Intravenous anesthetics and epinephrine-induced arrhythmias.

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1. It is well known that halothane and other hydrocarbon anesthetics enhance the epinephrine-induced arrhythmias. Regarding to intravenous anesthetics, thiopental has been reported to enhance the epinephrine-induced arrhythmias to a greater extent than did halothane. However, the effect of other intravenous anesthetics on epinephrine-induced arrhythmias has not been well discussed. Our study was designed to clarify the effect of propofol and etomidate on epinephrine-induced arrhythmias in dogs. The result is that, we clarified that propofol enhanced epinephrine-induced arrhythmias whereas etomidate did not have significant effect on epinephrine-induced arrhythmias. In addition, we determined that the action of propofol was dose-dependent in the presence of a background of etomidate. (Anesthesiology, 1991)2. Thiopental has been reported to sensitize the heart to the arrhythmogenic action of epinephrine, but the adrenoceptor mechanism involved in the arrhythmogenicity of thiopental remains unknown. We investigated comparative roles of alphal and beta adrenoceptors in myocardial sensitization by thiopental in dogs, and demonstrated that both alphal and beta adrenoceptor activities are important for myocardial sensitization by thiopental to the arrhythmogenic action of epinephrine.3. In order to extent our previous work on adrenoceptor mechanism of epinephrine-induced arrhythmias, we designed an experimental model to clarify the role of betal and beta2 adrenoceptor using halothane-anesthetized dogs. (Can J Anaesth, 1992) In our next work, we intend to elucidate the role of subtypes of beta adrenoceptor in the genesis of arrhythmias during thiopental anesthesia using this experimental model.