Vagally induced hyperpolarization in atrioventricular node

1986 ◽  
Vol 251 (3) ◽  
pp. H631-H643 ◽  
Author(s):  
T. Mazgalev ◽  
L. S. Dreifus ◽  
E. L. Michelson ◽  
A. Pelleg
Keyword(s):  
Action Potentials ◽  
Cycle Length ◽  
Time Course ◽  
Vagal Stimulation ◽  
Sinus Node ◽  
Atrioventricular Node ◽  
Conduction Time ◽  
Sinus Cycle Length ◽  
Atrioventricular Nodal Conduction ◽  
The Moment

The effects of postganglionic vagal stimulation on atrioventricular nodal conduction were studied in 12 rabbit atrial-atrioventricular nodal preparations. Vagal stimulation was introduced in the sinus and atrioventricular nodes, separately or in combination, using single bursts of subthreshold stimuli. The sinus cycle length was scanned to identify the phasic effect of vagal stimulation. Action potentials from cells in the AN, N, and NH regions of the atrioventricular node were recorded by microelectrode techniques. Vagally induced hyperpolarization of cells in the atrioventricular node resulted in a phase-dependent prolongation of conduction time and reflected the level of residual hyperpolarization at the moment of arrival of the next atrial beat at the atrioventricular nodal input region. Vagally induced hyperpolarization was membrane potential dependent, although its overall time course was similar at different phases. Increased diastolic depolarization followed the maximal hyperpolarization. This "rebound" observed at certain phases was responsible for paradoxical shortening of the conduction time after vagal stimulation. The predominant effects of local vagal stimulation in the atrioventricular node were observed in cells in or near the N region. Slower rate of rise, shorter amplitude and duration, as well as step formations were among the changes in action potentials recorded from these cells. The effects of vagal stimulation were inhomogeneous between different regions of the atrioventricular node as well as within the N region, producing alternative pathways of conduction and the potential for reentry. The concomitant changes in sinus cycle length resulting from vagal stimulation in the sinus node region altered the phasic effects of vagal stimulation introduced in the atrioventricular node. This was related to a direct influence of the prolonged sinus cycle length on atrioventricular nodal refractoriness as well as an indirect effect on the degree of residual vagally induced hyperpolarization at the moment of arrival of the delayed atrial beat. These findings provide mechanistic explanations for the complex effects of vagal stimulation on atrioventricular nodal conduction.

Phasic effects of postganglionic vagal stimulation on atrioventricular nodal conduction

1986 ◽  
Vol 251 (3) ◽  
pp. H619-H630
Author(s):  
T. Mazgalev ◽  
L. S. Dreifus ◽  
E. L. Michelson ◽  
A. Pelleg ◽  
R. Price
Keyword(s):  
Cycle Length ◽  
Vagal Stimulation ◽  
Sinus Node ◽  
Conduction Time ◽  
Vagal Activity ◽  
Experimental Conditions ◽  
Sinus Cycle Length ◽  
Atrioventricular Nodal Conduction ◽  
Effective Phase ◽  
Vagal Influence

The effects of postganglionic vagal stimulation (PGVS) on atrioventricular nodal conduction were studied in 15 rabbit atrial-atrioventricular nodal preparations. PGVS was introduced, and sinus cycle length was scanned as independent bursts of subthreshold stimuli were produced in the sinus node and atrioventricular node (AVN). Changes in conduction of atrial impulses to the bundle of His were studied under the following experimental conditions: changes in sinus cycle length resulting from vagal influence on the sinus node, direct vagal stimulation exclusively to the AVN, and during both simultaneous or nonsimultaneous vagal stimulation to sinus node and AVN. The results of the present study showed that the direct effect of PGVS on AVN conduction time at a constant sinus cycle length is phase dependent with maximal prolongation achieved in the first or second beat after introduction of the burst. The interval between the onset of PGVS producing maximal prolongation of conduction time and the following atrial beat was designated the "optimal effective phase." It was shown that the optimal effective phase was a constant parameter for a given preparation and in the present experiments was 321 +/- 16 ms. However, when PGVS was introduced in combination to both nodes while scanning the cycle length, AVN conduction was variable, reflecting both the direct effects of PGVS on the AVN as well as the indirect effects resulting from changes in the sinus cycle length. Notably, it was found that simultaneous PGVS to both the sinus node and AVN usually diminished, whereas appropriate nonsimultaneous PGVS accentuated the typical phasic dependency of AVN conduction time. Additionally, vagally induced prolongation of the sinus cycle length was found to be accompanied by changes in the time of depolarization of the inputs to the AVN, thus influencing AVN conduction and facilitating reentry. These interactions between changes in the sinus cycle length and concomitant changes in the effectiveness of vagal influence on the AVN can be used to explain complexities of AVN conduction during increased vagal activity.

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

1999 ◽  
Vol 90 (1) ◽  
pp. 60-65 ◽  
Author(s):  
Michael D. Sharpe ◽  
Daniel J. Cuillerier ◽  
John K. Lee ◽  
Magdi Basta ◽  
Andrew D. Krahn ◽  
...  
Keyword(s):  
Cycle Length ◽  
Sinoatrial Node ◽  
Sinus Node ◽  
Accessory Pathway ◽  
Atrioventricular Node ◽  
Conduction Time ◽  
White Syndrome ◽  
The Right ◽  
Ablative Procedures ◽  
Wolff Parkinson White Syndrome

Background The effects of sevoflurane on the electrophysiologic properties of the human heart are unknown. This study evaluated the effects of sevoflurane on the electrophysiologic properties of the normal atrioventricular conduction system, and on the accessory pathways in patients with Wolff-Parkinson-White syndrome, to determine its suitability as an anesthetic agent for patients undergoing ablative procedures. Methods Fifteen patients with Wolff-Parkinson-White syndrome undergoing elective radiofrequency catheter ablation were studied. Anesthesia was induced with alfentanil (20-50 microg/kg) and midazolam (0.15 mg/kg), and vecuronium (20 mg) and maintained with alfentanil (0.5 to 2 microg x kg(-1) x min(-1)) and midazolam (1 or 2 mg every 10-15 min, as required). An electrophysiologic study measured the effective refractory period of the right atrium, atrioventricular node, and accessory pathway; the shortest conducted cycle length of the atrioventricular node and accessory pathway during atrial pacing; the effective refractory period of the right ventricle and accessory pathway; and the shortest retrograde conducted cycle length of the accessory pathway during ventricular pacing. Parameters of sinoatrial node function included sinus node recovery time, corrected sinus node recovery time, and sinoatrial conduction time. Intraatrial conduction time and the atrial-His interval were also measured. Characteristics of induced reciprocating tachycardia, including cycle length, atrial-His, His-ventricular, and ventriculoatrial intervals, also were measured. Sevoflurane was administered to achieve an end-tidal concentration of 2% (1 minimum alveolar concentration), and the study measurements were repeated. Results Sevoflurane had no effect on the electrophysiologic parameters of conduction in the normal atrioventricular conduction system or accessory pathway, or during reciprocating tachycardia. However, sevoflurane caused a statistically significant reduction in the sinoatrial conduction time and atrial-His interval but these changes were not clinically important. All accessory pathways were successfully identified and ablated. Conclusions Sevoflurane had no effect on the electrophysiologic nature of the normal atrioventricular or accessory pathway and no clinically important effect on sinoatrial node activity. It is therefore a suitable anesthetic agent for patients undergoing ablative procedures.

Modulation of electrophysiological properties of neonatal canine heart by tonic parasympathetic stimulation

1990 ◽  
Vol 258 (1) ◽  
pp. H38-H44 ◽  
Author(s):  
A. S. Pickoff ◽  
A. Stolfi
Keyword(s):  
Cycle Length ◽  
Parasympathetic Nervous System ◽  
Vagal Stimulation ◽  
Sinus Node ◽  
Right Atrial ◽  
Conduction Time ◽  
Canine Heart ◽  
Electrophysiological Properties ◽  
Refractory Periods ◽  
The Right

The effects of tonic right and left vagal stimulation (RVS and LVS) on electrophysiological properties of the immature myocardium and specialized conduction system were evaluated in 11 neonatal canines pretreated with propranolol (1 mg/kg iv). Electrophysiological studies were performed by recording intracardiac electrograms from multiple endocardial catheters during programmed electrical stimulation. Assessments were made of sinus node function, intra-atrial, atrioventricular (AV) nodal and His-Purkinje conduction, and atrial and ventricular refractoriness in the control state and during RVS and LVS at 4–12 Hz. Vagal stimulation prolonged the sinus cycle length; RVS produced a 38% increase and LVS a 25% increase at 8 Hz (P less than 0.01). There were no changes in the intra-atrial or His-Purkinje conduction times. Comparable increases occurred during RVS and LVS in the paced cycle length resulting in AV nodal Wenckebach, the AV nodal conduction time at a paced cycle length of 340 ms, and the effective and functional refractory periods of the AV node, suggesting symmetrical influences of the right and left vagus on neonatal AV nodal function. Right atrial effective and functional refractory periods shortened significantly during vagal stimulation (ERP, 36% RVS and 23% LVS; FRP, 27% RVS and 15% LVS), and in 5 of 11 neonates, a sustained regular atrial tachyarrhythmia was induced during atrial extra-stimulation. Small yet significant increases were observed in the right ventricular ERP and FRP during vagal stimulation. This study provides information regarding the functional integrity of the parasympathetic nervous system and its potential role as a modulator of the electrophysiological properties of the newborn heart.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of propafenone on sinus node function in the rabbit heart

1990 ◽  
Vol 68 (7) ◽  
pp. 851-855 ◽  
Author(s):  
Charles R. Kerr
Keyword(s):  
Cycle Length ◽  
Sinus Node ◽  
Rabbit Heart ◽  
Conduction Time ◽  
Supraventricular Arrhythmias ◽  
Sinus Cycle Length ◽  
Cycle Lengths ◽  
Dose Dependent ◽  
Control State

Propafenone is a type 1C antiarrhythmic drug with efficacy for both ventricular and supraventricular arrhythmias. We investigated the effects of propafenone on properties of sinus node function in an in vitro preparation of rabbit sinus node and surrounding atrium. Spontaneous sinus cycle length (SCL), atriosinus conduction time (ASCT), and sinus node effective refractory period (SNERP) at multiple pacing cycle lengths were measured in the control state and during superfusion with propafenone (2.3 μM). SNERP prolonged from 175 ± 25 ms in the control state to 220 ± 45 ms (p < 0.001) with propafenone. ASCT also prolonged significantly (p < 0.01) from 50 ± 20 to 65 ± 20 ms whereas SCL did not change. In four experiments, multiple concentrations of propafenone were utilized and there appeared to be a dose-dependent prolongation of SNERP. Thus, propafenone has a significant effect on SNERP and ASCT in an isolated rabbit sinus node preparation.Key words: propafenone, sinus node, atrium.

Differential vagal effects on antegrade vs. retrograde atrioventricular conduction

1987 ◽  
Vol 253 (5) ◽  
pp. H1059-H1068 ◽  
Author(s):  
T. Mitsuoka ◽  
T. Mazgalev ◽  
L. S. Dreifus ◽  
E. L. Michelson
Keyword(s):  
Vagal Stimulation ◽  
Atrioventricular Node ◽  
Rabbit Heart ◽  
Heart Tissue ◽  
Atrioventricular Conduction ◽  
Conduction Time ◽  
Crista Terminalis ◽  
Time Optimal ◽  
Fixed Phase ◽  
Atrioventricular Nodal Conduction

The influence of postganglionic vagal stimulation (PGVS) on antegrade and retrograde atrioventricular nodal conduction was studied in 17 isolated rabbit heart tissue preparations by pacing at the crista terminalis or His bundle, respectively. The effect of short bursts of PGVS on prolongation of atrioventricular conduction was phase dependent with respect to the cardiac cycle. This phasic dependency was more pronounced during antegrade atrioventricular conduction. Although the control retrograde atrioventricular conduction time was longer than the antegrade (P less than 0.05) at or near the time in the cycle during which vagal stimulation caused maximal prolongation of conduction time (optimal phase), PGVS-induced maximal prolongation of the antegrade atrioventricular conduction time was significantly greater than that of the retrograde (P less than 0.02). Moreover, when PGVS was introduced at a fixed phase in the cycle, but with increasing amplitude, antegrade atrioventricular conduction time was progressively prolonged, and block was observed first in the antegrade direction, whereas retrograde atrioventricular conduction continued. Microelectrode recordings during these experiments showed consistently that PGVS-induced hyperpolarization in the N region of the atrioventricular node was greater during antegrade atrioventricular conduction. This suggests that vagal effects depended not only on the intensity and phase of stimulation, but also on electronic influences which apparently are different during antegrade and retrograde conduction.

Supersensitivity to acetylcholine of canine sinus and AV nodes after parasympathetic denervation

1988 ◽  
Vol 255 (3) ◽  
pp. H534-H539 ◽  
Author(s):  
S. Kaseda ◽  
D. P. Zipes
Keyword(s):  
Dose Response ◽  
Cycle Length ◽  
Vagal Stimulation ◽  
Conduction Time ◽  
Av Block ◽  
Response Curves ◽  
Parasympathetic Ganglia ◽  
Sinus Cycle Length ◽  
Alpha Chloralose ◽  
Complete Av Block

Supersensitivity of the sinus (SAN) and atrioventricular (AVN) nodes to acetylcholine (ACh) after parasympathetic denervation has not been demonstrated conclusively. In this study, we denervated the SAN and AVN by surgically removing parasympathetic ganglia and painting the area with phenol. Sham dogs underwent thoracotomy without denervation. Four to 9 days later, vagal denervation was proved by supramaximal bilateral vagal stimulation, which prolonged the sinus cycle length (SCL) only 32 +/- 7% (mean +/- SE) and the AVN conduction time (AH interval) 15 +/- 7% in denervated dogs. We tested for supersensitivity by obtaining dose-response curves to ACh (1 ml, 10(-8.0) to 10(-4.0) M in 10(0.5) steps) infused over 15 s into the sinus nodal and posterior septal arteries in open chest-denervated (Den) dogs and in sham-operated (Sham) dogs that were anesthetized with alpha-chloralose. ACh concentration (Log[ACh], M) required to prolong SCL 50, 100, and 300% was -5.7 +/- 0.1, -5.6 +/- 0.1, and -5.4 +/- 0.1 in 10 Sham dogs vs. -6.4 +/- 0.1 (P less than 0.001), -6.3 +/- 0.1 (P less than 0.001) and -6.1 +/- 0.1 (P less than 0.001) in 11 Den dogs. ACh concentration necessary to produce second degree and complete AV block was -5.7 +/- 0.1 and -5.3 +/- 0.1 in 11 Sham dogs vs. -6.3 +/- 0.1 (P less than 0.001) and -5.8 +/- 0.1 (P less than 0.01) in 10 Den dogs. Because significantly lower doses of ACh prolonged SCL or produced AV block in Den compared with Sham dogs, we conclude that dogs with vagally denervated SAN and AVN develop a supersensitive response to ACh.

Atrioventricular nodal conduction during atrial fibrillation in rabbit heart

1982 ◽  
Vol 243 (5) ◽  
pp. H754-H760 ◽  
Author(s):  
T. Mazgalev ◽  
L. S. Dreifus ◽  
J. Bianchi ◽  
E. L. Michelson
Keyword(s):  
Atrial Fibrillation ◽  
Action Potentials ◽  
Atrioventricular Node ◽  
Interatrial Septum ◽  
Rabbit Heart ◽  
Relative Timing ◽  
Crista Terminalis ◽  
His Bundle ◽  
Atrioventricular Nodal Conduction ◽  
Variable Interaction

Atrial fibrillation was induced in 15 superfused rabbit atrial-atrioventricular nodal preparations in which surface bipolar electrograms were recorded simultaneously from the crista terminalis, interatrial septum, and His bundle along with microelectrode action potentials from cells in the atrionodal (AN), nodal (N), and nodal-His (NH) regions of the atrioventricular node. Effective engagement of the atrioventricular node with propagation to the His bundle was critically dependent on the relative timing of activation at the crista terminalis and interatrial septal input regions of the atrioventricular node. Conduction through the AN and N regions appeared dependent on the relative timing of activation wave fronts emerging from the two input regions. Asynchronous engagement of AN and N regions resulted in both distortion of action potentials and concealed conduction, with delayed conduction and block to the NH region and His bundle. Successful engagement of the NH region always produced a 1:1 NH-to-His bundle relationship. It is concluded that during atrial fibrillation 1) activation of the AN region occurs as a result of the variable interaction of inputs from the crista terminalis and interatrial septum; 2) predictably, effective synchronous engagement of the AN and consequently the N region is responsible for conduction to the NH and His bundle regions; 3) conversely, asynchronous activation inputs from the crista terminalis and interatrial septum result in fragmented, asynchronous as well as concealed conduction within the AN and N regions with block in the atrioventricular node and variable conduction to the His bundle.

Dynamic counterbalance between direct and indirect vagal controls of atrioventricular conduction in cats

1999 ◽  
Vol 277 (6) ◽  
pp. H2129-H2135 ◽  
Author(s):  
Shi-Liang Chen ◽  
Toru Kawada ◽  
Masashi Inagaki ◽  
Toshiaki Shishido ◽  
Hiroshi Miyano ◽  
...  
Keyword(s):  
Transfer Function ◽  
Vagal Stimulation ◽  
Normal Sinus Rhythm ◽  
Gaussian White Noise ◽  
Atrioventricular Node ◽  
Atrioventricular Conduction ◽  
Step Response ◽  
Conduction Time ◽  
Pass Filter ◽  
Low Pass Filter

The vagal system regulates the atrioventricular conduction time ( T AV) via two opposing mechanisms: a direct effect on the atrioventricular node and an indirect effect through changes in heart period ( T AA). To evaluate how dynamic vagal activation affects T AV, we stimulated the vagal nerve with frequency-modulated Gaussian white noise and estimated the transfer function from vagal stimulation to the T AV response under conditions of no pacing and constant pacing in anesthetized cats. The effect of changes in T AA on T AV was estimated by a random-pacing protocol. The transfer function from vagal stimulation to T AV has low-pass filter characteristics. Constant pacing increased the maximum step response in T AV(2.4 ± 1.2 vs. 6.3 ± 2.2 ms/Hz, P < 0.01). The time constant did not differ between the vagal effect on T AV and that on T AA (2.9 ± 1.2 vs. 2.3 ± 0.5 s). Because changes in T AA reciprocally affected T AVwithout significant delay, the direct and indirect effects were dynamically counterbalanced and exerted stable T AV transient response during vagal stimulation under normal sinus rhythm.

Vagal-mediated atrial premature beats: a computer model

1993 ◽  
Vol 265 (4) ◽  
pp. H1195-H1202
Author(s):  
R. T. Whitney ◽  
G. J. Rozanski
Keyword(s):  
Experimental Data ◽  
Computer Model ◽  
Recovery Time ◽  
Cycle Length ◽  
Sinus Node ◽  
Primary Operation ◽  
Sinus Cycle Length ◽  
Overdrive Suppression ◽  
Ectopic Pacemaker ◽  
Premature Beats

A computer algorithm is described that used experimental data to model the arrhythmogenic interaction of phasic vagal stimuli and atrial ectopic pacemakers. The model consisted of a dominant sinus node and a single ectopic pacemaker center separated by conducting atrial tissue. Its primary operation was to predict the timing and incidence of atrial premature beats resulting from transient escape of ectopic automatic impulses when vagal-induced entrance block of the sinus impulse was simulated near the ectopic focus. These predictions were based on a series of experimentally derived phase-response and corrected recovery time curves, describing the modulation of ectopic pacemaker periodicity by vagal input and overdrive suppression, respectively. Depending on the combination of curves tested, the model predicted premature beats to develop only with critically timed vagal stimuli. The coupling intervals of vagal-induced premature beats were > 300 ms and varied as a function of vagal timing and sinus cycle length. The model suggests therefore that phasic vagal stimuli within the atrium may transiently protect ectopic pacemaker foci from conducted sinus impulses and mediate the genesis of atrial extrasystoles with long coupling intervals.

Atrioventricular nodal activation during periodic premature stimulation of the atrium

1987 ◽  
Vol 252 (1) ◽  
pp. H163-H177 ◽  
Author(s):  
J. Billette
Keyword(s):  
Cycle Length ◽  
Cell Activation ◽  
Atrioventricular Node ◽  
Rabbit Heart ◽  
Propagation Time ◽  
Conduction Time ◽  
Activation Time ◽  
Refractory Periods ◽  
Complete Sequences ◽  
Stimulation Of

To study the intranodal origin of the functional properties of the atrioventricular node, progressive changes in nodal cell activation time and cycle length occurring during complete sequences of periodic premature stimulation of the atrium were determined for 419 nodal cells recorded in 11 isolated rabbit heart preparations. The conduction time in proximal nodal cells including the N cells increased only at very short coupling intervals. Conduction time in the distal node (NH and H cells) first increased and then decreased with increasing prematurity. The major fraction of the basic and premature delays developed between N and NH cell activation, a period devoid of upstrokes. The effective and functional refractory periods were related to the minimum intervals between successive upstrokes at the node entrance and outlet, respectively. These results suggest that the cycle-length dependency of nodal conduction is the result of complex changes in propagation time occurring at three levels in the node, whereas the effective and functional refractory periods reflect reactivation limits of cells located at the node entrance and outlet, respectively.

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