Effects of bepridil and lidocaine on the intravenctricular conduction in acutely ischaemic and infarcted canine myocardium

Abstract

Effects of bepridil, an antiarrhythmic and antianginal drug, on intraventricular conduction in acutely ischaemic and infarcted myocardium were examined in anaesthetized dogs, and compared with those of lidocaine. Bepridil at doses of 2 and 5 mg/kg markedly prolonged the conduction time of a premature excitation induced by a ventricular stimulation in the infarcted zone. The effect of bepridil was dependent on a coupling time of the stimulation. Bepridil showed a marked effect at a coupling time of 150 ms, while it showed no significant effect at a prolonged coupling time of 1 s. In other words, the effect of bepridil was interval-dependent. Lidocaine showed a similar interval-dependent effect, but the effect of lidocaine at a longer coupling time was less than that of bepridil. The premature stimulation produced severely delayed conduction which resulted in reentrant beats. Bepridil blocked these conductions, thereby preventing reentrant beats. In contrast to the depressant effect of bepridil in the infarcted myocardium, bepridil prevented the prolongation of conduction time during acute ischaemia. The alternation of the ST-T complex during acute ischaemia which is also an important arrhythmogenic factor was also attenuated by bepridil. Contrary to bepridil, lidocaine significantly enhanced the conduction delay and the alternation in the ST-T complex. In conclusion, bepridil as well as lidocaine showed an interval-dependent depression of the conduction in the infarcted zone of the heart, whereas during acute ischaemia bepridil in contrast to lidocaine attenuated the conduction delay and ST-T alternans.

Coupling Interval-Related Effects of Class I Antiarrhythmic Drugs, Mexiletine, Cibenzoline and Disopyramide, on Ventricular Activation in Canine Myocardial Infarction.

“…In other words, these drugs selectively depressed the activation in the infarcted zone. A similar effect was also observed with other class I antiarrhythmic drugs, lidocaine and SUN-1165 (9,10). In in vitro studies, several class I anti arrhythmic drugs such as lidocaine, mexiletine and pirmenol depressed more markedly the maximum rate of depolarization in depressed action potentials than in normal action poten tials (7,8).…”

“…However, their effects on in traventricular conduction have not been fully examined in myocardial infarction models. Previously we studied the effects of lidocaine, bepridil and SUN-1165 on intraventricular conduction in a canine model of myocardial infarction (9,10). In the present study, we in vestigated coupling interval-related effects of class I antiarrhythmic drugs, mexiletine, ciben zoline and disopyramide (1,2,(11)(12)(13), a fast, an intermediate and a slow kinetic drug (2,3,7,8), respectively, on ventricular activation in a canine model of myocardial infarction.…”

Electrophysiologic effects of volatile anesthetics, sevoflurane and halothane, in a canine myocardial infarction model

“…A markedly delayed activation may lead to reentrant arrhythmias, and the blockade of the activation with antiarrhythmic drugs prevents arrhythmias [16,[21][22][23]. In the two animals in which ventricular ~r"h'"hmias were induced by the premature stimulation, which were suppressed during the inhalation of sevoflurane or halothane.…”