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.

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.

Reflex regulation of atrioventricular conduction

1987 ◽  
Vol 252 (6) ◽  
pp. H1077-H1085
Author(s):  
M. R. Warner ◽  
J. M. Loeb
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Time Course ◽  
Atrial Pacing ◽  
Av Node ◽  
Reflex Regulation ◽  
Absolute Value ◽  
Intact State ◽  
Anesthetized Dogs ◽  
Induced Changes

We evaluated the time course of baroreflex modulation of atrioventricular (AV) nodal conduction in anesthetized dogs (n = 28). Beat-by-beat changes in heart rate (HR) and AV interval (AVI) evoked by transient alterations in arterial pressure (AP) were recorded in the intact state, after vagotomy, and following stellectomy. Under each experimental condition, alterations in AP induced parallel changes in HR and AVI with maximum HR and AVI responses occurring simultaneously. In three animals, AP alterations elicited pacemaker shifts that markedly altered AVI. Reflex changes in AVI were also examined during atrial pacing. When pacing at a low (120 beats/min) versus a high (190 beats/min) level of heart rate, reductions in AP decreased AVI to a significantly lower absolute value in the intact state, after vagotomy, and following stellectomy. However, under each experimental condition, decreases in AP elicited marked changes in AVI at either level of pacing. We conclude that baroreflex-induced changes in sympathetic and parasympathetic activity influence the sinoatrial and AV nodes simultaneously, predominate over the effects of changes in HR at the AV node, and may induce pacemaker shifts that influence the measurement of AVI.

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.

Blood pressure responses to cyclic blood volume changes in awake and anesthetized dogs

1989 ◽  
Vol 256 (4) ◽  
pp. R827-R835 ◽  
Author(s):  
D. R. Brown ◽  
A. W. Cowley ◽  
D. B. Young
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Blood Volume ◽  
Cycle Length ◽  
Volume Changes ◽  
Total Blood ◽  
Forcing Function ◽  
Cycle Lengths ◽  
Anesthetized Dogs ◽  
Blood Pressure Responses

A dynamic analysis of blood pressure regulation was performed in conscious and anesthetized dogs. The mean arterial pressure (MAP) responses to 5 and 10% sinusoidal changes in total blood volume with cycle lengths of 1, 4, and 8 min were measured in anesthetized 1) control dogs, 2) carotid and vagal baroreflex (CVB)-denervated animals, and 3) spinal-ablated dogs; in addition, the MAP responses to 10% sinusoidal blood volume changes with cycle lengths ranging from 0.25 to 8 min were measured in conscious control and CVB-denervated dogs. The presence of the baroreflexes in both the conscious and anesthetized control dogs essentially eliminated MAP excursions during the cyclic volume changes. The MAP changes in both the conscious and anesthetized denervated dogs were large. However, the responses in the anesthetized denervated dogs were linear, stationary, and cycle-length insensitive with respect to the sinusoidal forcing function, whereas the responses in the conscious CVB-denervated dogs were nonlinear, nonstationary, and cycle-length dependent. These results indicate that the cardiovascular system in the anesthetized CVB-denervated and spinal-ablated dogs is passive or "hydraulic" in nature; conversely, factors other than the carotid and vagal baroreflexes appear to exist that alter the arterial pressure responses to cyclic blood volume perturbations in the conscious CVB-denervated dogs.

Facilitated ventriculoatrial conduction: effects of sequential pacing interval and basic cycle length

1995 ◽  
Vol 268 (1) ◽  
pp. H384-H390
Author(s):  
A. F. Kuguoglu ◽  
D. W. Wallick ◽  
P. J. Martin
Keyword(s):  
Refractory Period ◽  
Cycle Length ◽  
Effective Refractory Period ◽  
Conduction Time ◽  
Time Intervals ◽  
Av Node ◽  
Anesthetized Dogs ◽  
Alpha Chloralose ◽  
Retrograde Conduction ◽  
Basic Cycle Length

We studied 1) the effects of pacing interval, 2) the timing of atrioventricular sequential pacing, and 3) the effects of successive premature intervals on retrograde conduction of the atrioventricular (AV) node in open-chest alpha-chloralose-anesthetized dogs. The ventricles and atria were sequentially paced at one of three levels of basic cycle length and one of six sequential time intervals (V1-A1) for three basic cycles (V1-V1). Then a premature ventricular impulse was introduced at various V1-V2 intervals, and the resultant retrograde conduction time (V2-A2 interval) was measured. Successive V1-V2 intervals were applied in an incremental or a decremental fashion. The V1-V2 intervals ranged from V1-V1 to V1-V2, at which the retrograde conduction was blocked. For each level of the above three factors, we plotted retrograde conduction time (V2-A2) as a function of the various premature intervals (V1-V2). We found that the time between atrial and ventricular activations was the most important factor in determining V1-V2 and in decreasing the effective refractory period of the AV node during retrograde conduction.

Vagal-induced tachycardia: release of vasoactive intestinal peptide and peptide HI

1994 ◽  
Vol 267 (5) ◽  
pp. H2019-H2024
Author(s):  
F. L. Anderson ◽  
A. C. Kralios ◽  
N. Cluff ◽  
G. R. Hanson
Keyword(s):  
Heart Rate ◽  
Vasoactive Intestinal Peptide ◽  
Coronary Sinus ◽  
Nicotinic Receptors ◽  
Vagal Stimulation ◽  
Concentration Difference ◽  
Anesthetized Dogs ◽  
Alpha Chloralose ◽  
The Relationship ◽  
Coronary Sinus Blood

The relationship between vagal-induced tachycardia (VT) and release of vasoactive intestinal peptide (VIP) and peptide HI (PHI) into cardiac lymph and coronary sinus blood was studied in 23 alpha-chloralose-anesthetized open-chest dogs that were autonomically decentralized and pretreated with atropine and propranolol. After simultaneous right and left cervical vagal stimulation at 5 V, 20 Hz for 3 min mean +/- SE, increase in heart rate was 38 +/- 6 beats/min, and increase in lymph VIP output from control was 0.308 +/- 0.093 pg/min (P = 0.004). The decrease in VIP arterial minus coronary sinus concentration was not significant. The increase in heart rate did not significantly correlate with increase in lymph VIP output (R2 = 0.141) or decrease in VIP arterial minus coronary sinus concentration (R2 = 0.059). The increases in heart rate and lymph VIP output were blocked by hexamethonium. Increase in lymph PHI output from control during VT (5 dogs) was 0.797 +/- 0.658 pg/min. Arterial-coronary sinus PHI concentration difference did not change in these dogs. These data indicate that VT is associated but not significantly correlated with VIP and PHI release into cardiac lymph. Cholinoceptive nicotinic receptors may mediate VIP release and VT in anesthetized dogs.

Propofol Has No Direct Effect on Sinoatrial Node Function or on Normal Atrioventricular and Accessory Pathway Conduction in Wolff-Parkinson-White Syndrome during Alfentanil/Midazolam Anesthesia

1995 ◽  
Vol 82 (4) ◽  
pp. 888-895. ◽  
Author(s):  
Michael D. Sharpe ◽  
Wojciech B. Dobkowski ◽  
John M. Murkin ◽  
George Klein ◽  
Raymond Yee
Keyword(s):  
Refractory Period ◽  
Cycle Length ◽  
Accessory Pathway ◽  
Right Atrial ◽  
Conduction Time ◽  
Av Node ◽  
White Syndrome ◽  
Sa Node ◽  
The Right ◽  
Wolff Parkinson White Syndrome

Background Propofol has been implicated as causing intraoperative bradyarrhythmias. Furthermore, the effects of propofol on the electrophysiologic properties of the sinoatrial (SA) node and on normal atrioventricular (AV) and accessory pathways in patients with Wolff-Parkinson-White syndrome are unknown. Therefore, this study examined the effects of propofol on the cardiac electrophysiologic properties in humans to determine whether propofol promotes bradyarrhythmias and its suitability as an anesthetic agent in patients undergoing ablative procedures. Methods Twelve patients with Wolff-Parkinson-White syndrome undergoing radiofrequency catheter ablation were studied. Anesthesia was induced with alfentanil (50 micrograms/kg), midazolam (0.15 mg/kg), and vecuronium (20 mg) and maintained with alfentanil (2 micrograms.kg-1.min-1) and midazolam (1-2 mg, every 15 min, as needed). A electrophysiologic study was performed consisting of measurement of the effective refractory period of the right atrium, AV node, and accessory pathway and the shortest cycle length of the AV node and accessory pathway during antegrade stimulation plus the effective refractory period of the right ventricle and accessory pathway and the shortest cycle length of the accessory pathway during retrograde stimulation. Determinants of SA node function including sinus node recovery time, corrected sinus node recovery time, and SA conduction time; intraatrial conduction time and atrial-His interval also were measured. Reciprocating tachycardia was induced by rapid right atrial or ventricular pacing, and the cycle length and atrial-His, His-ventricular, and ventriculoatrial intervals were measured. Alfentanil/midazolam was then discontinued. Propofol was administered (bolus 2 mg/kg + 120 micrograms.kg-1.min-1), and the electrophysiologic measurements were repeated. Results Propofol caused a statistically significant but clinically unimportant prolongation of the right atrial refractory period. The effective refractory periods of the AV node, right ventricle, and accessory pathway, as well as the shortest cycle length, were not affected. Parameters of SA node function and intraatrial conduction also were not affected. Sustained reciprocating tachycardia was inducible in 8 of 12 patients, and propofol had no effect on its electrophysiologic properties. All accessory pathways were successfully identified and ablated. Conclusions Propofol has no clinically significant effect on the electrophysiologic expression of the accessory pathway and the refractoriness of the normal AV conduction system. In addition, propofol has no direct effect on SA node activity or intraatrial conduction; therefore, it does not directly induce bradyarrhythmias. It is thus a suitable agent for use in patients undergoing ablative procedures who require either a neuroleptic or general anesthetic.

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.

Nonuniform Distribution of Vagal Effects on the Atrial Refractory Period

1958 ◽  
Vol 194 (2) ◽  
pp. 406-410 ◽  
Author(s):  
R. Alessi ◽  
M. Nusynowitz ◽  
J. A. Abildskov ◽  
G. K. Moe
Keyword(s):  
Arterial Pressure ◽  
Refractory Period ◽  
Vagal Stimulation ◽  
Nonuniform Distribution ◽  
Right Atrial ◽  
Vagus Nerves ◽  
Anesthetized Dogs ◽  
The Right ◽  
Stimulation Of

The refractory period (RP) was measured at several points on the right atrial surface in anesthetized dogs. Under control conditions with vagi cut the values recorded at various points varied by no more than 40 msec. During stimulation of the vagus nerves, singly or together, the RP varied widely. At some points marked effects were observed, while at others little or no effect was apparent. Reflex excitation of the vagi, induced by increased arterial pressure, yielded similar results. It was concluded that the effects of vagal stimulation are not uniformly distributed.

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