Phasic influences of vagal stimulation on atrioventricular conduction

1988 ◽  
Vol 66 (9) ◽  
pp. 1198-1205 ◽  
Author(s):  
Margaret R. Warner ◽  
Jerod M. Loeb
Keyword(s):  
Sympathetic Activity ◽  
Cycle Length ◽  
Cardiac Cycle ◽  
Vagal Stimulation ◽  
Response Patterns ◽  
Constant Frequency ◽  
Stimulus Interval ◽  
Av Conduction ◽  
Anesthetized Dogs ◽  
Interval Response

The beat-by-beat changes in atrioventricular (AV) conduction evoked by constant frequency and phase-coupled vagal stimulation were examined both qualitatively and quantitatively in 13 anesthetized dogs. The effects of pacing cycle length and sympathetic activity on the vagally induced phasic changes in AV conduction were also characterized. When the vagal stimulus interval was nearly equal to the pacing cycle length and the vagal stimulus moved progressively through the cardiac cycle, AV interval oscillated in a rhythmic fashion. The rhythmicity of the vagally induced AV interval oscillations was altered substantially by changes in either the vagal stimulus interval or the pacing cycle length. The vagally induced AV interval oscillations were abolished during phase-coupled vagal stimulation; however, the magnitude of the resultant steady-state AV interval depended on the time relative to the phase of the cardiac cycle that the vagal stimulus was delivered. In the presence or absence of sympathetic stimulation, a vagal stimulus falling approximately 200 ms prior to atrial depolarization evoked the greatest prolongation in AV interval, regardless of the pacing cycle length. Additionally, the effects of combined sympathetic and phase-dependent vagal stimulation on the AV interval were additive. These data confirm that the influence of a vagal stimulus on AV interval can be predicted from the phase in the cardiac cycle that the vagal stimulus is delivered. Moreover, this phase dependency of vagal effects evokes marked qualitative variations in AV interval response patterns when either the vagal stimulus interval or the pacing cycle length is altered.

Effect of phasic vagal stimulation and atrial pacing site on atrioventricular conduction time

1997 ◽  
Vol 272 (5) ◽  
pp. H2289-H2298 ◽  
Author(s):  
D. A. Igel ◽  
D. W. Wallick ◽  
P. J. Martin ◽  
M. N. Levy
Keyword(s):  
Coronary Sinus ◽  
Cycle Length ◽  
Vagal Stimulation ◽  
Interatrial Septum ◽  
Conduction Time ◽  
Atrial Pacing ◽  
Av Conduction ◽  
Recovery Times ◽  
Anesthetized Dogs ◽  
The Right

We tested the hypothesis that the effect of phasic vagal stimulation on atrioventricular (AV) conduction time is affected by the site of atrial pacing in anesthetized dogs. We paced the right atrium at a constant cycle length from the interatrial septum (IAS), superior coronary sinus (SCS), or inferior coronary sinus (ICS) regions, and we evaluated the time-dependent effects of vagal stimulation on AV conduction at each pacing site. When we stimulated the vagi at stimulus (St)-A phases greater than 136 +/- 40 ms and less than the phase that blocked AV conduction (182 +/- 70 ms), IAS pacing prolonged A-V intervals by 8.6 +/- 8.2 ms more than ICS pacing. A change in pacing site affected the A-V intervals by up to 30 ms when we stimulated the vagus at those times that caused the A-V intervals to prolong maximally. Furthermore, the effect of atrial pacing site on A-V intervals was modulated by AV nodal recovery times during the second or third cycles after the vagal stimulus.

Changes in vagal phasic chronotropic responses with sympathetic stimulation in the dog

1981 ◽  
Vol 241 (6) ◽  
pp. H850-H856 ◽  
Author(s):  
S. L. Stuesse ◽  
D. W. Wallick ◽  
H. Zieske ◽  
M. N. Levy
Keyword(s):  
Cycle Length ◽  
Temporal Relationship ◽  
Cardiac Cycle ◽  
Vagal Stimulation ◽  
Cardiac Response ◽  
Sympathetic Stimulation ◽  
Pacemaker Cells ◽  
Paradoxical Response ◽  
Chronotropic Response ◽  
Anesthetized Dogs

Sympathetic stimulation both shortens the cardiac cycle and potentiates the cardiac response to vagal stimulation. In the present study the effects of sympathetic stimulation on the chronotropic responses of the heart to brief bursts of vagal stimulation were determined in open-chest anesthetized dogs. The sinoatrial nodal pacemaker cells demonstrate a paradoxical response to repetitive bursts of vagal stimuli over a certain portion of the cardiac cycle. That is, the cardiac cycle length does not increase but actually decreases as the vagal stimulation frequency is raised. Background levels of sympathetic stimulation do not significantly alter the range over which this “paradoxical” response occurs. Sympathetic stimulation decreases the cardiac chronotropic response to short bursts of vagal stimuli regardless of the time in the cardiac cycle that the stimulus is given; however, it does not decrease the time from the minimum vagal chronotropic response to the subsequent atrial depolarization although the total cardiac cycle is shortened. Since sympathetic stimulation shifts the overall temporal relationship between vagal stimulation and pacemaker response, small changes in sympathetic tone may greatly alter the cardiac response to phasic vagal stimulation if the vagal stimulus is given at certain times in the cardiac cycle.

Effects of vagus nerve on heart rate and ventricular contractility in chicken

1989 ◽  
Vol 256 (5) ◽  
pp. H1295-H1302
Author(s):  
S. A. Lang ◽  
M. N. Levy
Keyword(s):  
Vagus Nerve ◽  
Cycle Length ◽  
Cardiac Cycle ◽  
Ventricular Contractility ◽  
Ventricular Contraction ◽  
Vagus Stimulation ◽  
Constant Frequency ◽  
The Right ◽  
Contraction And Relaxation ◽  
Left Vagus

We determined the effects of vagus nerve stimulation on cardiac cycle length and on ventricular contraction and relaxation in 18 chickens anesthetized with pentobarbital. Right vagus stimulation at a constant frequency of 35 Hz prolonged cycle length by 190%, whereas left vagus stimulation at the same frequency increased cycle length by 136%. When one burst of stimuli was delivered to the right vagus nerve each cardiac cycle, but the timing of the stimuli was changed within the cardiac cycle, the response of the avian pacemaker cells varied substantially with the timing of the stimuli. Right and left vagus stimulation at a constant frequency of 20 Hz depressed ventricular contraction by 62 +/- 6 and 52 +/- 6%, respectively, and depressed ventricular relaxation by 56 +/- 7 and 53 +/- 7%, respectively. These results indicate that in the chicken the chronotropic effects of right vagus stimulation are greater than those of left vagus stimulation, whereas right and left vagus stimulation are approximately equipotent on ventricular contraction and relaxation.

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.

scholarly journals Heart rate variability: Response to graded head up tilt in healthy men

1970 ◽  
Vol 7 (3) ◽  
pp. 252-257 ◽  
Author(s):  
P Sharma ◽  
BH Paudel ◽  
PN Singh ◽  
P Linmbu
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Sympathetic Activity ◽  
Cycle Length ◽  
Cardiac Cycle ◽  
Test Results ◽  
Successive Cycle ◽  
Head Up Tilt ◽  
Bonferroni Test ◽  
Lying Down

Background: Heart rate variability is actually a misnomer for R to R variability in cardiac cycle. Variation in successive cycle length is called the heart rate variability (HRV). Head-up tilt is a model of studying cardiovascular haemodynamics, which reflects in heart rate variability (HRV). Objectives: To study the effect of 10° and 70° head-up tilt on HRV. Materials and methods: The study was done in the Department of Physiology using graded head up tilt (passive orthostatism). HRV measurement was done at 10° and 70° tilt and compared with supine using standardised methods on 30 consenting healthy males (age 25.37±3.89 years). The HRV variables across postures were compared by ANOVA and Bonferroni test. Results: The heart rate increased at 70° compared to 10° and supine (70.48±8.17 Vs 70.22±8.67 and 88.51±12.84 bpm, p<0.001). The 70° tilt decreased vagal HRV indicators compared to 10° and supine: SDNN (31.13±8.12 Vs 38.07±11.29 and 38.13±10.89 ms, p<0.05), RMSSD (20.06 ±8.47 Vs 34.23±14.22 and 36.16±12.22 ms, p<0.001), NN50 count (13.03±20.58 Vs 45.07±44.44 and 55.27±44.10, p<0.01), pNN50 (3.28±6.08 Vs 14.06±15.65 and 16.65±14.23, p<0.01), HF power (197.20±143.76 Vs 218.17±155.85 and 216.87±150.98 Hz, p<0.05), HFnu unit (24.28±14.16 Vs 45.48±16.34 and 47.67±19.89, p<0.001). The 70° tilt increased LF power% (197.20±143.76 Vs 218.17±155.85 and 216.87±150.98, p<0.001). LFnu unit (75.72±14.76 Vs 54.52±16.34 and 52.32±19.89, p<0.001), LF: HF (4.96±4.08 Vs 1.53±1.138 and 1.69±1.67, p<0.001) compared to 10° and supine. Conclusion: At 70° tilt, HRV measures, reflecting vagal contribution to cardiac-cycle length, decreased with reciprocal increase in sympathetic activity compared to 10° or supine leading to increase in sympathetic predominance. A 10° tilt, which is almost equivalent to lying down with pillow, did not change HRV from supine. Key words: Cardiac cycle; cardiovascular haemodynamics; head-up-tilt; heart rate variability; sympathetic activity; parasympathetic activity DOI: 10.3126/kumj.v7i3.2733 Kathmandu University Medical Journal (2009) Vol.7, No.3 Issue 27, 252-257

Brief vagal bursts can induce Wenckebach arrhythmia

1989 ◽  
Vol 257 (3) ◽  
pp. H935-H941
Author(s):  
D. W. Wallick ◽  
P. J. Martin
Keyword(s):  
Feedback Control ◽  
Cardiac Cycle ◽  
Vagal Stimulation ◽  
Feedback Control System ◽  
Pentobarbital Sodium ◽  
Control Loops ◽  
Av Conduction ◽  
Retrograde Conduction ◽  
Ventricular Depolarization ◽  
Wenckebach Arrhythmia

We hypothesized that a brief burst of vagal stimulation applied in each cardiac cycle could elicit an atrioventricular (AV) nodal Wenckebach arrhythmia. Twenty-six dogs were anesthetized with pentobarbital sodium (30 mg/kg iv) and were given propranolol (1 mg/kg iv). We varied the timing of a vagal stimulus burst in steps of 25-50 ms relative to the onset of atrial or ventricular depolarization. In four of nine experiments, a Wenckebach arrhythmia occurred despite changing the timing of stimuli. By prolonging the effects of vagal stimulation on AV conduction with physostigmine, the timing of the stimuli no longer influenced the severity of the arrhythmia. We did experiments to open one of the feedback control loops; these results indicated that this arrhythmia has elements of a positive feedback control system. We also studied the effects of vagal stimulation on the arrhythmia during retrograde conduction. We found that the timing of vagal stimulation was critical in eliciting the arrhythmia in only 4 of the 10 dogs.

Effects of spatial dispersion of acetylcholine release on AV conduction responses to vagal stimulation in dogs

1991 ◽  
Vol 261 (2) ◽  
pp. H392-H397 ◽  
Author(s):  
T. N. Yang ◽  
J. Cheng ◽  
P. Martin ◽  
M. N. Levy
Keyword(s):  
Cardiac Cycle ◽  
Spatial Dispersion ◽  
Vagal Stimulation ◽  
Nerve Fibers ◽  
Vagal Nerve ◽  
Conduction Time ◽  
Vagal Activity ◽  
Ach Release ◽  
Response Curves ◽  
Av Conduction

We determined the effects on atrioventricular (AV) conduction of changing the spatial dispersion of acetylcholine (ACh) release from vagal nerve fibers in anesthetized dogs. We paced the atria at a constant rate and stimulated the vagus nerves with one stimulus burst per cardiac cycle. We varied the spatial heterogeneity of ACh release in the cardiac tissues by changing the stimulus voltage, and we varied the quantity of ACh release from each excited nerve fiber by changing the number of pulses per stimulus burst. We slightly changed the stimulus timing with each heartbeat to scan the entire cardiac cycle. We constructed phase-response curves (PRCs) by plotting the changes in AV conduction time as a function of the timing of vagal stimulation. We found that the amplitude of the PRC varied directly with average AV conduction time (AV), whereas the minimum-to-maximum phase difference of the PRC varied inversely with AV. However, for any given change in AV, the specific characteristics of the PRCs did not depend on whether we varied the number of pulses per burst or the stimulus voltage. Therefore, the phase-dependent characteristics of the dromotropic responses appear to be unaffected by the spatial dispersion of ACh release from the vagal nerve endings. The effects of vagal activity on the AV conduction time are determined by those conducting fibers that are the least restrained by neurally released ACh.

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.

Sustained increases in heart rate induced by timed repetition of vagal stimulation in dogs

1985 ◽  
Vol 249 (4) ◽  
pp. H703-H709
Author(s):  
T. Yang ◽  
M. D. Jacobstein ◽  
M. N. Levy
Keyword(s):  
Cycle Length ◽  
Cardiac Cycle ◽  
Vagal Stimulation ◽  
Sinus Node ◽  
Critical Time ◽  
Critical Value ◽  
Chronotropic Effect ◽  
Chronotropic Response ◽  
The Right ◽  
Positive Chronotropic Effect

We determined the influence of the "free-running cycle length" (tau FR) on chronotropic responses to one burst of right vagal stimuli per cardiac cycle in anesthetized dogs (tau FR, cycle length that prevailed in absence of right vagal stimulation). We varied tau FR by the following methods: 1) tonic left vagal stimulation in pentobarbital-anesthetized animals; 2) tonic left vagal stimulation plus sinus node cooling in pentobarbital-anesthetized animals; and 3) anesthesia with fentanyl, droperidol, and pentobarbital. When tau FR was less than a critical value [1,019 +/- 60 (SE) ms], right vagal stimulus bursts always had the expected negative chronotropic effect. However, when the tau FR was increased beyond critical value, right vagal stimulus bursts delivered within a specific portion of cardiac cycle actually had a positive chronotropic effect; i.e., cycle lengths diminished to values below tau FR. As tau FR was progressively increased beyond critical value, positive chronotropic response became greater and could be evoked by stimulus bursts delivered within a greater fraction of cardiac cycle. The right vagal stimuli that elicited the maximum positive chronotropic effect were those that were given approximately 235 ms prior to beginning of next atrial depolarization. This critical time probably occurs near the end of the period of phase 4 depolarization of sinus node automatic cells.

Sensitivity differences of SA and AV node to vagal stimulation: attenuation of vagal effects at SA node

1981 ◽  
Vol 241 (5) ◽  
pp. H684-H690 ◽  
Author(s):  
J. M. Loeb ◽  
D. P. Dalton ◽  
J. M. Moran
Keyword(s):  
Arterial Pressure ◽  
Cycle Length ◽  
Vagal Stimulation ◽  
Chronotropic Effect ◽  
Av Node ◽  
Sa Node ◽  
Anesthetized Dogs ◽  
Stimulation Period ◽  
The Relationship ◽  
Rule Out

The present study sought to characterize vagally induced desensitization at the sinoatrial (SA) node of the intact dog and to determine whether these findings could be extended to atrioventricular (AV) Nodal conduction. Autonomically decentralized anesthetized dogs were instrumented to record electrocardiograms, arterial pressure, and electrograms from the SA node, right atrium, right ventricle, and His bundle. During right- or left-vagal stimulation for 60 s, cycle length (CL) increased initially, followed by a gradual recovery toward control during stimulation; atrio-His (AH) interval remained prolonged throughout the stimulation. Atrial drive increased AH interval during stimulation, but AH prolongation was maintained throughout the stimulation period. To rule out acetylcholine (ACh) depletion, ACh was administered before and during vagal stimulation. Although control CL and AH interval were lengthened by ACh, no significant CL increases occurred when ACh was given during stimulation, but the AH interval became longer. Propranolol increased control CL and AH interval but did not alter the relationship between vagal stimulation and CL or AH interval. Thus the negative chronotropic effect of ACh at the SA node is diminished upon prolonged vagal stimulation, whereas the negative dromotropic effect upon AV nodal conduction remains unaltered. These results suggest differences in muscarinic receptor behavior at the SA and AV nodes.

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