The effects of lidocaine on intracellular and extracellular potentials, activation, and ventricular arrhythmias during acute regional ischemia in the isolated porcine heart.

Cardinal, René; Janse, Michiel J.; Eeden, I van; Werner, Guido; d’Alnoncourt, C. Naumann; Durrer, D

doi:10.1161/01.res.49.3.792

Cited by 79 publications

(19 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Comparison of studies on the electrophysiologic effects of lidocaine on refractoriness in infarcted myocardium with composite electrode recordings and epicardial isochronal mapping have shown that results are consistent.25 26 This suggests that observations on changes in cycle length-dependent fractionation and block of infarct-zone late potentials, as recorded by the composite electrogram,25 are likely to correspond to the demonstrable slow conduction, unidirectional block, or inexcitability that can be recorded directly by epicardial isochronal mapping.26 Nevertheless, the problems of determining the refractoriness of areas of delayed depolarization in ischemic myocardium by the composite electrode technique are considerable and the results obtained in this study should be interpreted with caution and verified by isochronal mapping studies.…”

Section: Discussionmentioning

confidence: 91%

Action of sotalol on potential reentrant pathways and ventricular tachyarrhythmias in conscious dogs in the late postmyocardial infarction phase.

Cobbe¹,

Hoffman²,

Ritzenhoff³

et al. 1983

Circulation

View full text Add to dashboard Cite

Sotalol is a ,3-adrenergic blocker that also prolongs action potential duration and myocardial refractoriness over the short term (class III effect). Its short-term antiarrhythmic effects were compared with those of metoprolol, which has neither short-term class III nor membranestabilizing action, on reentrant ventricular arrhythmias produced by programmed stimulation in 17 conscious dogs 3 to 8 days after myocardial infarction. Ventricular arrhythmias were prevented or significantly slowed by sotalol in 11 of 19 studies (58%) compared with in one of 14 (7%) studies with metoprolol. Sotalol prolonged refractoriness in the infarct zone, measured from an implanted "composite" electrode, by 41 45% (mean ± SD, p < .01), which was significantly greater than the increases it produced in effective refractory period of the normal ventricle (14.0 + 5.5%) or QT interval (12.5 ± 7.8%). Metoprolol had no effect on infarct-zone refractoriness. Sotalol differentially increases refractoriness in potential reentry circuits in ischemic myocardium. Its antiarrhythmic effect in this model is not due to /8-blockade, and is presumably related to prolongation of action potential duration. Circulation 68, No. 4, 865-871, 1983. SOTALOL is unique among currently available 38-adrenergic blockers in that it produces short-term prolongation of myocardial action potential duration and effective refractory period (ERP) in vitro. According to Vaughan-Williams' classification,3 therefore, sotalol has class III as well as class II antiarrhythmic properties. It has recently been shown that sotalol prolongs monophasic action potential duration in man,4'5 and produces acute increases in the ERPs of human atria, ventricles, and atrioventricular accessory pathways.6 7The purpose of this study was to examine the shortterm effects of sotalol on reentrant ventricular arrhythmias and epicardial infarct-zone potentials in experimental canine myocardial infarction.8 9 The effects of sotalol were compared with those of metoprolol, a cardioselective /3-adrenergic blocker that is devoid of short-term class III

show abstract

Section: Discussionmentioning

confidence: 91%

Action of sotalol on potential reentrant pathways and ventricular tachyarrhythmias in conscious dogs in the late postmyocardial infarction phase.

Cobbe¹,

Hoffman²,

Ritzenhoff³

et al. 1983

Circulation

View full text Add to dashboard Cite

show abstract

“…49, No. 5, NOVEMBER 1981 regional ischemia in isolated perfused hearts, lidocaine depressed or abolished the slow transmembrane action potentials in the center of the ischemic zone, making it very likely that these potentials are initiated by the rapid sodium inward current (Cardinal et al, 1980). Unfortunately, no information is available on the effect of slow channel-blocking agents on the shape and duration of the transmembrane action potential during ischemia in the intact heart.…”

Section: Changes In Resting Membrane Potentialmentioning

confidence: 99%

Electrophysiological changes and ventricular arrhythmias in the early phase of regional myocardial ischemia.

Janse¹,

Kléber²

1981

Circulation Research

Self Cite

297

121

View full text Add to dashboard Cite

“…In contrast, inactivated state blockers may be more eVective in conditions where tissue becomes depolarised-experimental evidence suggests that the eYcacy of lignocaine and the risk of proarrhythmia are both enhanced in acutely ischaemic myocardium. 27 In addition to the eVects of membrane potential depolarisation on block, the low pH associated with ischaemia can also slow the time constant of drug dissociation, enhancing the cumulative level of channel block. 26 …”

Section: Figure 3 (A) Ion Channels Undergo Changes In Protein Conformmentioning

confidence: 99%

Echohistological correlation in Candida albicans endocarditis

Serrador¹

2000

Heart

View full text Add to dashboard Cite

The effects of lidocaine on intracellular and extracellular potentials, activation, and ventricular arrhythmias during acute regional ischemia in the isolated porcine heart.

Cited by 79 publications

References 29 publications

Action of sotalol on potential reentrant pathways and ventricular tachyarrhythmias in conscious dogs in the late postmyocardial infarction phase.

Action of sotalol on potential reentrant pathways and ventricular tachyarrhythmias in conscious dogs in the late postmyocardial infarction phase.

Electrophysiological changes and ventricular arrhythmias in the early phase of regional myocardial ischemia.

Echohistological correlation in Candida albicans endocarditis

Contact Info

Product

Resources

About