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.

Sympathetic neural effects on regional atrial recovery properties and cardiac rhythm

1981 ◽  
Vol 240 (4) ◽  
pp. H590-H596
Author(s):  
F. A. Kralios ◽  
C. K. Millar
Keyword(s):  
Left Atrial ◽  
Sinus Node ◽  
Stellate Ganglion ◽  
Sympathetic Nerves ◽  
Substantial Effect ◽  
Cardiac Nerve ◽  
Anesthetized Dogs ◽  
Functional Distribution ◽  
The Right ◽  
Stimulation Of

The functional distribution of the cardiac sympathetic nerves to the atria and their arrhythmiogenic effects were determined in 16 open-chest pentobarbital-anesthetized dogs. Shortening of refractory periods at four right and two left atrial sites during stimulation of the nerves was taken as a criterion of their distribution. Stimulation of right stellate ganglion, craniovagal, and right stellate cardiac nerves produced localized shortening on the right atrium, particularly at the sinus node area, and invariably induced sinus tachycardia. The recurrent cardiac nerve produced little shortening at all sites and less arrhythmiogenic effect. The left stellate ganglion and ventrolateral cardiac nerve affected only left atrial sites and induced atrioventricular junctional rhythm. The ventromedial cardiac nerve affected all sites and had no consistent arrhythmiogenic effect. The innominate nerve had no substantial effect. We concluded that the functional distribution of the cardiac sympathetic nerves is localized, and that rate, rhythm, and refractory period changes induced by stimulation of these nerves are characteristic of the area of distribution.

scholarly journals Stimulation of left stellate ganglion prolongs Q-T interval in patients with palmar hyperhidrosis

1997 ◽  
Vol 273 (4) ◽  
pp. H1696-H1698 ◽  
Author(s):  
Cheuk-Wah Wong
Keyword(s):  
Heart Rate ◽  
Stellate Ganglion ◽  
Sympathetic Ganglia ◽  
Palmar Hyperhidrosis ◽  
The Third ◽  
Video Assisted ◽  
Stellate Ganglia ◽  
Left Stellate Ganglion ◽  
The Right ◽  
Stimulation Of

With the advent of transthoracic video-assisted endoscopic electrocautery of the second and the third sympathetic ganglia for the treatment of palmar hyperhidrosis, it is possible to approach the stellate ganglia with ease. To see whether stimulation of stellate ganglia in humans is similar to the case in dogs, we stimulated the sympathetic ganglia in 18 palmar hyperhidrosis patients with a coagulation power of 5 W at a frequency of three times every 2 s. We found that left stellate stimulation prolongs the Q-T interval and increases the heart rate, whereas right stellate stimulation affects the Q-T interval and heart rate insignificantly, just like the case in dogs in which the left stellate ganglion predominates the right one in determining the Q-T interval. Left stellate stimulation after destruction of the left second and third ganglia also prolongs the Q-T interval, suggesting that the left stellate ganglion is more important in determining the Q-T interval.

Epinephrine release from the heart during left stellate ganglion stimulation in dogs

1988 ◽  
Vol 254 (4) ◽  
pp. R659-R662 ◽  
Author(s):  
F. Peronnet ◽  
R. Nadeau ◽  
G. Boudreau ◽  
R. Cardinal ◽  
D. Lamontagne ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
High Performance ◽  
Stellate Ganglion ◽  
Blood Samples ◽  
Radioenzymatic Assay ◽  
Left Stellate Ganglion ◽  
Anesthetized Dogs ◽  
Significant Uptake ◽  
Stimulation Of

Plasma epinephrine (E) and norepinephrine (NE) concentrations were measured (radioenzymatic assay) in blood samples simultaneously withdrawn from the aorta (Ao) and coronary sinus (CS) on 10 anesthetized dogs immediately before and during a 1-min period of electrical stimulation of the left stellate ganglion (4 V, 4 ms, 10 Hz). Heart rate and systolic blood pressure significantly increased in response to electrical stimulation (152 +/- 8 to 180 +/- 15 beats/min and 128 +/- 12 to 149 +/- 12 mmHg, mean +/- SE; P less than 0.05). Plasma NE concentrations were not significantly different in the Ao and the CS (432 +/- 110 and 319 +/- 67 pg/ml) before the stimulation, whereas a net removal of E was present across the myocardium (Ao, 172 +/- 61; CS, 71 +/- 22 pg/ml). A large NE spillover in the CS was observed during the stimulation (Ao, 1,555 +/- 513; CS, 10,583 +/- 3,753 pg/ml). A significant output of E from the myocardium was also present (Ao, 165 +/- 42; CS, 291 +/- 74 pg/ml) during the stimulation. Determination of NE and E concentrations by high-performance liquid chromatography in five of the dogs confirmed the observation made with the radioenzymatic assay, i.e., a significant uptake (66%) of blood-borne E was present across the myocardium in the control situation (Ao, 320 +/- 97; CS, 110 +/- 23 pg/ml), whereas plasma E concentrations in the CS (280 +/- 61 pg/ml) were 1.5 times the values found in Ao (184 +/- 56 pg/ml) under electrical stimulation. These observations give further support to the hypothesis that endogenous tissue E can act as a cotransmitter of sympathetic fibers.

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.

Evaluation of β-Adrenerglc Blocking Agents in Presence of Adrenergic Tone

1972 ◽  
Vol 50 (5) ◽  
pp. 381-388
Author(s):  
Victor Elharrar ◽  
Reginald A. Nadeau
Keyword(s):  
Dose Response ◽  
Sinus Node ◽  
Stellate Ganglion ◽  
Sodium Pentobarbital ◽  
Response Curves ◽  
Chronotropic Response ◽  
Blocking Agents ◽  
Sinus Node Artery ◽  
Anesthetized Dogs ◽  
The Right

The importance of the level of adrenergic tone in the determination of the dose–response curve to noradrenaline (NA) and in the evaluation of β-adrenergic blocking agents was studied in open-chest sodium pentobarbital anesthetized dogs by injecting drugs directly into the sinus node artery. Changes in the level of adrenergic tone by stimulating the right stellate ganglion resulted in variation of the observed chronotropic response to NA and of its ED50. The chronotropic responses were corrected by taking into account the underlying adrenergic tone. The negative chronotropic effect of dl-propranolol (1 and 10 μg) appeared to be related to its β-blocking properties and not to its quinidine-like effects as shown by the lack of effect of d-propranolol injected at the same doses. The magnitude of the negative chronotropic effects of 10 μg of propranolol and 100 μg of practolol, oxprenolol, and sotalol was shown to be related to the initial heart rate and consequently to the level of adrenergic tone. The comparison of these four β-blocking agents was carried out on corrected dose-response curves to NA. Their relative potencies were found to be: propranolol > oxprenolol > practolol > sotalol, corresponding to ratios of 1, [Formula: see text], [Formula: see text], and [Formula: see text]

Blood Pressure and Pulse Rate in the Foetal Sheep

1945 ◽  
Vol 22 (1-2) ◽  
pp. 63-74
Author(s):  
JOSEPH BARCROFT ◽  
D. H. BARRON
Keyword(s):  
Blood Pressure ◽  
Central Nervous System ◽  
Nervous System ◽  
Pulse Rate ◽  
Umbilical Artery ◽  
The Central Nervous System ◽  
The Right ◽  
First Moment ◽  
Left Vagus ◽  
Stimulation Of

1. A method (the needle method) is described for the measurement of the pressure in the stream going through a vessel. 2. In the foetal sheep the needle method applied to the umbilical artery gives substantially the same results as the mercurial manometer applied to the carotid, until about half-way through the gestation period. 3. As gestation proceeds the needle method applied at the first moment at which it can be applied to the umbilical artery (or a branch) gives readings substantially lower, and increasingly lower as gestation proceeds, than does the mercurial manometer read at the first moment at which it can be read. 4. The discrepancy is due to the sum of a number of causes which are discussed, but of these the most important is an actual rise of pressure between the time of delivery and the completion of the dissections contingent on the use of the mercurial manometer. 5. The cause of this is not at present demonstrated, but either or both of two factors may be concerned: (a) a dulling of the central nervous system which weakens the depressor reflex; (b) the establishment of a greater degree of vasomotor tone consequent on the bombardment of the central nervous system with sensory stimuli. 6. The pulse rates in utero and just after delivery of the foetus into a saline bath at 39-40°C. (the umbilical circulation being unimpaired) are not significantly different. 7. The pulse rate quickens up to the 70th-80th day, after which it becomes slower as gestation proceeds. 8. If both vagi be severed, the pulse rate te to quicken throughout gestation. The pulse, therefore, comes increasingly under vagus inhibition from the 80th-90th day onwards. 9. Even after the vagi have been cut after the 120th day (it has not been tried before) adrenalin in sufficient quantity will cause a further quickening of the pulse. 10. The earliest date at which stimulation of the peripheral end of the right vagus was observed to slow the heart was the 77th day. On the 85th day peripheral stimulation of the left vagus also failed, but succeeded on the 101st day. 11. Central stimulation of the left vagus, with the right vagus intact, produced slowing on the 77th day. 12. Slowing of the heart synchronous with rise of arterial pressure has been observed on the 111th day. 13. Slowing of the heart which bears evidence of being reflex has been obtained by raising the blood pressure (clamping the cord) on the 121st day and by injection of adrenalin on the 118th day. 14. Approaching term both the carotid sinus and cardiac depressor mechanisms are functional. 15. Lowering of the blood pressure as the result of stimulation of the central end of the vagus and with both vagi severed can be demonstrated late in gestation.

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.

Pulmonary C-fibers reflexly increase secretion by tracheal submucosal glands in dogs

1985 ◽  
Vol 58 (3) ◽  
pp. 907-910 ◽  
Author(s):  
H. D. Schultz ◽  
A. M. Roberts ◽  
C. Bratcher ◽  
H. M. Coleridge ◽  
J. C. Coleridge ◽  
...  
Keyword(s):  
Gland Secretion ◽  
Right Atrial ◽  
Vagus Nerves ◽  
C Fibers ◽  
Airway Secretion ◽  
Submucosal Glands ◽  
C Fiber ◽  
Anesthetized Dogs ◽  
The Right ◽  
Stimulation Of

Stimulation of bronchial C-fibers evokes a reflex increase in secretion by tracheal submucosal glands, but the influence of pulmonary C-fibers on tracheal gland secretion is uncertain. In anesthetized dogs with open chests, we sprayed powdered tantalum on the exposed mucosa of a segment of the upper trachea to measure the rate of secretion by submucosal glands. Secretions from the gland ducts caused elevations (hillocks) in the tantalum layer. We counted hillocks at 10-s intervals for 60 s before and 60 s after we injected capsaicin (10–20 micrograms/kg) into the right atrium to stimulate pulmonary C-fiber endings. Right atrial injection of capsaicin increased the rate of hillock formation fourfold, but left atrial injection had no significant effect. The response was abolished by cutting the vagus nerves or cooling them to 0 degree C. We conclude that the reflex increase in tracheal submucosal gland secretion evoked by right atrial injection of capsaicin was initiated as capsaicin passed through the pulmonary vascular bed, and hence that pulmonary C-fibers, like bronchial C-fibers, reflexly increase airway secretion.

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.

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