Enhancement of cardiac vagal action during ischaemia of the sino-atrial node

1986 ◽  
Vol 71 (4) ◽  
pp. 449-451 ◽  
Author(s):  
Erica K. Potter ◽  
D. I. McCloskey ◽  
Gillian P. Courtice
Keyword(s):  
Heart Rate ◽  
Vagus Nerve ◽  
Sinoatrial Node ◽  
Vagal Stimulation ◽  
Arterial Supply ◽  
The Right

1. The effect of ischaemia of the sino-atrial node on cardiac vagal action was studied in anaesthetized dogs. 2. The cut, cardiac end of the right vagus nerve was stimulated with a standard supramaximal stimulus every 10 s. The arterial supply to the sinoatrial node was occluded for periods of 1–3 min during this intermittent vagal stimulation. 3. Vagal action on heart rate was potentiated during ischaemia of the sino-atrial node.

Long-term effects of hyperpolarization-activated inward current blockade on cardiac parasympathetic activity

EP Europace ◽  
2021 ◽  
Vol 23 (Supplement_3) ◽  
Author(s):  
A Scridon ◽  
VB Halatiu ◽  
AI Balan ◽  
DA Cozac ◽  
GV Moldovan ◽  
...  
Keyword(s):  
Heart Rate ◽  
Vagus Nerve ◽  
Vagal Stimulation ◽  
Sinus Node ◽  
Vagal Tone ◽  
Right Atrial ◽  
The Right

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): This work was supported by a grant of the Romanian Ministry of Education and Research, CNCS - UEFISCDI Background The autonomic control of the pacemaker current, If, and the molecular mechanisms underlying parasympathetic If modulation are well understood. Conversely, the effects of chronic If blockade on the parasympathetic nervous system and on the heart rate (HR) response to acute parasympathetic changes are still largely unknown. Such interactions could significantly influence the course of patients undergoing chronic therapy with the If blocker ivabradine. Purpose We aimed to assess the effects of long-term If blockade using ivabradine on cardiac autonomic modulation and on the cardiovascular response to acute in vivo and in vitro parasympathetic stimulation. Methods Radiotelemetry ECG transmitters were implanted in 6 Control and 10 ivabradine-treated male Wistar rats (IVA; 3 weeks, 10 mg/kg/day); sympathetic and parasympathetic heart rate variability parameters were assessed. At the end of the study, the right atrium was removed and right atrial HCN(1-4) RNA expression levels were analyzed. The HR and systolic blood pressure (SBP) responses to in vivo electrical stimulation of the right vagus nerve (2–20 Hz) and the spontaneous sinus node discharge rate (SNDR) response to in vitro cholinergic receptors stimulation using carbamylcholine (10-9–10-6 mol/L) were assessed in 6 additional Control and 10 IVA rats. Results At the end of the study, mean 24-h HR was significantly lower in the IVA compared with the Control rats (301.3 ± 7.5 bpm vs. 341.5 ± 8.3 bpm; p< 0.01). Ivabradine administration led to a significant increase in vagal tone and shifted the sympatho-vagal balance towards vagal dominance (awake, asleep, and over 24-h; all p< 0.05). In the Control rats, in vivo vagus nerve stimulation induced a progressive decrease in both the SBP (p = 0.0001) and the HR (p< 0.0001). Meanwhile, in the IVA rats, vagal stimulation had no effect on the HR (p = 0.16) and induced a significantly lower drop in SBP (p< 0.05). Ivabradine-treated rats also presented a significantly lower SNDR drop in response to carbamylcholine (p< 0.01) and significantly higher HCN4 expression (p = 0.02). Conclusion Long-term If blockade using ivabradine caused a significant increase in vagal tone and shifted the autonomic balance towards vagal dominance in rats. Given the highly proarrhythmic effects of vagal activation at the atrial level, these findings could provide an explanation for the increased risk of atrial fibrillation associated with ivabradine use in clinical trials. In addition, ivabradine reduced the HR response to direct muscarinic receptors stimulation, canceled the cardioinhibitory response and blunted the hemodynamic response to in vivo vagal stimulation, and led to significant sinus node HCN4 up-regulation. These data suggest that ivabradine-induced HCN4 and the consequent If up-regulation could render the sinus node less sensitive to acute vagal inputs and could thus protect against excessive bradycardia induced by acute vagal activation.

AV blocking due to asynchronous vagal stimulation in rats

2000 ◽  
Vol 278 (1) ◽  
pp. H67-H73 ◽  
Author(s):  
P. Schiereck ◽  
N. Sanna ◽  
W. L. Mosterd
Keyword(s):  
Heart Rate ◽  
Nervous System ◽  
Sinoatrial Node ◽  
Parasympathetic Nervous System ◽  
Vagal Stimulation ◽  
Stimulation Protocol ◽  
Av Node ◽  
Vagal Nerves ◽  
The Right ◽  
Conduction Properties

The parasympathetic nervous system innervates the heart through two cervical vagal branches. The right vagal branch mainly influences the heart rate by the modulation of the rhythmogenesis of the sinoatrial node. The left branch predominantly influences the conduction properties of the atrioventricular (AV) node. We investigated the effect of asynchronous stimulation by the vagal nerves on the occurrence of irregularities in heart rate. In rats, the vagal nerves were isolated and cut. Different vagal stimulation patterns (continuous, pulsed) were applied. The heart was beating spontaneously under continuous vagal stimulation. In case of pulsed vagal stimulation, the atria were paced at different rates. Asynchronicity was induced by delaying the right stimulus with respect to the left stimulus (early right) or the left stimulus with respect to the right stimulus (early left). The value of the fraction of deviated R-R or P-Q intervals in the distribution in the histogram was used to characterize irregularities during a stimulation protocol (duration in case of continuous stimulation: 20 s; pulsed stimulation: 120 s). Under both stimulation patterns (continuous or pulsed), we found that early left vagal stimulation introduced a much larger fraction of deviated intervals in the R-R or P-Q histogram (in R-R: 29.1 ± 4.9%; in P-Q: 12.90 ± 1.95%) than early right vagal stimulation (in R-R: 7.4 ± 2.0%; in P-Q: 1.05 ± 0.50%) or synchronous stimulation (in R-R: 8.2 ± 3.6%; in P-Q: 2.15 ± 0.75%). We conclude that early stimulation by the left vagal nerve can introduce irregularities in heart rate, mainly due to different degrees of AV nodal blockade.

Central vascular flow patterns in the alligator Alligator mississipiensis

1995 ◽  
Vol 269 (5) ◽  
pp. R1133-R1139 ◽  
Author(s):  
G. M. Malvin ◽  
J. W. Hicks ◽  
E. R. Greene
Keyword(s):  
Vagus Nerve ◽  
Swirling Flow ◽  
Vagal Stimulation ◽  
Contrast Echocardiography ◽  
Flow Patterns ◽  
Left Ventricular ◽  
Vascular Flow ◽  
The Right ◽  
Alligator Mississipiensis ◽  
Central Circulation

Many different flow patterns have been described through the central circulation of crocodilian reptiles. We tested the hypothesis that the vagus nerve stimulation promotes right-to-left (R-L) shunting in the alligator. Flow patterns were investigated before and during stimulation of the intact left vagus nerve using three methods. 1) Atrial and aortic PO2 were measured simultaneously and continuously by gas probes. 2) Atrial outflows were tracked with a blood tracer (helium). 3) Flows were assessed with echocardiography. Four different flow patterns were observed before vagal stimulation: left ventricular (LV) blood flowed into both the right (RAo) and left (LAo) aortas, whereas right ventricular (RV) blood flowed only into the LAo; both aortas received a mixture of LV and RV blood; only LV blood perfused both aortas; and RV blood flowed into both aortas, but LV blood flowed only into the RAo. During vagal stimulation, both aortas received a mixture of LV and RV blood in half of the animals, and in the other half, both aortas received RV blood, but LV blood flowed only into the RAo. Doppler and contrast echocardiography demonstrated swirling flow in the foramen of Panizza and the base of the LAo during systole. These data indicate that vagal stimulation either maintains or produces R-L shunting, flow patterns are variable, and blood can swirl in the foramen of Panizza and LAo base.

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.

Regulatory peptides as modulators of vagal influence on cardiac rhythm

1995 ◽  
Vol 73 (9) ◽  
pp. 1235-1245 ◽  
Author(s):  
Vladimir M. Pokrowsky ◽  
Oleg E. Osadchiy
Keyword(s):  
Heart Rate ◽  
Vagus Nerve ◽  
Regulatory Peptides ◽  
Burst Stimulation ◽  
Different Types ◽  
Delta Sleep ◽  
Heart Contraction ◽  
The Right ◽  
Delta Sleep Inducing Peptide ◽  
Vagal Influence

When the right vagus nerve of anesthetized cats was stimulated with repetitive bursts of pulses, decelerated heart rate became synchronized to the rhythm of the vagal bursts. Each burst applied to the vagus was followed by a single heart contraction. Within defined limits an increase in the frequency of vagal bursts evoked a proportional acceleration of the heart, whereas a decreased frequency diminished the heart rate. Therefore, over the range of synchronization the heart rate was precisely controlled by changing the vagal stimulation rate. We concluded that the chronotropic effect evoked by vagal bursts was composed of two functionally different types of influence, namely, inhibitory tonic and synchronizing. The vagotropic influence of intravenously injected regulatory peptides was found to be selective for either the tonic or synchronizing component. For instance, dalargin (D-Ala2-Leu5-Arg6-enkephalin) and neokyotorphin selectively diminished the inhibitory tonic vagal influence, whereas delta sleep inducing peptide and neurotensin potentiated it. The magnitude of synchronizing vagal influence was not modified by these peptides. In contrast, secretin selectively inhibited the synchronizing vagal effect, but the tonic one was not affected. Somatostatin potentiated the synchronizing effect but diminished the tonic one. These data support the hypothesis that certain regulatory peptides can modulate the effects of repetitive vagal bursts on pacemaker activity.Key words: vagus nerve, burst stimulation, controlled bradycardia, regulatory peptides.

Supersensitivity to l-norepinephrine of the denervated sinoatrial node

1965 ◽  
Vol 208 (2) ◽  
pp. 255-259 ◽  
Author(s):  
David E. Donald ◽  
John T. Shepherd
Keyword(s):  
Vagus Nerve ◽  
Sinoatrial Node ◽  
Sinus Node ◽  
Sympathetic Nerves ◽  
Cardiac Denervation ◽  
Cervical Vagotomy ◽  
Cervical Ganglia ◽  
The Right ◽  
Cardiac Nerves ◽  
Stimulation Of

Following attempted denervation of the heart by the technic of regional neural ablation, dogs with incomplete cardiac denervation were shown to have the same supersensitivity to l-norepinephrine as dogs in which the denervation of the heart was complete. Dogs with chronic bilateral stellate ganglionectomy or those pretreated with reserpine had cardiac acceleration in response to the administration of tyramine or to stimulation of the stellate cardiac nerves, but did not demonstrate supersensitivity to l-norepinephrine. No supersensitivity was seen in dogs with chronic bilateral cervical vagotomy. Excision of the right stellate and caudal cervical ganglia and the immediately adjacent right vagus nerve resulted in supersensitivity to l-norepinephrine. In these animals cardiac acceleration resulted from stimulation of the left stellate cardiac nerves or from the administration of tyramine. The supersensitivity was lost after excision of the sinoatrial node. It is concluded that one can uniquely denervate the sinus node and that dogs so treated will develop supersensitivity to l-norepinephrine despite the presence of functional sympathetic nerves to the rest of the heart.

Sympathetic-parasympathetic interaction and accentuated antagonism in conscious dogs

1991 ◽  
Vol 260 (2) ◽  
pp. H335-H340 ◽  
Author(s):  
M. Stramba-Badiale ◽  
E. Vanoli ◽  
G. M. De Ferrari ◽  
D. Cerati ◽  
R. D. Foreman ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Rate ◽  
Sympathetic Activity ◽  
Vagal Stimulation ◽  
Inhibitory Effect ◽  
Conscious Dogs ◽  
Exercise Heart Rate ◽  
Bipolar Electrode ◽  
The Right ◽  
Frequency Of Stimulation

The heart rate response to vagal stimulation and the interaction with sympathetic activity was evaluated in conscious dogs at rest and during exercise; the latter was used as a tool to physiologically elevate sympathetic activity. In 20 dogs with a healed myocardial infarction and in 7 healthy dogs a bipolar electrode was chronically implanted around the right cervical vagus. Vagal stimulation (3 ms; 2.1 +/- 0.7 mA; 2, 4, 6, 8, 10, 12 Hz) was performed while dogs stood on the treadmill (heart rate 120 +/- 25 beats/min) and while they exercised (201 +/- 17 beats/min). Gradual increases of the frequency of vagal stimulation gradually enhanced the inhibitory effect on heart rate both before and during exercise. During exercise, heart rate reduction was significantly greater than that produced at rest at any frequency of stimulation (P less than 0.001). This difference widened as the frequency of stimulation increased and the interaction with or without the presence of exercise was significant (P less than 0.02). Vagal stimulation produced similar effects in the seven dogs without myocardial infarction. These data demonstrate that the vagal-sympathetic "accentuated antagonism" described in anesthetized animals is also present in conscious dogs.

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.

Effects of catecholamines on cardiac chronotropic response to vagal stimulation in the dog

1983 ◽  
Vol 245 (5) ◽  
pp. H721-H724 ◽  
Author(s):  
C. Chassaing ◽  
P. Duchene-Marullaz ◽  
M. J. Veyrac
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Vagus Nerve ◽  
Neurotransmitter Release ◽  
Acetylcholine Release ◽  
Vagal Stimulation ◽  
Norepinephrine Release ◽  
Chronotropic Response ◽  
Anesthetized Dogs ◽  
Stimulation Of

The influence of isoproterenol, norepinephrine, and dopamine on the cardiomoderator effects of moderate vagal stimulation was studied in anesthetized dogs. The drugs were administered at increasing doses in successive perfusions. Stimulation of the vagus nerve, the parameters of which remained constant throughout each experiment, was performed immediately before each sequence of perfusion and after 10-min perfusion. Isoproterenol at 0.025, 0.05, 0.1, and 0.2 microgram X kg-1 X min-1 raised heart rate dose relatedly but did not alter heart rate under vagal stimulation. Thus the amplitude of vagal bradycardic effects increased dose relatedly. Norepinephrine at 0.125, 0.25, 0.5, and 1 microgram X kg-1 X min-1 lowered heart rate through reflex hypertension. Heart rate under vagal stimulation remained constant. Thus the effects of vagal stimulation decreased as dose increased, finally becoming null. Dopamine at 0.5, 1, 2.5, and 5 micrograms X kg-1 X min-1 did not significantly alter heart rate, but at 10 and 20 micrograms X kg-1 X min-1, like norepinephrine, it raised blood pressure, causing a reflex fall in heart rate. At all doses, heart rate under vagal stimulation remained stable. Consequently, at the highest doses, the net effects of vagal stimulation were slight. These results suggest the simultaneous involvement of sympathetic-parasympathetic interactions both post- and prejunctionally. In the latter case, different mechanisms of regulation of neurotransmitter release are involved during vagal stimulation according to the sympathomimetic used. With isoproterenol, norepinephrine release seems more particularly affected, whereas with norepinephrine and dopamine, acetylcholine release is apparently inhibited.

Cholinesterase affects dynamic transduction properties from vagal stimulation to heart rate

1998 ◽  
Vol 275 (2) ◽  
pp. R541-R547 ◽  
Author(s):  
Tsutomu Nakahara ◽  
Toru Kawada ◽  
Masaru Sugimachi ◽  
Hiroshi Miyano ◽  
Takayuki Sato ◽  
...  
Keyword(s):  
Heart Rate ◽  
Transfer Function ◽  
Vagus Nerve ◽  
White Noise ◽  
Vagal Stimulation ◽  
Dynamic Properties ◽  
Gaussian White Noise ◽  
Corner Frequency ◽  
Nerve Activity ◽  
Noise Pattern

Recent investigations in our laboratory using a Gaussian white noise technique showed that the transfer function representing the dynamic properties of transduction from vagus nerve activity to heart rate had characteristics of a first-order low-pass filter. However, the physiological determinants of those characteristics remain to be elucidated. In this study, we stimulated the vagus nerve according to a Gaussian white noise pattern to estimate the transfer function from vagal stimulation to the heart rate response in anesthetized rabbits and examined how changes in acetylcholine kinetics affected the transfer function. We found that although increases in the mean frequency of vagal stimulation from 5 to 10 Hz did not change the characteristics of the transfer function, administration of neostigmine (30 μg ⋅ kg−1 ⋅ h−1iv), a cholinesterase inhibitor, increased the dynamic gain from 8.19 ± 3.66 to 11.7 ± 4.88 beats ⋅ min−1 ⋅ Hz−1( P < 0.05), decreased the corner frequency from 0.12 ± 0.05 to 0.04 ± 0.01 Hz ( P < 0.01), and increased the lag time from 0.17 ± 0.12 to 0.27 ± 0.08 s ( P < 0.05). These results suggest that the rate of acetylcholine degradation at the neuroeffector junction, rather than the amount of available acetylcholine, plays a key role in determining the dynamic properties of transduction from vagus nerve activity to heart rate.

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