• Y Hayashi, T Kamibayashi, K Sumikawa, A Yamatodani, M Kuro, and I Yoshiya.
• Department of Anesthesiology, Osaka University Medical School, Japan.
• Am. J. Physiol. 1993 Oct 1; 265 (4 Pt 2): H1380-5.

AbstractThe authors investigated the role of alpha 1- and beta-adrenoceptors on induction of ventricular arrhythmias during thiopental anesthesia in dogs and compared with that during halothane anesthesia. Throughout this study, arrhythmogenic threshold of epinephrine during thiopental anesthesia was designed to be comparable with that during halothane anesthesia. Phenylephrine, an alpha 1-agonist, and isoproterenol, a beta-agonist, consistently failed to provoke arrhythmias during thiopental or halothane anesthesia. The interaction between phenylephrine and isoproterenol in inducing arrhythmias was synergistic and additive during halothane and thiopental anesthesia, respectively, indicating that adrenoceptor mechanism in thiopental-epinephrine arrhythmias is different from that in halothane-epinephrine arrhythmias. During thiopental anesthesia, incidence of arrhythmias with blood pressure elevation by epinephrine, phenylephrine, or angiotensin II was not different, and increasing heart rate by electrical pacing did not replace isoproterenol in the arrhythmogenic interaction between isoproterenol and phenylephrine. The results indicate that blood pressure elevation due to the combined inotropic action of alpha 1- and beta-adrenoceptor agonists is a critical factor in the genesis of thiopental-epinephrine arrhythmias.

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