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.

Effects of calcium channel antagonists on the vagally mediated cardiac chronotropic response in dogs

1990 ◽  
Vol 68 (10) ◽  
pp. 1363-1367 ◽  
Author(s):  
Don W. Wallick ◽  
Sherry L. Stuesse ◽  
Paul Martin
Keyword(s):  
Electrical Stimulation ◽  
Vagus Nerve ◽  
Calcium Channel ◽  
Total Dose ◽  
Cycle Length ◽  
Cardiac Cycle ◽  
Vagal Stimulation ◽  
Calcium Channel Antagonists ◽  
Chronotropic Response ◽  
Stimulation Of

A brief electrical stimulation of the vagus nerve may elicit a triphasic response comprising (i) an initial prolongation of the same or the next cardiac cycle, (ii) a return of the subsequent cardiac cycle to about the level prior to vagal stimulation, and (iii) a secondary prolongation of cardiac cycle length that lasts several beats. We compared the effects of two calcium channel antagonists, verapamil and nifedipine, on this triphasic response to vagal stimulation in chloralose-anesthetized, open-chest dogs. In the absence of vagal stimulation, nifedipine (doses of 10, 40, and 50 μg/kg for a total dose of 100 μg/kg, i.v.) and verapamil (two doses of 100 μg/kg each, i.v.) increased the cardiac cycle length (A–A interval) by 16% (429 ± 20 to 496 ± 21 ms) and 29% (470 ± 33 to 605 ± 54 ms), respectively. Nifedipine (100 μg/kg total) attenuated the initial vagally mediated prolongation of the A–A interval, from 474 ± 19 to 369 ± 42 ms above the basal A–A interval. Following the initial prolongation of the vagal effect, other A–A intervals were not affected. In contrast, verapamil potentiated the vagally mediated initial prolongation in cardiac cycle length at the first dose administered (100 μg/kg) from 492 ± 17 to 561 ± 14 ms, but other increases in dosages had no further effect. Thus these two calcium channel antagonists have different effects on the sinoatrial chronotropic responses caused by brief vagal stimulation.Key words: autonomic control, parasympathetic, heart, calcium.

Effects of digoxin on the chronotropic responses to repetitive vagal stimules bursts in the dog

1984 ◽  
Vol 62 (11) ◽  
pp. 1411-1415 ◽  
Author(s):  
Daniel G. Pace ◽  
Yukitaka Masuda ◽  
Isaac Eisenstein ◽  
Matthew N. Levy
Keyword(s):  
Vagus Nerve ◽  
Cumulative Dose ◽  
Cardiac Cycle ◽  
Vagal Stimulation ◽  
Cardiac Pacemaker ◽  
Pacemaker Cells ◽  
Chronotropic Response ◽  
Cycle Lengths ◽  
Anesthetized Dogs

We studied the effects of digoxin on the chronotropic responses of the heart to repetitive bursts of vagal stimulation in chloralose-anesthetized dogs. The frequency of the stimulus bursts was increased linearly with time. Over a certain range of frequencies, the cardiac pacemaker became synchronized with the vagal stimulation in a 1:1 ratio of heart beats to stimulus bursts. Digoxin increased the range of cardiac cycle lengths over which 1:1 synchronization occurred during repetitive vagal stimulation. This increment in the range of synchronization varied directly with the dose of digoxin. Before digoxin was given, the range of cardiac cycle lengths over which synchronization occurred when the vagus nerve was stimulated with 10 pulses per burst was 272 ± 50 (mean ± SE) ms. However, after a cumulative dose of 120 μg/kg−1 digoxin had been given, the range of 1:1 synchronization increased to 396 ± 32 ms. Digoxin did not appear to have a proportionately greater effect on those processes that take place in the phase of the cardiac cycle during which the pacemaker cells are maximally responsive than on those processes that occur in the phase of the cycle during which the pacemaker cells are minimally responsive. Therefore, we conclude that the augmented entrainment induced by digoxin is ascribable to its tendency to enhance the chronotropic response to vagal stimulation.

Prolonged Apnea, Vagal Overactivity, and Sudden Infant Death

PEDIATRICS ◽  
1973 ◽  
Vol 51 (4) ◽  
pp. 755-755
Author(s):  
David S. Bachman
Keyword(s):  
At Risk ◽  
Vagus Nerve ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Vagal Stimulation ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
Prolonged Apnea ◽  
Stimulation Of

The article on prolonged apnea and the sudden infant death syndrome (SIDS) by Steinschneider1 is very exciting in that it suggests the possibility of identifying infants at risk from SIDS before the final event. Obviously, it is of great importance to learn the mechanism causing the preceding apneic episodes. Do they represent vagal overactivity? Stimulation of the intact vagus nerve in the unanesthetized monkey causes apnea, as well as bradycardia and even arrhythmias.2 In fact, we have seen myocardial myocytolysis secondary to vagal stimulation.3

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.

Participation of central alpha-receptors on hemodynamic response to E. coli endotoxin

1984 ◽  
Vol 247 (4) ◽  
pp. R655-R662
Author(s):  
S. Koyama
Keyword(s):  
Blood Pressure ◽  
Central Nervous System ◽  
Heart Rate ◽  
Time Course ◽  
Hypotensive Effect ◽  
Control Group ◽  
E Coli ◽  
Alpha Receptors ◽  
Anesthetized Dogs ◽  
The Central Nervous System

The time course of changes in mean blood pressure (MBP), heart rate (HR), and renal blood flow (RBF) in a control group of anesthetized dogs given only endotoxin (1 mg/kg iv) was compared with groups pretreated with alpha-antagonists either intravenously or intracisternally (ic). The decreases in MBP and RBF in the control group were abolished by intracisternal prazosin (0.1 mg/kg ic). MBP response to endotoxin after intravenous prazosin did not differ from that of the control group; however, the endotoxin-induced decrease in RBF after intravenous prazosin was significantly greater than that in the control group. HR responses to endotoxin were not altered by either intracisternal or intravenous prazosin. MBP and RBF responses to endotoxin after intravenous or intracisternal yohimbine (0.5 mg/kg iv or ic) did not differ from the control responses. However, significant differences occurred in the time course of changes in HR only when yohimbine was administered intracisternally. These observations suggest that the hypotensive effect and reduction of RBF due to endotoxin may be mediated by alpha 1-adrenoceptors at least in the central nervous system and that of HR response may be mediated alpha 2-adrenoceptors.

Neural mechanism underlying basilar arterial constriction by intracisternal L-NNA in anesthetized dogs

1993 ◽  
Vol 265 (1) ◽  
pp. H103-H107 ◽  
Author(s):  
N. Toda ◽  
K. Ayajiki ◽  
T. Okamura
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cerebral Arteries ◽  
Neural Mechanism ◽  
Systemic Blood Pressure ◽  
Systemic Blood ◽  
Anesthetized Dogs ◽  
Arterial Constriction ◽  
Synthase Inhibitor

Basilar arterial diameters were angiographically measured in anesthetized dogs in which systemic blood pressure and heart rate were also monitored. Injections of NG-nitro-L-arginine (L-NNA), a NO synthase inhibitor, into the cisterna magna produced a significant, persistent decrease in arterial diameter, the effect being reversed by intracisternal injections of L-arginine. The vasoconstrictor effect of L-NNA was diminished in dogs treated with hexamethonium. On the other hand, treatment with phentolamine in a dose sufficient to lower blood pressure to a level similar to that attained with hexamethonium did not inhibit, but rather potentiated, the effect of intracisternal L-NNA. Nicotine injected into the vertebral artery significantly dilated the basilar artery. The effect was abolished by treatment with L-NNA applied intracisternally, the inhibition being reversed by the addition of L-arginine. Systemic blood pressure and heart rate were not altered by intracisternally applied L-NNA and L-arginine. These findings support the hypothesis that basilar arterial constriction caused by intracisternal L-NNA is associated with a suppression of NO synthesis in nitroxidergic nerves innervating the cerebroarterial wall rather than an elimination of basal release of NO from the endothelium. Functional importance of nitroxidergic vasodilator innervation in cerebral arteries in vivo is thus clarified.

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.

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