Coronary sinus norepinephrine concentrations during ventricular tachycardia induced by left stellate ganglion stimulation in dogs

1988 ◽  
Vol 66 (4) ◽  
pp. 419-421 ◽  
Author(s):  
Réginald Nadeau ◽  
Daniel Lamontagne ◽  
René Cardinal ◽  
Jacques de Champlain ◽  
J. Andrew Armour
Keyword(s):  
Ventricular Tachycardia ◽  
Coronary Sinus ◽  
Nerve Stimulation ◽  
Stellate Ganglion ◽  
Normal Myocardium ◽  
Sympathetic Stimulation ◽  
Sodium Thiopental ◽  
Cardiac Nerve ◽  
Left Stellate Ganglion ◽  
Ventricular Tachycardias

Coronary sinus catecholamine overflow was measured in open-chest dogs, anesthetized with sodium thiopental and α-chloralose, during left sympathetic stimulation. Uniform ventricular tachycardias were induced in 9 out of 16 dogs during either left stellate ganglion or left ventrolateral cardiac nerve stimulations. Significant increases in norepinephrine (8.1 ng/mL, plasma) and epinephrine (0.19 ng/mL, plasma) overflows were obtained after 30 and 90 s of stimulation, respectively. Maximum norepinephrine overflow was significantly higher in dogs with ventricular tachycardia than in those without it (16.0 vs. 7.4 ng/mL, p < 0.05). This suggests that the induction of ventricular tachycardia in the normal myocardium is related to the amount of local secretion of norepinephrine during nerve stimulation.

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 Mechanism of ventricular premature beats elicited by left stellate ganglion stimulation during acute ischaemia of the anterior left ventricle

2020 ◽  
Author(s):  
Bastiaan J D Boukens ◽  
Michael Dacey ◽  
Veronique M F Meijborg ◽  
Michiel J Janse ◽  
Joseph Hadaya ◽  
...  
Keyword(s):  
Stellate Ganglion ◽  
Underlying Mechanism ◽  
Normal Myocardium ◽  
Acute Ischaemia ◽  
Ischaemic Myocardium ◽  
Ventricular Premature Beats ◽  
Left Stellate Ganglion ◽  
The Right ◽  
Premature Beats ◽  
T Waves

Abstract Aims Enhanced sympathetic activity during acute ischaemia is arrhythmogenic, but the underlying mechanism is unknown. During ischaemia, a diastolic current flows from the ischaemic to the non-ischaemic myocardium. This ‘injury’ current can cause ventricular premature beats (VPBs) originating in the non-ischaemic myocardium, especially during a deeply negative T wave in the ischaemic zone. We reasoned that shortening of repolarization in myocardium adjacent to ischaemic myocardium increases the ‘injury’ current and causes earlier deeply negative T waves in the ischaemic zone, and re-excitation of the normal myocardium. We tested this hypothesis by activation and repolarization mapping during stimulation of the left stellate ganglion (LSG) during left anterior descending coronary artery (LAD) occlusion. Methods and results In nine pigs, five subsequent episodes of acute ischaemia, separated by 20 min of reperfusion, were produced by occlusion of the LAD and 121 epicardial local unipolar electrograms were recorded. During the third occlusion, left stellate ganglion stimulation (LSGS) was initiated after 3 min for a 30-s period, causing a shortening of repolarization in the normal myocardium by about 100 ms. This resulted in more negative T waves in the ischaemic zone and more VPBs than during the second, control, occlusion. Following the decentralization of the LSG (including removal of the right stellate ganglion and bilateral cervical vagotomy), fewer VPBs occurred during ischaemia without LSGS. During LSGS, the number of VPBs was similar to that recorded before decentralization. Conclusion LSGS, by virtue of shortening of repolarization in the non-ischaemic myocardium by about 100 ms, causes deeply negative T waves in the ischaemic tissue and VPBs originating from the normal tissue adjacent to the ischaemic border.

Ventricular distensibility and pressure-volume curve during sympathetic stimulation

1963 ◽  
Vol 204 (1) ◽  
pp. 1-4 ◽  
Author(s):  
Edmund H. Sonnenblick ◽  
John H. Siegel ◽  
Stanley J. Sarnoff
Keyword(s):  
Heart Rate ◽  
Left Ventricle ◽  
Nerve Stimulation ◽  
Sympathetic Stimulation ◽  
Cardiac Nerve ◽  
Ventricular Relaxation ◽  
Volume Curve ◽  
Pressure Volume Curve ◽  
Volume Relation ◽  
Ventricular Distensibility

Experiments with an isovolumically contracting canine left ventricle preparation do not indicate that sympathetic cardiac nerve stimulation induces any alteration in ventricular distensibility. If the heart rate is sufficiently high to produce incomplete ventricular relaxation, sympathetic stimulation, by shortening systole, restores the relaxed pressure-volume relation without any indication, however, that ventricular distensibility is changed.

Parasympathetic Cardiac Nerve Stimulation with Implanted Coronary Sinus Lead

2004 ◽  
Vol 15 (5) ◽  
pp. 588-590 ◽  
Author(s):  
HAJNALKA VÁGÓ ◽  
ATTILA RÓKA ◽  
GYÖRGY ACSÁDY ◽  
BÉLA MERKELY
Keyword(s):  
Coronary Sinus ◽  
Nerve Stimulation ◽  
Cardiac Nerve ◽  
Coronary Sinus Lead

Coronary artery compliance in the dog

1982 ◽  
Vol 60 (7) ◽  
pp. 942-951 ◽  
Author(s):  
G. A. Klassen ◽  
A. Y. K. Wong
Keyword(s):  
Coronary Artery ◽  
Arterial Pressure ◽  
Coronary Flow ◽  
Arterial Wall ◽  
Coronary Circulation ◽  
Stellate Ganglion ◽  
Sympathetic Stimulation ◽  
Intramyocardial Pressure ◽  
Left Stellate Ganglion

Measurement of left anterior descending coronary arterial pressure, phasic coronary flow, and intramyocardial pressure in an open-chest dog provided data, which when entered into the computer model of the coronary circulation, permitted calculation of coronary artery compliance and resistance during systole and diastole. Resting in vivo compliance averaged 0.21 × 10−3 mL/mmHg (1 mmHg = 133.322 Pa) while systolic resistance averaged 4.05 mmHg∙min−1∙mL−1 and during diastole 2.06 mmHg∙min−1∙mL−1. Left stellate ganglion stimulation or vasodilation caused minimal changes in compliance but glutaraldehyde applied to arterial wall caused a decrease in compliance. Sympathetic stimulation and vasodilation decreased both diastolic and systolic resistance. Transmural distribution of coronary flow was not significantly altered by the experimental changes in compliance and resistance.

Mapping of ventricular tachycardia induced by thoracic neural stimulation in dogs

1986 ◽  
Vol 64 (4) ◽  
pp. 411-418 ◽  
Author(s):  
René Cardinal ◽  
Pierre Savard ◽  
J. Andrew Armour ◽  
Réginald Nadeau ◽  
D. Leigh Carson ◽  
...  
Keyword(s):  
Ventricular Tachycardia ◽  
Stellate Ganglion ◽  
Sympathetic Ganglia ◽  
Posterior Aspect ◽  
Cardiac Nerve ◽  
Surface Ecg ◽  
Cervical Ganglion ◽  
Potential Gradients ◽  
The Right ◽  
Stimulation Of

To investigate ventricular tachycardias produced in healthy canine myocardium by stimulation of sympathetic ganglia or cardiac nerves, we simultaneously recorded a surface ECG and 63 ventricular electrograms in anesthetized open-chest dogs. Isochronal and isopotential maps were generated off-line by computer. Ventricular tachycardia with uniform beat-to-beat morphology was induced in 13 or 22 dogs by electrical stimulation of the left stellate ganglion (five experiments), the left middle cervical ganglion (four experiments), the left caudal pole cardiopulmonary nerve (two experiments), or the ventrolateral cardiac nerve (eight experiments). It was not inducible by stimulation of the right-sided major cardiopulmonary nerves or ganglia. In most instances the earliest measured electrical excitation occurred on the posterior aspect of the ventricles. Isochronal maps demonstrated a radial spread of the impulse away from the area of earliest excitation. Changes in the region of earliest excitation and (or) activation pattern were accompanied by changes in QRS morphology. The potential gradients measured between areas displaying positive and negative T waves on the anterior and left lateral aspects of the ventricles were significantly increased by ventrolateral cardiac nerve stimulation. However, the ventricular regions where these potential gradients existed differed from the regions of earliest excitation during ventricular tachycardia. These results demonstrate that the thoracic autonomic nervous system can induce repetitive ventricular excitation originating from consistent loci.

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