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

Hashimoto, Hisakuni; Imamura, Satoshi; Ikeda, Kazuyuki; Nakashima, Mitsuyoshi

doi:10.1007/bf02482763

Cited by 8 publications

(1 citation statement)

References 24 publications

(28 reference statements)

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“…The present study showed that volatile anesthetics and class I antiarrhythmic drugs depressed the delayed activa tion in infarcted zones of canine ventricles, which is con sistent with previous results (5,15,16). In the present study, the effects of sevoflurane and isoflurane were exam ined, because these are now frequently used.…”

Section: Discussionsupporting

confidence: 91%

Electrophysiologic Interaction between Class I Antiarrhythmic Drugs and Volatile Anesthetics in Depressant Effects on Ventricular Activation in a Canine Myocardial Infarction Model

Hashimoto

Imamura

Ikeda

et al. 1994

Japanese Journal of Pharmacology

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ABSTRACT-Previous studies showed that volatile anesthetics depressed ventricular delayed activation in a canine myocardial infarction model. It is well known that class I antiarryhthmic drugs depress the ven tricular activation in the infarcted myocardium. In the present study, we examined the electrophysiologic interaction between volatile anesthetics (sevoflurane, isoflurane) and class I antiarrhythmic drugs (lidocaine, procainamide) in effects on the ventricular delayed activation in a canine myocardial infarction model. The conduction time of the premature stimulation-induced ventricular excitation was measured in both normal and infarcted zones of the ventricle. An interval from the premature stimulus artifact to the epicardial ac tivation was measured on bipolar electrograms as an index of conduction time, i.e., activation time. In the infarcted zone, the volatile anesthetics and class I antiarrhythmic drugs prolonged the activation time in the infarcted zone, and the combination of the volatile anesthetics and the class I antiarrhythmic drugs mark edly prolonged the activation time or blocked the delayed activation. In the normal zone, a similar synergistic interaction was observed, but the effect of these drugs was less compared with that in the infarcted zone. From these results, possible mechanisms to explain the synergistic interaction were discussed.

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Section: Discussionsupporting

confidence: 91%