Accurate control of the heart rate in monkeys by burst stimulation of the vagus nerve

1987 ◽  
Vol 104 (3) ◽  
pp. 1180-1182
Author(s):  
V. M. Pokrovskii ◽  
Yu. R. Sheikh-Zade ◽  
V. M. Kruchinin ◽  
T. G. Urmancheeva
Keyword(s):  
Heart Rate ◽  
Vagus Nerve ◽  
Burst Stimulation ◽  
Stimulation Of

Heart rate control by burst stimulation of the vagus nerve in rats

1984 ◽  
Vol 97 (4) ◽  
pp. 386-388
Author(s):  
M. V. Pokrovskii
Keyword(s):  
Heart Rate ◽  
Vagus Nerve ◽  
Rate Control ◽  
Heart Rate Control ◽  
Burst Stimulation ◽  
Stimulation Of

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.

Effect of met-enkephalin on sinus arrhythmia caused by burst stimulation of the vagus nerve

1993 ◽  
Vol 116 (1) ◽  
pp. 759-761
Author(s):  
O. E. Osadchii ◽  
V. M. Pokrovskii ◽  
I. L. Cherednik ◽  
A. N. Kurzanov
Keyword(s):  
Vagus Nerve ◽  
Burst Stimulation ◽  
Sinus Arrhythmia ◽  
Stimulation Of

Effect of neurotensin and epinephrine on sinus arrhythmia caused by burst stimulation of the vagus nerve

1997 ◽  
Vol 123 (5) ◽  
pp. 427-430 ◽  
Author(s):  
O. E. Osadchii ◽  
V. M. Pokrovskii ◽  
O. G. Kompaniets ◽  
A. N. Kurzanov
Keyword(s):  
Vagus Nerve ◽  
Burst Stimulation ◽  
Sinus Arrhythmia ◽  
Stimulation Of

Effects of sino-atrial ischaemia on the heart rate response to phasic burst stimulation of the right cervical vagus in the dog

1984 ◽  
Vol 18 (8) ◽  
pp. 486-496 ◽  
Author(s):  
J. BILLETTE ◽  
J.-P. BONIN ◽  
A. ARSENAULT ◽  
P. GAUTHIER
Keyword(s):  
Heart Rate ◽  
Heart Rate Response ◽  
Burst Stimulation ◽  
The Right ◽  
Stimulation Of

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.

scholarly journals Development and characterization of a chronic implant mouse model for vagus nerve stimulation

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Ibrahim T Mughrabi ◽  
Jordan Hickman ◽  
Naveen Jayaprakash ◽  
Dane Thompson ◽  
Umair Ahmed ◽  
...  
Keyword(s):  
Heart Rate ◽  
Vagus Nerve ◽  
Nerve Stimulation ◽  
Vagus Nerve Stimulation ◽  
Axonal Pathology ◽  
Device Implantation ◽  
Preclinical And Clinical Studies ◽  
Stimulation Of

Vagus nerve stimulation (VNS) suppresses inflammation and autoimmune diseases in preclinical and clinical studies. The underlying molecular, neurological, and anatomical mechanisms have been well characterized using acute electrophysiological stimulation of the vagus. However, there are several unanswered mechanistic questions about the effects of chronic VNS, which require solving numerous technical challenges for a long-term interface with the vagus in mice. Here, we describe a scalable model for long-term VNS in mice developed and validated in 4 research laboratories. We observed significant heart rate responses for at least 4 weeks in 60-90% of animals. Device implantation did not impair vagus-mediated reflexes. VNS using this implant significantly suppressed TNF levels in endotoxemia. Histological examination of implanted nerves revealed fibrotic encapsulation without axonal pathology. This model may be useful to study the physiology of the vagus and provides a tool to systematically investigate long-term VNS as therapy for chronic diseases modeled in mice.

Closed-loop control of the heart rate by electrical stimulation of the vagus nerve

2006 ◽  
Vol 44 (3) ◽  
pp. 161-169 ◽  
Author(s):  
Marco Tosato ◽  
Ken Yoshida ◽  
Egon Toft ◽  
Vitas Nekrasas ◽  
Johannes J. Struijk
Keyword(s):  
Heart Rate ◽  
Electrical Stimulation ◽  
Vagus Nerve ◽  
Closed Loop ◽  
Closed Loop Control ◽  
Loop Control ◽  
Stimulation Of
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