Heart rate response to sympathetic stimulation before and after sodium pentobarbital

1975 ◽  
Vol 228 (5) ◽  
pp. 1568-1574 ◽  
Author(s):  
MJ Cowan ◽  
AM Scher ◽  
J Hildebrandt
Keyword(s):  
Heart Rate ◽  
Heart Rate Response ◽  
Stellate Ganglion ◽  
Sodium Pentobarbital ◽  
Sympathetic Stimulation ◽  
Initial Decrease ◽  
Before And After ◽  
The Right ◽  
Main Effects ◽  
Stimulation Of

Heart rate response to electrical stimulation of the right stellate ganglion of vagotomized cats was studied before and after the administration of sodium pentobarbital. The increase and decrease of heart rate with the initiation and cessation of sympathetic stimulation could be accurately described by separate exponential time functions. The time constants of rise and decline, the maximum steady-state heart rate, and the time between cessation of stimulation and initial decrease of heart rate (lag) were functions of the frequency and voltage of stimulation. The main effects of sodium pentobarbital were: 1) to prolong the rise of heart rate by 20-30 percent (P smaller than 0.0001),2) to prolong the decay of heart rate by 36-56 percent (P smaller than 0.005), and 3) to decrease the resting heart rate. The effects were observed 10 min after administration of the drug and lasted at least 4 h.

scholarly journals Recording Intrinsic Nerve Activity at the Sinoatrial Node in Normal Dogs with High-density Mapping

2021 ◽  
Author(s):  
Yufan Yang ◽  
Yuan Yuan ◽  
Johnson Wong ◽  
Michael C. Fishbein ◽  
Peng-Sheng Chen ◽  
...  
Keyword(s):  
Heart Rate ◽  
Sinoatrial Node ◽  
Stellate Ganglion ◽  
High Density ◽  
Nerve Activity ◽  
Density Mapping ◽  
Sinus Rate ◽  
Intrinsic Nerve ◽  
The Right ◽  
Stimulation Of

Background - It is known that autonomic nerve activity controls the sinus rate. However, the coupling between local nerve activity and electrical activation at the sinoatrial node (SAN) remains unclear. We hypothesized that we would be able to record nerve activity at the SAN to investigate if right stellate ganglion (RSG) activation can increase the local intrinsic nerve activity, accelerate sinus rate, and change the earliest activation sites (EASs). Methods - High-density mapping of the epicardial surface of the right atrium (RA) including the SAN was performed in 6 dogs during stimulation of the RSG, and after RSG stellectomy. A radiotransmitter was implanted into 3 additional dogs to record RSG and local nerve activity at the SAN. Results - Heart rate accelerated from 108±4 bpm at baseline to 125±7 bpm after RSG stimulation ( P =0.001), and to 132±7 bpm after apamin injection ( P <0.001). Both electrical RSG stimulation and apamin injection induced local nerve activity at the SAN with the average amplitudes of 3.60±0.72 µV and 3.86±0.56 µV, respectively. RSG stellectomy eliminated the local nerve activity and decreased the heart rate. In ambulatory dogs, local nerve activity at the SAN had a significantly higher average Pearson correlation to heart rate (0.72±0.02, P =0.001) than RSG nerve activity to HR (0.45±0.04 P =0.001). Conclusions - Local intrinsic nerve activity can be recorded at the SAN. Short bursts of these local nerve activities are present before each atrial activation during heart rate acceleration induced by stimulation of the right stellate ganglion.

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.

Diabetes reduces right atrial β-adrenergic signaling but not agonist stimulation of heart rate in swine

2001 ◽  
Vol 79 (4) ◽  
pp. 346-351 ◽  
Author(s):  
William C Stanley ◽  
Justin J Dore ◽  
Jennifer L Hall ◽  
C Dawn Hamilton ◽  
Robert D Pizzurro ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Heart Rate ◽  
Adenylyl Cyclase ◽  
Right Atrium ◽  
Heart Rate Response ◽  
Signal Transduction Pathway ◽  
Adrenergic Stimulation ◽  
Adenylyl Cyclase Activity ◽  
The Right ◽  
Stimulation Of

This study assessed the effects of streptozotocin diabetes in swine on the heart rate response to β-adrenergic stimulation the adenylyl cyclase signal transduction pathway. Diabetic animals (n = 9) were hyperglycemic compared to the control group (n = 10) (12.6 ± 1.0 vs. 3.53 ± 0.29 mM). There were no significant differences between the diabetic and nondiabetic groups in the heart rate response to isoproterenol, however, there was a significant reduction (14%) in β-adrenergic receptor density in the right atrium in the diabetic (61 ± 3 fmol/mg protein) versus the nondiabetic group (71 ± 3) (P < 0.05). The content of guanosine triphosphate binding regulatory proteins (Gs and Gi) in the right atrium was not affected by diabetes, nor was adenylyl cyclase activity under unstimulated conditions or with receptor-dependent stimulation with isoproterenol. On the other hand, adenylyl cyclase activity was 34% lower when directly stimulated with forskolin, and it was reduced by 23% when stimulated through Gs with Gpp(NH)p. In conclusion, beta-adrenergic stimulation of heart rate with isoproteronol and the receptor-dependent signal transduction pathway remained intact in the right atrium of diabetic swine despite reduced beta-adrenergic receptor density, G-protein content, and direct stimulation of adenylyl cyclase activity.Key words: diabetes, G-proteins, heart rate, receptors, signal transduction.

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]

Effect of canine cardiac nerves on heart rate, rhythm, and pacemaker location

1986 ◽  
Vol 250 (4) ◽  
pp. H630-H644 ◽  
Author(s):  
R. B. Schuessler ◽  
J. P. Boineau ◽  
A. C. Wylds ◽  
D. A. Hill ◽  
C. B. Miller ◽  
...  
Keyword(s):  
Heart Rate ◽  
Right Atrium ◽  
General Trend ◽  
Canine Model ◽  
Right Atrial ◽  
Sympathetic Stimulation ◽  
Open Chest ◽  
Left Posterior ◽  
The Right ◽  
Cardiac Nerves

In open-chest dogs, right- and left-sided cardiac nerves were stimulated to determine their effect on heart rate, rhythm, and pacemaker location. The majority of the nerves produced chronotropic changes; 72% of the induced rhythms originated from within the atrial pacemaker complex. Ten percent of the stimulations produced an atrio-ventricular (AV) nodal rhythm; most of the time this was induced by the left posterior and anterior ansae and ventrolateral nerves. The dominance of a lateral right atrial pacemaker was observed in 8% of the stimulations; the dorsal cardiac and innominate nerves induced this rhythm the majority of the time. The general trend was for a cranial shift in the location of the pacemaker within the pacemaker complex with sympathetic stimulation and a caudal shift with parasympathetic stimulation. Exceptions to the pattern may be explained by the preferential effect of the nerves on the pacemakers in the right atrium. The study demonstrates, in the canine model, that in addition to the sinus and AV nodes, there is a system of pacemakers controlled by the cardiac nerves.

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.

Intermittent hypoxia modulates nNOS expression and heart rate response to sympathetic nerve stimulation

2001 ◽  
Vol 281 (1) ◽  
pp. H132-H138 ◽  
Author(s):  
R. M. Mohan ◽  
S. Golding ◽  
D. J. Paterson
Keyword(s):  
Heart Rate ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Intermittent Hypoxia ◽  
Stellate Ganglion ◽  
No Synthase ◽  
Sympathetic Nerve Stimulation ◽  
Synthase Inhibitor ◽  
The Right ◽  
And Control

Nitric oxide (NO) decreases norepinephrine (NE) release and the heart rate (HR) response to sympathetic nerve stimulation (SNS). We tested the hypothesis that the enhanced HR response to sympathetic activation following chronic intermittent hypoxia (IH) results from a peripheral modulation of pacemaking by NO. Isolated guinea pig double atrial/right stellate ganglion preparations were studied from animals that had been exposed to IH ( n = 20) and control animals ( n = 22). The HR response to SNS was significantly enhanced in the IH group compared with the controls. However, the increase in HR with cumulative doses (0.1–10 μM) of bath-applied NE was similar in both groups. Western blot analysis showed less neuronal NO synthase in the right atria from the IH group. In IH animals, the NO synthase inhibitor, N ω-nitro-l-arginine (l-NNA; 100 μM) did not alter the increased HR response to SNS, whereas in control animals l-NNA significantly increased the HR response to SNS; an effect that was reversed with excess l-arginine. In conclusion, the enhanced HR response to SNS after IH may be related to a decreased inhibitory action of NO on presynaptic NE release.

Dynamic vagosympathetic interaction augments heart rate response irrespective of stimulation patterns

1997 ◽  
Vol 272 (5) ◽  
pp. H2180-H2187 ◽  
Author(s):  
T. Kawada ◽  
M. Sugimachi ◽  
T. Shishido ◽  
H. Miyano ◽  
Y. Ikeda ◽  
...  
Keyword(s):  
Heart Rate ◽  
Transfer Function ◽  
Heart Rate Response ◽  
Rate Regulation ◽  
Heart Rate Regulation ◽  
Two Systems ◽  
Tonic Stimulation ◽  
White Noises ◽  
Dynamic Stimulation ◽  
Stimulation Of

We previously demonstrated that tonic stimulation of either the sympathetic or the vagal nervous system augmented the dynamic heart rate response to the other of the two systems. We characterized the phenomenon as bidirectional augmentation of heart rate regulation. The question remained unanswered, however, as to whether such augmentation could occur under simultaneous dynamic stimulation of the two systems. The transfer characteristics from nerve stimulation to heart rate were well described by linear systems analysis, although no attention was paid to the aphasic nature of the stimuli in relation to each R-R interval. When we stimulated the two nerves with statistically independent Gaussian white noises, gain of the transfer function increased by 63.2 +/- 47.4% relative to individual stimulation (P < 0.05). When we stimulated the two nerves with mutually reciprocal Gaussian white noises, gain of the transfer function increased by 54.9 +/- 49.1% (P < 0.05). Thus simultaneous dynamic stimulation of the sympathetic and vagal systems bidirectionally augmented heart rate regulation irrespective of the pattern of the stimulation signals.

Effect of cervical vagal stimulation on chicken heart rate and atrioventricular conduction

1983 ◽  
Vol 244 (2) ◽  
pp. R235-R243
Author(s):  
J. M. Goldberg ◽  
M. H. Johnson ◽  
K. D. Whitelaw
Keyword(s):  
Heart Rate ◽  
Vagal Stimulation ◽  
Atrioventricular Conduction ◽  
Right Atrial ◽  
Atrial Pacing ◽  
Chicken Heart ◽  
Av Conduction ◽  
Supramaximal Stimulation ◽  
The Right ◽  
Stimulation Of

The effects of supramaximal stimulation of the right and left cervical vagi on heart rate, pacemaker localization, and atrioventricular (AV) conduction were investigated in 15 anesthetized open-chest chickens before and after atropine sulfate. Epicardial bipolar electrograms were recorded from selected atrial sites and right ventricle. A back lead electrocardiogram was also recorded. The effect of stimulation on atrioventricular conduction was evaluated during pacing from one of the right atrial recording sites. Supramaximal stimulation of either cervical vagus produced bradycardia but not cardiac arrest. Heart rate was reduced from an average spontaneous rate of 282 +/- 13 (SE)/min to 161 +/- 13/min with stimulation of the right and left cervical vagus. Pacemaker shifts occurred in over 50% of the vagal stimulations. The most frequent shift occurred to the lower AV node or ventricles. Pacemaker shifts to the AV junctional region producing almost simultaneous activation of the atria and ventricles were not observed. Vagal stimulation during atrial pacing produced minimal prolongation in AV conduction time [right vagus, 13 +/- 3 (SE) ms; left vagus, 8 +/- 2 ms]. Second and third degree heart blocks were not observed during pacing. Vagal stimulation after atropine indicates that the cervical vagi do not contain sympathetic fibers going to pacemaker or AV conduction tissues.

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