Atrioventricular nodal activation during periodic premature stimulation of the atrium

1987 ◽  
Vol 252 (1) ◽  
pp. H163-H177 ◽  
Author(s):  
J. Billette

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.

1995 ◽  
Vol 269 (4) ◽  
pp. H1258-H1267 ◽  
Author(s):  
J. Billette ◽  
J. Zhao ◽  
A. Shrier

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.


1992 ◽  
Vol 262 (6) ◽  
pp. H1899-H1907 ◽  
Author(s):  
J. Zhao ◽  
J. Billette

The roles of changes in refractory and recovery properties of the atrioventricular node as affected by facilitation and fatigue in the genesis of Wenckebach periodicity were studied in isolated rabbit heart preparations. The contribution of nodal recovery time, facilitation, and fatigue to beat-to-beat changes in nodal conduction time (NCT) and effective (ERPN) and functional refractory periods of node (FRPN) occurring during stable 4:3 Wenckebach cycles was determined with premature stimulation protocols performed during these cycles. Fatigue prolonged, equally for each beat, NCT, ERPN, and FRPN, and therefore did not contribute to Wenckebach periodicity. Beat-to-beat increases in facilitation broadened the range of recovery times for which conduction was successful and decreased NCT, ERPN, and FRPN below the values expected from fatigue alone. However, ERPN and NCT increased overall from beat to beat because of NCT-induced (effects of NCT on ensuing refractoriness) increases in nodal refractoriness and consequent shortenings of the recovery time. These findings establish a complementary role for the recovery and refractory properties in generating the Wenckebach periodicity and demonstrate the modulating roles of facilitation and fatigue on this phenomenon.


1999 ◽  
Vol 90 (1) ◽  
pp. 60-65 ◽  
Author(s):  
Michael D. Sharpe ◽  
Daniel J. Cuillerier ◽  
John K. Lee ◽  
Magdi Basta ◽  
Andrew D. Krahn ◽  
...  

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.


1986 ◽  
Vol 251 (3) ◽  
pp. H631-H643 ◽  
Author(s):  
T. Mazgalev ◽  
L. S. Dreifus ◽  
E. L. Michelson ◽  
A. Pelleg

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.


2002 ◽  
Vol 92 (1) ◽  
pp. 225-229 ◽  
Author(s):  
L. Such ◽  
A. Rodriguez ◽  
A. Alberola ◽  
L. Lopez ◽  
R. Ruiz ◽  
...  

We have studied the intrinsic modifications on myocardial automatism, conduction, and refractoriness produced by chronic exercise. Experiments were performed on isolated rabbit hearts. Trained animals were submitted to exercise on a treadmill. The parameters investigated were 1) R-R interval, noncorrected and corrected sinus node recovery time (SNRT) as automatism index; 2) sinoatrial conduction time; 3) Wenckebach cycle length (WCL) and retrograde WCL, as atrioventricular (A-V) and ventriculoatrial conduction index; and 4) effective and functional refractory periods of left ventricle, A-V node, and ventriculoatrial retrograde conduction system. Measurements were also performed on coronary flow, weight of the hearts, and thiobarbituric acid reagent substances and glutathione in myocardium, quadriceps femoris muscle, liver, and kidney, to analyze whether these substances related to oxidative stress were modified by training. The following parameters were larger ( P < 0.05) in trained vs. untrained animals: R-R interval (365 ± 49 vs. 286 ± 60 ms), WCL (177 ± 20 vs. 146 ± 32 ms), and functional refractory period of the left ventricle (172 ± 27 vs. 141 ± 5 ms). Corrected SNRT was not different between groups despite the larger noncorrected SNRT obtained in trained animals. Thus training depresses sinus chronotropism, A-V nodal conduction, and increases ventricular refractoriness by intrinsic mechanisms, which do not involve changes in myocardial mass and/or coronary flow.


1990 ◽  
Vol 258 (1) ◽  
pp. H38-H44 ◽  
Author(s):  
A. S. Pickoff ◽  
A. Stolfi

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)


1990 ◽  
Vol 68 (7) ◽  
pp. 851-855 ◽  
Author(s):  
Charles R. Kerr

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.


1987 ◽  
Vol 253 (5) ◽  
pp. H1059-H1068 ◽  
Author(s):  
T. Mitsuoka ◽  
T. Mazgalev ◽  
L. S. Dreifus ◽  
E. L. Michelson

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.


1976 ◽  
Vol 40 (1) ◽  
pp. 74-78 ◽  
Author(s):  
S. Teague ◽  
S. Collins ◽  
D. Wu ◽  
P. Denes ◽  
K. Rosen ◽  
...  

The AV nodal conduction curve generated by the atrial extrastimulus technique has been described only qualitatively in man, making clinical comparison of known normal curves with those of suspected AV nodal dysfunction difficult. Also, the effects of physiological and pharmacological interventions have not been quantifiable. In 50 patients with normal AV conduction as defined by normal AH (less than 130 ms), normal AV nodal effective and functional refractory periods (less than 380 and less than 500 ms), and absence of demonstrable dual AV nodal pathways, we found that conduction curves (at sinus rhythm or longest paced cycle length) can be described by an exponential equation of the form delta = Ae-Bx. In this equation, delta is the increase in AV nodal conduction time of an extrastimulus compared to that of a regular beat and x is extrastimulus interval. The natural logarithm of this equation is linear in the semilogarithmic plane, thus permitting the constants A and B to be easily determined by a least-squares regression analysis with a hand calculator.


2021 ◽  
Vol 9 (6) ◽  
pp. 1305
Author(s):  
Carlos Alonso Domínguez-Alemán ◽  
Luis Alberto Sánchez-Vargas ◽  
Karina Guadalupe Hernández-Flores ◽  
Andrea Isabel Torres-Zugaide ◽  
Arturo Reyes-Sandoval ◽  
...  

A common hallmark of dengue infections is the dysfunction of the vascular endothelium induced by different biological mechanisms. In this paper, we studied the role of recombinant NS1 proteins representing the four dengue serotypes, and their role in promoting the expression and release of endocan, which is a highly specific biomarker of endothelial cell activation. We evaluated mRNA expression and the levels of endocan protein in vitro following the stimulation of HUVEC and HMEC-1 cell lines with recombinant NS1 proteins. NS1 proteins increase endocan mRNA expression 48 h post-activation in both endothelial cell lines. Endocan mRNA expression levels were higher in HUVEC and HMEC-1 cells stimulated with NS1 proteins than in non-stimulated cells (p < 0.05). A two-fold to three-fold increase in endocan protein release was observed after the stimulation of HUVECs or HMEC-1 cells with NS1 proteins compared with that in non-stimulated cells (p < 0.05). The blockade of Toll-like receptor 4 (TLR-4) signaling on HMEC-1 cells with an antagonistic antibody prevented NS1-dependent endocan production. Dengue-infected patients showed elevated serum endocan levels (≥30 ng/mL) during early dengue infection. High endocan serum levels were associated with laboratory abnormalities, such as lymphopenia and thrombocytopenia, and are associated with the presence of NS1 in the serum.


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