Rate-dependent functional properties of retrograde atrioventricular nodal conduction in experimental animals

1993 ◽  
Vol 265 (4) ◽  
pp. H1257-H1264 ◽  
Author(s):  
G. O'Hara ◽  
R. Gendreau ◽  
J. Billette ◽  
F. Amellal ◽  
M. Nayebpour ◽  
...  

While rate-dependent atrioventricular (AV) nodal functional properties play a major role in determining antegrade AV nodal conduction, their existence and characteristics have not been assessed during retrograde AV nodal impulse propagation. Pacing protocols were used to study selectively AV nodal recovery, facilitation, and fatigue in 6 isolated, superfused rabbit AV nodal preparations and in 11 morphine-chloralose anesthetized dogs. All three properties were identifiable during retrograde AV nodal activation in rabbits. Retrograde recovery and fatigue were clearly demonstrated in dogs, but facilitation could not be evaluated because of echo beats during retrograde premature stimulation. Functional properties were qualitatively similar during retrograde and antegrade propagation; however, important quantitative differences were noted. The time constant for recovery from activation was significantly greater in the retrograde [rabbits, 69 +/- 8 (SE) ms; dogs, 93 +/- 11 ms] compared with the antegrade direction (rabbits, 50 +/- 5 ms; dogs, 58 +/- 4 ms; P < 0.05 vs. retrograde for each species). The magnitude of fatigue resulting from sustained increases in rate was also substantially greater in the retrograde direction in both rabbits (17 +/- 2 vs. 10 +/- 1 ms antegrade, P = 0.01) and dogs (20 +/- 4 vs. 6 +/- 1 ms antegrade, P < 0.01). Conduction time and refractory period were both greater in the retrograde compared with antegrade direction, and directional differences in conduction properties were magnified as activation rate increased.(ABSTRACT TRUNCATED AT 250 WORDS)

1981 ◽  
Vol 241 (1) ◽  
pp. H26-H33 ◽  
Author(s):  
J. Billette

The number of short cardiac cycles necessary to induce, and normal cycles to dissipate, a rate-dependent shortening in atrioventricular (AV) nodal functional refractory period (FRP) and conduction time (CT) was determined in six anesthetized dogs. For the induction study, the periodic premature stimulation procedure was performed at control and repeated six times while 1, ..., 6 conditioning short prepremature cycles (PPC) were introduced between the last basic cycle and the premature cycle. In all dogs, FRP was maximally shortened and the recovery curve was maximally shifted to the left when the premature cycle was preceded by 1 PPC. Adding 2, ..., 6 PPC resulted in slightly fewer but persistent shortenings of both FRP and CT. The dissipation of the FRP and CT shortenings produced by 2 and 6 PPC was studied subsequently in the same dogs by introducing 1, ..., 6 normal basic cycles between the last PPC and the test premature cycle. The FRP and CT shortenings induced by 2 or 6 PPC were almost completely dissipated after one normal basic cycle. Thus, one short cycle produces a maximum shortening in AV nodal FRP and CT, and one normal basic cycle is sufficient to dissipate these effects.


1986 ◽  
Vol 251 (5) ◽  
pp. H920-H925 ◽  
Author(s):  
J. Billette ◽  
J. P. Gossard ◽  
L. Lepanto ◽  
R. Cartier

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.


1991 ◽  
Vol 261 (2) ◽  
pp. H292-H300 ◽  
Author(s):  
M. Nayebpour ◽  
M. Talajic ◽  
S. Nattel

A number of functional properties of the atrioventricular (AV) node have been described in response to changes in the atrial input rate. The purpose of this study was 1) to develop quantitative descriptors of these properties, and 2) to determine whether they can account for rate-dependent changes in AV nodal conduction. The delay in AV nodal conduction of single premature beats (recovery) was found to be an exponential function of coupling interval with a time constant of 66 +/- 2 (+/- SE) ms. A single abbreviated (facilitation) cycle did not alter the time constant of recovery or basal conduction for a subsequent beat but shifted its recovery curve to the left to an extent exponentially related to the facilitation cycle length. The induction of a tachycardia with HA interval fixed so as to control the recovery and facilitation variables resulted in a first-order onset of AV conduction slowing (fatigue). The fatigue process had a time constant in the range of 70 beats and a magnitude that was a decaying exponential function of HA interval. An equation incorporating quantitative descriptors of recovery, facilitation, and fatigue accurately predicted rate-dependent changes in AH interval. We conclude that 1) the AV nodal properties of recovery, facilitation, and fatigue are amenable to quantitative characterization, and 2) rate-dependent changes in AV nodal conduction time can be well described in terms of these underlying properties.


1995 ◽  
Vol 268 (1) ◽  
pp. H384-H390
Author(s):  
A. F. Kuguoglu ◽  
D. W. Wallick ◽  
P. J. Martin

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.


1984 ◽  
Vol 62 (12) ◽  
pp. 1479-1486 ◽  
Author(s):  
Jean-Paul Clozel ◽  
Jacques Billette ◽  
Gilles Caillé ◽  
Pierre Théroux ◽  
Richard Cartier

Atrial and atrioventricular conduction variables were studied at control and at the end of each of six consecutive 45-min diltiazem administration periods in eight closed chest-anesthetized dogs. Diltiazem was given as a bolus (50 μg/kg, i.v.) followed by an infusion (0.5 μg∙kg−1∙min−1); doses were doubled in subsequent periods. The plasma concentrations, measured by gas–liquid chromatography, ranged from 8 to 1400 ng/mL and correlated strongly with the doses (r = 0.92; p < 0.01). The Wenckebach cycle length, basic conduction time, and functional refractory period of the atrioventricular (AV) node increased proportionally with plasma concentration (respective r = 0.90, 0.89, 0.80; p < 0.01). The minimum mean plasma concentrations affecting these variables significantly were 37, 83, and 175 ng/mL, respectively. Second or third degree AV blocks developed in all dogs for plasma concentrations between 379 and 1400 ng/mL. In four dogs which were given isoproterenol (0.2 μg∙kg−1∙min−1), these blocks disappeared within 1 min. Atrial conduction time and functional refractory period were slightly but significantly shortened by diltiazem with mean plasma concentrations of 175 ng/mL and over. His–Purkinje intervals were not significantly changed by diltiazem. Systolic and diastolic arterial pressures were decreased by diltiazem (r = −0.64, r = −0.79; p < 0.01) starting with a mean plasma concentration of 83 ng/mL. We conclude that AV nodal conduction variables are progressively prolonged with increasing plasma concentrations of diltiazem; plasma concentrations affecting blood pressure and AV nodal variables overlap; and the AV blocks produced by toxic concentrations of diltiazem can be corrected by isoproterenol.


1957 ◽  
Vol 191 (3) ◽  
pp. 481-486 ◽  
Author(s):  
M. J. Oppenheimer ◽  
P. R. Lynch ◽  
G. Ascanio

Slow conduction velocities play a role in pulsus alternans and digitalis intoxication and possibly in the arrhythmia due to a rapidly discharging atrial aconitine focus. In the ventricle mephentermine increases conduction velocity, shortens refractory period and A-V conduction time. The present study investigates the usefulness of mephentermine in these conditions. Pulsus alternans was reverted to a normal series of mechanical contractions by mephentermine. The same agent provided periods of regular rhythm during the presence of an atrial aconitine focus; in two cases a permanent sinus rhythm was established. The prolonged P-R interval due to intoxication with acetyl strophanthidin was restored to normal by mephentermine. The action of mephentermine is specific since compounds with addition or subtraction of one methyl group or the hydroxy-mephentermine were ineffective against a circus flutter.


1995 ◽  
Vol 268 (1) ◽  
pp. H17-H24 ◽  
Author(s):  
W. Y. Lew

Load-dependent relaxation was studied in six anesthetized dogs by inflating an intra-aortic balloon to increase peak left ventricular (LV) pressure by 1–20 mmHg within a single cardiac cycle. A series of timed and graded pressure loads was produced by inflating the balloon either during diastole (early loads) or midsystole (midsystolic pressure loads). The rate of LV pressure fall was measured with the time constant (tau). There was a significant increase in tau with 63 midsystolic pressure load [tau increased 1.4 +/- 0.1% (SE)/mmHg increase in peak LV pressure] but not with 67 early pressure loads (-0.5 +/- 0.1%/mmHg). This difference remained with LV pacing-induced asynchrony (tau increased 1.8 +/- 0.1%/mmHg with 54 midsystolic pressure loads compared with -0.2 +/- 0.1%/mmHg with 56 early pressure loads) and after 5 micrograms/kg of intravenous ryanodine (tau increased 1.0 +/- 0.2%/mmHg with 58 midsystolic pressure loads compared with -0.7 +/- 0.1%/mmHg with 59 early pressure loads). When compared with control, asynchrony significantly augmented and ryanodine significantly attenuated the effects of midsystolic pressure loads. In conclusion, asynchrony and ryanodine modulate the extent of load-dependent relaxation in the intact left ventricle.


1995 ◽  
Vol 79 (6) ◽  
pp. 1930-1935 ◽  
Author(s):  
S. Magder

The time constant of venous drainage (tau v) is an important determinant of the return of blood to the heart. The lower the tau v, the higher the flow for a given volume. To determine whether the tau v of muscle decreases during muscle contraction, we anesthetized dogs with pentobarbital sodium and mechanically ventilated them. We isolated the vasculature of the gastrocnemius muscle and attached the muscle to a force transducer. The muscle was pump perfused, and flows were measured with electromagnetic flow probes on the artery and vein. Pressure in the venous compliant region (Pel) was obtained by simultaneously occluding the artery and vein. Changes in volume (delta V) were produced by changing inflow and obtaining the integral of the difference between inflow and outflow. The tau v was obtained from delta V divided by change in flow. Compliance was calculated from delta V divided by change in Pel from before to after a change in flow. The venous resistance was calculated from tau v divided by venous compliance. The muscle was set at the optimal length, and contractions were produced by stimulating the nerve to the muscle with supramaximal voltage at either 1- or 5-Hz trains with stimulations at 20 Hz, 0.2-ms duration, and duty cycle of 0.25. The tau v at rest was 4.06 +/- 2.16 s and decreased to 2.44 +/- 1.07 s (P < 0.05) at 1 Hz and to 1.81 +/- 0.4 s at 5 Hz. There were no significant changes in venous compliance or venous resistance. In conclusion, muscle contractions can reduce the time constant of venous drainage of muscle and could thereby contribute to the increased venous return and cardiac output during exercise.


1987 ◽  
Vol 65 (11) ◽  
pp. 2329-2337 ◽  
Author(s):  
Jacques Billette ◽  
Marie St-Vincent

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).


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