The Decrease in the Automatism of Thepurkinje Pacemaker Fibers Provoked Byhigh Frequencies of Stimulation

Alanís, J; Benítez, Daisy

doi:10.2170/jjphysiol.17.556

Cited by 42 publications

(15 citation statements)

References 14 publications

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“…The dominance of the pacemaker site may be determined not only by its intrinsic firing rate, but also by its susceptibility to overdrive suppression. 21 " 23 We considered the possibility that the gradation of intensity of automatic activity might be related in part to the density of distribution of sympathetic nerve endings. The findings during /3-adrenergic blockade both in vivo and in vitro effectively dispelled that possibility.…”

Section: Discussionmentioning

confidence: 99%

Hierarchy of ventricular pacemakers.

Hope¹,

Scherlag²,

El‐Sherif³

et al. 1976

Circulation Research

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SUMMARY To characterize the pattern of pacemaker dominance in the ventricular specialized conduction system (VSCS), escape ventricular pacemakers were localized and quantified in vivo and in vitro, in normal hearts and in hearts 24 hoars after myocardial infarction. Escape pacemaker fod were localized in vivo during vagally induced atria! arrest by means of electrograms recorded from the His bundle and proximal bundle branches and standard electrocardiographk limb leads. The VSCS was isolated using a modified Ellzari preparation or preparations of each bundle branch. Pacemakers were located by extra-and lntracellular recordings. Escape pacemaker foci in vivo were always in the proximal conduction system, usually the left bundle branch. The rate was 43 ± 11 (mean ± SD) beats/min. After /3-adrenergic blockade, the mean rate feD to 31 ± 10 beats/min, bat there were no shifts in pacemaker location. In the infarcted hearts, pacemakers were located in the peripheral left bundle branch. The mean rate was 146 ± 20 beats/min. In isolated normal preparations, the dominant pacemakers usually were in the His bundle, firing at a mean rate of 43 ± 10 beats/min. The rates of pacemakers diminished with distal progression. In infarcted hearts, the pacemakers invariably were in the infant zone. The mean firing rates were not influenced by /3-adrenergic blockade. The results indicate that the dominant pacemakers are normally in the very proximal VSCS, bnt after myocardial infarction pacemaker dominance is shifted into the infarct. Distribution of pacemaker dominance is independent of sympathetic influence.IT HAS BEEN stated that in the ventricles there is a hierarchy of pacemakers analogous to that in atria; the more proximal the locus in the specialized conduction system, the greater the intrinsic automaticity.1 ' 2 However, data to substantiate this assertion are lacking. Recent attempts to localize ventricular escape pacemakers in the normal canine heart were interpreted to indicate that pacemaker activity is confined to the atrioventricular (AV) junction.3 There have been no systematic attempts to quantify and compare regional pacemaker activity within the ventricular specialized conduction system (VSCS).In the later phase of ventricular arrhythmias after coronary occlusion 4 there is an enhancement of the rate of firing of automatic foci.6 ' 6 It has not been determined whether there is an acceleration of normally dominant pacemakers or whether there is a displacement of pacemaker dominance after coronary occlusion. This report describes the results of a study of the distribution of pacemaker dominance within the normal VSCS and its alteration after coronary occlusion. Since the rate of firing of cells of the VSCS is strongly dependent on catecholamine stimulation, 7 we investigated the possibility that the normal distribution of pacemaker dominance might be related to regional differences in catecholamine influence. Correspondingly, we investigated the possibility that the accelerated firing of Purkinje fibers within an infa...

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Section: Discussionmentioning

confidence: 99%

Hierarchy of ventricular pacemakers.

Hope¹,

Scherlag²,

El‐Sherif³

et al. 1976

Circulation Research

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“…This phenomenon, which is counter to the previously described suppression of Purkinje fiber automaticity by pacing (Alanis and Benitez, 1967;Vassalle, 1970), is thought to arise by a mechanism which is fundamentally different from that which underlies classical spontaneous automaticity in Purkinje fibers Rosen et al, 1973a;Ferrier, 1977). When induced in the presence of cardiotonic steroids, the degree of this automaticity has been shown to increase with the rate and duration of stimulation (Davis, 1973;Hogan et al, 1973;Ferrier, 1977).…”

mentioning

confidence: 80%

Pacing-induced automaticity in sheep Purkinje fibers.

Wald¹,

Waxman²

1981

Circulation Research

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SUMMARY The induction and decay of pacing-induced automaticity were studied in 15 sheep Purkinje fiber preparations superfused with modified Tyrode's solution containing norepinephrine, 2.5 x 10"' M. All preparations were quiescent prior to pacing. Spontaneous automacity could be induced in each preparation provided a sufficient number of pacing stimuli were applied at a fast enough rate. Once the minimum pacing requirements for induction of automaticity were exceeded, the number, total duration, and fastest rate of the induced beats were proportional to the number and rate of the pacing stimuli up to a maximum which could not be exceeded. Consecutive trains of stimuli were additive in inducing automaticity, provided that the pauses between them were short enough to preclude the timedependent return of automatic properties to their pre-pacing level. Prolonged sequences of fixed pacing trains resulted in stable degrees of automaticity which depended on the length of the pause between them. These observations permit a semiquantitative description of induced automatic behavior and help establish a model that may be useful in future studies. Circ Res 48: 531-538, 1981PACING-INDUCED automaticity has been demonstrated in the specialized ventricular conduction tissues of several animal species under a variety of pharmacological and altered ionic conditions (Vassalle and Carpentier, 1972;Davis, 1973;Hogan et al., 1973;Ferrier and Moe, 1973; Cranefield and Aronson, 1974). This phenomenon, which is counter to the previously described suppression of Purkinje fiber automaticity by pacing (Alanis and Benitez, 1967;Vassalle, 1970), is thought to arise by a mechanism which is fundamentally different from that which underlies classical spontaneous automaticity in Purkinje fibers Rosen et al., 1973a;Ferrier, 1977). When induced in the presence of cardiotonic steroids, the degree of this automaticity has been shown to increase with the rate and duration of stimulation (Davis, 1973;Hogan et al., 1973;Ferrier, 1977). This suggested that this phenomenon was responsible for some pacing-sensitive ventricular arrhythmias which develop in vivo during digitalis intoxication (Vassalle et al., 1962;Wittenberg et al., 1970;Wittenberg et al., 1972). The temporal correlation of ouabain-induced delayed afterdepolarizations in vitro with the appearance of ventricular arrhythmias in vivo was strongly supportive of this relationship (Rosen at al., 1973b).First described by Vassalle and Carpentier (1972), pacing-induced automaticity, or, as the authors termed it, "overdrive excitation" in lamb Pur- Received April 7, 1978; accepted for publication October 29, 1980. kinje fibers in a normal ionic environment and in the presence of norepinephrine, 8.8 X 10~? M, represents one of the conditions closest to physiological under which the phenomenon has been described in ventricular tissues. Vassalle et al. (1976b) have demonstrated that overdrive excitation related ventricular arrhythmias in the heart-blocked dog in vivo was dependent on shortening o...

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“…It should be pointed out that Alanis & Benitez (1967) have observed on Purkinje fibres a slowing in rhythm after rapid stimulation and they also adduce an increase in K permeability as the mechanism. However, they suppose that the K conductance of the membrane is increased by rapid stimulation and do not discuss the possibility of a release of ACh nor do they test the effect of atropine.…”

Section: Discussionmentioning

confidence: 94%

“…A transitory slowing of the spontaneous rhythm after a period of rapid repetitive artificial stimulation has been observed frequently in the adult heart (Gaskell, 1883;Vincenzi & West, 1963;Lu, Lange & Brooks, 1965;Chiang & Leaders, 1966; Whitacre, Long & Whalen, 1966;Alanis & Benitez, 1967;Kennedy & West, 1967). This post-stimulation inhibition has generally been attributed to the negative chronotropic effect of acetylcholine (ACh) liberated from intracardiac nervous terminations under the effect of electrical pulses applied to the heart.…”

Section: Introductionmentioning

confidence: 99%

Release of acetylcholine by chick embryo heart before innervation

Coraboeuf¹,

Douarin²,

Obrecht-Coutris³

1970

The Journal of Physiology

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SUMMARY1. In chick embryo hearts, 3-day-old and not yet innervated, repetitive direct stimulation causes a transitory inhibition of the spontaneous rhythm.2. The degree of post-stimulation inhibition depends on the frequency and duration of the artificial stimulation and on the concentration of K and Ca ions in the extracellular solution.3. After treatment with atropine (10-5 g/ml.) post-stimulation inhibition is no longer observed. The spontaneous rhythm is accelerated by atropine. The findings therefore suggest that an ACh-like substance is released from the non-innervated embryonic heart during activity.4. By use of the dorsal muscle of the leech for biological assay the liberation of an ACh-like substance from the non-innervated embryonic heart was confirmed.

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The Decrease in the Automatism of Thepurkinje Pacemaker Fibers Provoked Byhigh Frequencies of Stimulation

Cited by 42 publications

References 14 publications

Hierarchy of ventricular pacemakers.

Hierarchy of ventricular pacemakers.

Pacing-induced automaticity in sheep Purkinje fibers.

Release of acetylcholine by chick embryo heart before innervation

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