous agonist for presynaptic beta 2-receptors and potentiates NE release.

Left Stellate Ganglion Block for Refractory Ventricular Tachycardia: A Case Series

2021 ◽  
Vol 104 (3) ◽  
pp. 506-511
Keyword(s):  
Ventricular Tachycardia ◽  
Ventricular Arrhythmia ◽  
Stellate Ganglion ◽  
Case Series ◽  
Stellate Ganglion Block ◽  
Definitive Treatment ◽  
Ganglion Block ◽  
Cardiac Implantable Electronic Devices ◽  
Left Stellate Ganglion ◽  
Life Threatening

Ventricular arrhythmias are usually well controlled with medical management, cardiac implantable electronic devices, or catheter ablation. However, the refractory ventricular tachycardia or fibrillation (VT/VF) is life threatening and challenging. The authors reported a case series of left stellate ganglion blocks (LSGB) in patients with refractory VT/VF, who failed pharmacological treatment and multiple traditional cardiac interventions. Five patients underwent six LSGB. Four patients had significant decreased in ventricular arrhythmia burden. Among the responders, the LSGB suppressed significant VT/VF for three to seven days. Blocks did not only temporary suppress ventricular arrhythmia, but also stabilized the condition and served as a bridge to definitive treatment such as EP ablation or heart transplantation. There was no significant hemodynamic change or devastating side effects. The outcome from the present case series suggested that LSGB could be an effective treatment and a lifesaving intervention frintractable VT/VF. Keywords: Stellate ganglion block, Refractory ventricular tachycardia, Sympathectomy

scholarly journals Effects of left stellate ganglion stimulation on left ventricular synchrony in dogs

1964 ◽  
Vol 207 (1) ◽  
pp. 181-186 ◽  
Author(s):  
Charles E. Osadjan ◽  
Walter C. Randall
Keyword(s):  
Electromechanical Coupling ◽  
Interventricular Septum ◽  
Stellate Ganglion ◽  
Left Ventricular ◽  
Cardiac Response ◽  
Time Interval ◽  
Ventricular Synchrony ◽  
Left Stellate Ganglion ◽  
Coupling Time ◽  
Stimulation Of

The cardiac response to excitation via the sympathetics has led to the inference that improved synchrony of contraction in the ventricular musculature is important to augmented performance. Pin electrodes and strain-gauge arches were fixed to several segments of the left ventricle, and the precise sequence of electrical excitation and mechanical shortening of the septum and epicardial segments of the apex and base compared during control periods and during electrical stimulation of the left stellate ganglion. During stimulation, augmentation in force of contraction was recorded from all segments, including the interventricular septum. In controls, one-half showed initial shortening at the apex and one-half at the base. During stimulation of the stellate, the base contracted first, and the electromechanical coupling time decreased significantly. The septum shortened last in all circumstances. The time interval between the first and the last segment to shorten decreased during stimulation, indicating increased synchrony of contraction. This undoubtedly contributes to the more rapid rise phase of the ventricular pressure pulse during sympathetic stimulation.

Myocardial catecholamines and stimulation of the stellate ganglion in hemorrhagic shock

1965 ◽  
Vol 209 (4) ◽  
pp. 751-756 ◽  
Author(s):  
Vincent V. Glaviano ◽  
Mary Ann Klouda
Keyword(s):  
Blood Pressure ◽  
Hemorrhagic Shock ◽  
Stellate Ganglion ◽  
Myocardial Contraction ◽  
Cardiac Contraction ◽  
Cardiac Responses ◽  
Left Stellate Ganglion ◽  
Anesthetized Dogs ◽  
The Right ◽  
Stimulation Of

Cardiac responses to electrical stimulation of the right or left stellate ganglion were recorded from 16 open-chest anesthetized dogs in hemorrhagic shock. Shock was induced by bleeding the animals to a mean blood pressure of 40 mm Hg. This level of pressure was maintained for 4 hr, during which time blood pressure, heart rate, force of myocardial contraction, and intraventricular pressures were recorded. Stimulation of the stellate ganglion for 15–40 sec every 30 min after hemorrhage showed a gradual decrease in these parameters to levels below control. The reinfusion of blood and the infusion of exogenous l-norepinephrine did not restore an increase in force of cardiac contraction to stellate stimulation. Myocardial epinephrine and norepinephrine levels in shock were found not to differ from those in 14 normal dog hearts. In contrast to almost complete myocardial refractoriness to stellate stimulation in hemorrhagic shock, stimulation of the vagus nerve elicited bradycardia and eventual cardiac arrest. The decrease observed in force of cardiac contraction to stimulation of the stellate ganglion in hemorrhagic shock may be due to depletion of norepinephrine stores in the heart.

scholarly journals Electroanatomic Remodeling of the Left Stellate Ganglion After Myocardial Infarction

2012 ◽  
Vol 59 (10) ◽  
pp. 954-961 ◽  
Author(s):  
Seongwook Han ◽  
Kenzaburo Kobayashi ◽  
Boyoung Joung ◽  
Gianfranco Piccirillo ◽  
Mitsunori Maruyama ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Stellate Ganglion ◽  
Left Stellate Ganglion

Slow cardioacceleration mediated by noncholinergic transmission in the stellate ganglion of the cat

1988 ◽  
Vol 66 (8) ◽  
pp. 1066-1074 ◽  
Author(s):  
Manjit Bachoo ◽  
Ehud Isacoff ◽  
Canio Polosa
Keyword(s):  
Heart Rate ◽  
Rate Increase ◽  
Stellate Ganglion ◽  
Low Frequency ◽  
Low Frequency Stimulation ◽  
Frequency Stimulation ◽  
Preganglionic Stimulation ◽  
Slow Onset ◽  
Inferior Cardiac Nerve ◽  
Stimulation Of

In C1-spinal, pentobarbital-anaesthetized or anemically decerebrated cats, the preganglionic input to the acutely decentralized right stellate ganglion was stimulated with 10- to 30-s trains at 20–40 Hz. Electrical stimulation consistently produced an increase in heart rate in the presence of blocking doses of hexamethonium and atropine or after depletion of acetylcholine from the preganglionic axons by prolonged low frequency stimulation in the presence of hemicholinium. The increase in heart rate had a delayed slow onset, lasted several minutes, and was abolished by propranolol or by section of the inferior cardiac nerve. The magnitude and duration of the heart rate increase were related to intensity, frequency, and duration of preganglionic stimulation. The response to stimulation of a given white ramus was progressively attenuated, and eventually irreversibly lost, during prolonged continuous stimulation of that ramus, while the response to stimulation of a different unstimulated ramus was unchanged. We conclude that the slow cardioacceleration results from a slow and prolonged excitation of postganglionic neurons by a noncholinergic transmitter released by the preganglionic axons.

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