Abnormal Automaticity in Canine Purkinje Fibers Focally Subjected to Low External Concentrations of Calcium

Sano, Toyomi; Sawanobori, Tohru

doi:10.1161/01.res.31.2.158

Cited by 32 publications

(5 citation statements)

References 19 publications

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“…As demonstrated here, the longer the period of pacing, the greater the hyperpolarization of the fiber and the longer the duration of overdrive suppression. showed EAD-induced triggered activity at a potassium concentration of 2 mM and at cesium concentrations of 5 to 10 mM, 17 (89%) showed rapid inhibition of triggering when the external potassium concentration was raised to 4 mM ( figure 1 1). EAD magnitude was 7.5 ± 0.4 units with 2 mM potassium and 1.8 + 0.7 units 10 min after raising the potassium concentration to 4 mM (n = 19, p < .001).…”

Section: Resultsmentioning

confidence: 99%

Effects of pacing on triggered activity induced by early afterdepolarizations.

Damiano¹,

Rosen²

1984

Circulation

250

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Early afterdepolarizations (EADs) are depolarizing potentials that occur during phase 2 or phase 3 of repolarization. They can induce triggered activity and have been proposed as a cause for arrhythmias in the heart in situ. To determine the response of EADs and triggered activity to interventions analogous to those used in the clinic for identifying arrhythmogenic mechanisms, we used a pacing protocol to study the response of EADs to sustained drive and extrastimuli. Cesium chloride (5 to 20 mM), which induces triggered arrhythmias in the intact dog, was used to induce EADs in isolated canine Purkinje fibers, and these were studied by microelectrode techniques. Cesium prolonged action potential duration and induced two types of EADs. At a potassium concentration of 4 mM, EADs occurred at membrane potentials of -3 to -30 mV. They were initiated 240 to 680 msec after the action potential upstroke and were 2 to 30 mV in amplitude. Their amplitude increased as drive cycle length increased, but their coupling interval to the action potential did not change with drive cycle length. These EADs did not induce triggered action potentials. At a potassium concentration of 2 mM, EADs usually occurred at higher membrane potentials (-50 to -70 mV) and longer coupling intervals (470 to 1360 msec) and were manifested as a delay.of phase 3 repolarization. These EADs induced triggered action potentials. When the triggered rhythms became sustained, premature stimuli either reset or terminated them, depending on the maximum diastolic potential. Termination occurred more frequently as the maximum diastolic potential increased. The extent of overdrive suppression induced by pacing for 15 sec to 3 min also increased as the maximum diastolic potential increased. In summary, cesium induced EADs at low or high membrane potentials. The former did not induce triggered activity, but the latter did. The triggered rhythms that occurred were similar to abnormal automatic mechanisms in their response to overdrive pacing and extrastimuli.

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Section: Resultsmentioning

confidence: 99%

Effects of pacing on triggered activity induced by early afterdepolarizations.

Damiano¹,

Rosen²

1984

Circulation

250

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“…Focal reexcitation has been demonstrated to occur by increasing inhomogeneity of repolarization in small segments of tissues. 17 A recent study also showed with experiments in vivo that ventricular arrhythmias were inducible in canine hearts in which dispersion of repolarization was induced by a combination of general hypothermia and selective coronary perfusion with warm blood. "8 The results of the present study, in agreement with those of previous reports,5-9 showed that ischemia produced by cessation of coronary perfusion shortened APD in affected myocardium, which may provide dispersion of repolarization between normal and ischemic myocardium in vivo.…”

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confidence: 96%

Simultaneous recording of action potentials from endocardium and epicardium during ischemia in the isolated cat ventricle: relation of temporal electrophysiologic heterogeneities to arrhythmias.

Kimura¹,

Bassett²,

Kohya³

et al. 1986

Circulation

120

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We studied the effects of ischemia on transmembrane action potentials, conduction time, and refractory periods of both endocardial and epicardial muscle cells of coronary-perfused cat left ventricles. Oxygenated Tyrode's solution was perfused through the left anterior descending coronary artery, while the preparation was superfused with Tyrode's solution gassed with 95% N2 and 5% CO2. Transmembrane action potentials recorded simultaneously from endocardial and epicardial cells were normal during coronary perfusion. When perfusion was discontinued ("ischemia"), rapid deterioration of action potentials and prolongation of conduction time were observed in both endocardial and epicardial cells. The magnitude of the reduction of action potential amplitude and action potential duration (APD), and of prolongation of conduction time, was greater in epicardial cells than in endocardial cells, although the change in resting membrane potential was almost the same. However, APD of endocardial cells decreased progressively during 30 min of ischemia, whereas APD of epicardial cells was reduced maximally at 10 min and then partially recovered. Shortening of refractory periods of endocardial cells paralleled APD shortening, whereas refractory periods of epicardial cells decreased for the first 10 min and then increased. At 10 min of ischemia, APD and refractory periods of epicardial cells were significantly shorter than those of endocardial cells. At 30 min of ischemia, refractory periods of epicardial cells exceeded those of endocardial cells because of development of greater postrepolarization refractoriness in epicardial cells. Accompanying these different changes in APD and refractory periods of endocardial and epicardial cells, spontaneous extrasystolic impulses increased and rapid runs of extrasystolic impulses could be induced by extrastimuli. Our data suggest that dispersion of repolarization and refractory period between endocardial and epicardial cells is related to the development of arrhythmias during early ischemia. In addition, heterogeneities of both the initial change in refractory period paralleling APD shortening and the late-developed postrepolarization refractoriness may be involved in the occurrence of acute ischemic arrhythmias. Circulation 74, No. 2, 401-409, 1986. EXPERIMENTAL preparations of coronary artery occlusion have been extensively studied in an attempt to understand the mechanisms of ischemia-induced ventricular arrhythmias. 1A Study of the electrophysiologic events that occur at a cellular level during ischemia can provide a more precise understanding of the mechanisms of such arrhythmias. Indeed, some investigators

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“…3 -* EADs have been induced in isolated cardiac tissue under a variety of conditions that increase inward current or reduce repolarizing current. These conditions include exposure to catecholamines, 7 acidosis, 8 low K + concentration, 9 low Ca 2+ concentration, 10 hypoxia, 11 and many drugs (e.g., aconitine, 12 quinidine, 5 7V-acetyl procainamide, 13 sotalol, 14 cesium chloride, 34 and clofilium 11 )-In vivo evidence of EAD and triggered activity as the underlying mechanism of polymorphic ventricular tachyarrhythmias in dogs exposed to cesium chloride was reported through the use of endocardial and epicardial monophasic action potentials. •Statistically significant (Student's t test, p<0.001); tstatistically significant (Student's t test, p<0.01).…”

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confidence: 99%

QTU prolongation and polymorphic ventricular tachyarrhythmias due to bradycardia-dependent early afterdepolarizations. Afterdepolarizations and ventricular arrhythmias.

El‐Sherif

Zeiler

Craelius

et al. 1988

Circulation Research

225

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Polymorphic ventricular tachyarrhythmias occurred spontaneously during bradycardia in dogs given the inotropic polypeptide anthopleurin-A (AP-A).The arrhythmia was investigated in in vitro and in vivo experiments. In in vitro experiments, AP-A (50 /ig/1) produced bradycardiadependent prolongation of action potential duration that was more pronounced in Purkinje than in muscle fibers. Only Purkinje fibers developed early afterdepolarizations (EAD) and triggered activity. These effects could be abolished by rapid pacing, lidocaine (4 mg/1), or tetrodotoxin (1 mg/1). In vivo experiments were conducted in anesthetized healthy dogs with simultaneous recording of surface ECG, monophask action potentials from the endocardia! and epicardial surface of the left ventricle by contact electrode catheter technique, and transmembrane action potentials from the epicardial surface of the left ventricle with a floating microelectrode technique. AP-A in a dose comparable to that used in vitro (4 /ig/kg, i.v. bolus) resulted in bradycardia-dependent marked prolongation of both monophasic and transmembrane action potentials. An EAD gradually appeared on both recordings but was more marked in endocardia! monophasic action potentials. Eventually, a premature ventricular depolarization arose from or very close to the peak of the EAD. The prolongation of action potentials was associated with similar prolongation of the QTU interval hi surface ECG, and in some experiments, the EAD corresponded to a distinct prominent U wave. A ventricular premature depolarization arose from the U or TU complex and initiated polymorphic ventricular tachyarrhythmias that terminated spontaneously or degenerated into ventricular fibrillation. These effects were reversed by rapid pacing or lidocaine (1 mg/kg). The present study provides evidence in support of the hypothesis that AP-A-induced ventricular tachyarrhythmias are due to bradycardia-dependent EAD and triggered activity.

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Abnormal Automaticity in Canine Purkinje Fibers Focally Subjected to Low External Concentrations of Calcium

Cited by 32 publications

References 19 publications

Effects of pacing on triggered activity induced by early afterdepolarizations.

Effects of pacing on triggered activity induced by early afterdepolarizations.

Simultaneous recording of action potentials from endocardium and epicardium during ischemia in the isolated cat ventricle: relation of temporal electrophysiologic heterogeneities to arrhythmias.

QTU prolongation and polymorphic ventricular tachyarrhythmias due to bradycardia-dependent early afterdepolarizations. Afterdepolarizations and ventricular arrhythmias.

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