Effect of Sustained Load on Dispersion of Ventricular Repolarization and Conduction Time in the Isolated Intact Rabbit Heart

1996 ◽  
Vol 7 (1) ◽  
pp. 9-16 ◽  
Author(s):  
MARKUS ZABEL ◽  
STUART PORTNOY ◽  
MICHAEL R. FRANZ
1958 ◽  
Vol 13 (3) ◽  
pp. 422-424 ◽  
Author(s):  
Benjamin G. Covino ◽  
W. R. Beavers
Keyword(s):  

1991 ◽  
Vol 25 (3) ◽  
pp. 205-213 ◽  
Author(s):  
Scott M. Balderston ◽  
Kenneth E. Johnson ◽  
Michael J. Reiter

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).


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 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.


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