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.

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.

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.

Functional origin of rate-induced changes in atrioventricular nodal conduction time of premature beats in the rabbit

1987 ◽  
Vol 65 (11) ◽  
pp. 2329-2337 ◽  
Author(s):  
Jacques Billette ◽  
Marie St-Vincent
Keyword(s):  
Recovery Time ◽  
Rabbit Heart ◽  
Inhibitory Effect ◽  
Facilitatory Effect ◽  
Conduction Time ◽  
Recovery Times ◽  
Atrioventricular Nodal Conduction ◽  
Premature Beats ◽  
Induced Changes ◽  
Nodal Properties

The characteristics and origin of the rate-induced changes in atrioventricular nodal conduction time of premature beats (A2H2 intervals) were studied in isolated rabbit heart preparations. Increasing the basic driving rate during a periodic premature stimulation prolonged (a net inhibitory effect) and shortened (a net facilitatory effect) significantly (p < 0.01, n = 17) the A2H2 intervals associated with long and short recovery times (H1A2 intervals), respectively. The origin of these responses was sought for by analyzing interactions between facilitation and fatigue. When the fatigue developed at a fast basic rate was estimated from changes in conduction time of basic beats and subtracted from the corresponding A2H2 intervals, the calculated A2H2 intervals showed enhanced facilitation but no fatigue. When independently obtained fatigue and facilitation effects were added to the control A2H2 intervals for corresponding H1A2 intervals, resulting A2H2 intervals correlated strongly with the ones observed at the equivalent fast basic rate (r = 0.99, p < 0.001). Moreover, changes in the A2H2 intervals of premature beats tested with constant coupling intervals during 5-min fast rates were biphasic, confirming the overlapping and competition between facilitation and fatigue effects. Hence, rate-induced deviations of premature nodal conduction time from that predicted by changes in recovery time are consistent and result from the interaction between the overlapping effects produced by two independent, antagonist, and dynamically distinct nodal properties (facilitation and fatigue).

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.

Common functional origin for simple and complex responses of atrioventricular node in dogs

1986 ◽  
Vol 251 (5) ◽  
pp. H920-H925 ◽  
Author(s):  
J. Billette ◽  
J. P. Gossard ◽  
L. Lepanto ◽  
R. Cartier
Keyword(s):  
Steady State ◽  
Atrioventricular Node ◽  
Sequential Patterns ◽  
Functional Domain ◽  
Conduction Time ◽  
Atrial Pacing ◽  
Av Node ◽  
Anesthetized Dogs ◽  
Atrioventricular Nodal Conduction ◽  
Transient And Steady State

The possibility that variations in atrioventricular nodal conduction time observed during transient and steady-state nodal responses share common characteristics was examined in six anesthetized dogs. Atrioventricular conduction times (AV intervals) obtained during transient (incremental atrial pacing rates, short frequency steps, and Wenckebach cycles) and steady state (periodic premature stimulation performed at 5 basic rates) responses were plotted together against the corresponding preceding ventriculoatrial (VA) intervals on a graph for each dog. Despite their diversity, nodal responses consistently resulted in AV intervals that fell within a well-defined, relatively narrow, crescent-shaped zone on the graphs. AV interval variations were small in the long VA interval range and increased slightly but predictably as the VA intervals decreased. AV intervals of transient and steady state nodal responses overlapped markedly. These results show that AV intervals of transient and steady-state nodal responses vary within a given common functional domain despite the diversity of their sequential patterns and suggest that the AV node may be obeying the same set of conduction rules during these very distinct responses.

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.

Morphology and electrophysiology of the mammalian atrioventricular node

1988 ◽  
Vol 68 (2) ◽  
pp. 608-647 ◽  
Author(s):  
F. L. Meijler ◽  
M. J. Janse
Keyword(s):  
Mammalian Species ◽  
Conduction Block ◽  
Atrioventricular Node ◽  
Conduction Delay ◽  
Conduction Time ◽  
Av Node ◽  
Crista Terminalis ◽  
His Bundle ◽  
Transitional Cells ◽  
Av Bundle

The AV node of those mammalian species in which it has been thoroughly investigated (rabbit, ferret, and humans) consists of various cell types: transitional cells, midnodal (or typical nodal cells), lower nodal cells, and cells of the AV bundle. There are at least two inputs to the AV node, a posterior one via the crista terminalis and an anterior one via the interatrial septum, where atrial fibers gradually merge with transitional cells. The role of a possible third input from the left atrium has not been investigated. Since the transition from atrial fibers to nodal fibers is gradual, it is very difficult to define the "beginning" of the AV node, and gross measurements of AV nodal length may be misleading. Histologically, the "end" of the AV node is equally difficult to define. At the site where macroscopically the AV node ends, at the point where the AV bundle penetrates into the membranous septum, typical nodal cells intermingle with His bundle cells. A conspicuous feature, found in all species studied, is the paucity of junctional complexes, most marked in the midnodal area. The functional counterpart of this is an increased coupling resistance between nodal cells. An electrophysiological classification of the AV nodal area, based on transmembrane action potential characteristics during various imposed atrial rhythms (rapid pacing, trains of premature impulses), into AN (including ANCO and ANL), N, and NH zones has been described by various authors for the rabbit heart. In those studies in which activation patterns, transmembrane potential characteristics, and histology have been compared, a good correlation has been found between AN and transitional cells, N cells and the area where transitional cells and cells of the beginning of the AV bundle merge with midnodal cells, and NH cells and cells of the AV bundle. Dead-end pathways correspond to the posterior extension of the bundle of lower nodal cells and to anterior overlay fibers. During propagation of a normal sinus beat, activation of the AN zone accounts for at least 25% of conduction time from atrium to His bundle, the small N zone being the main source of AV nodal delay. Cycle length-dependent conduction delay is localized in the N zone. Conduction block of premature atrial impulses can occur both in the N zone and in the AN zone, depending on the degree of prematurity. Several factors determining AV nodal conduction delay have been identified.(ABSTRACT TRUNCATED AT 400 WORDS)

Mechanisms of conduction time hysteresis in rabbit atrioventricular node

1995 ◽  
Vol 269 (4) ◽  
pp. H1258-H1267 ◽  
Author(s):  
J. Billette ◽  
J. Zhao ◽  
A. Shrier
Keyword(s):  
Functional Properties ◽  
Cycle Length ◽  
Atrioventricular Node ◽  
Intrinsic Property ◽  
Rabbit Heart ◽  
Fatigue Properties ◽  
Conduction Time ◽  
Cycle Lengths ◽  
Respective Contribution ◽  
Nodal Properties

The functional origin of atrioventricular nodal hysteresis was studied in isolated rabbit heart preparations. This hysteresis is characterized by asymmetric changes in nodal conduction time (NCT) occurring for symmetric changes in cycle length. The respective contribution of the nodal properties of recovery, facilitation, and fatigue to the beat-to-beat changes in NCT observed during paired symmetric ramps of decreasing and increasing cycle length was determined with specifically design stimulation protocols. Nodal hysteresis was found to be entirely accounted for by variations in the contribution of nodal recovery and fatigue properties observed at corresponding cycle lengths. The study establishes how this contribution varies on a beat-to-beat basis as a result of cycle length history. This holds true for the numerous changes in hysteresis observed in response to changes in the sequence and slope of the ramps. Facilitation clearly affected NCT during these responses but did not contribute to the hysteresis. Moreover, the study demonstrates that there is no inherent change in the characteristics of nodal function with the direction of the ramp that could account for the hysteresis. Thus nodal hysteresis arises from nodal functional properties of recovery and fatigue but does not constitute a distinct independent intrinsic property of the node.

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