The study demonstrates that the apparent failure of dichloroisoproterenol to block adrenaline-induced bigeminy is a result of its intrinsic sympathomimetic activity coupled with adrenaline-induced blood pressure elevation.
DCI's ISA may confound early beta-blocker arrhythmia studies; leaves open whether ISA-free agents better suppress catecholamine-induced bigeminy.
We reported previously that in cyclopropane-anesthetized dogs dichloroisoproterenol (DCI) sometimes fails to block adrenaline-induced bigeminal cardiac rhythm although it always prevents ventricular fibrillation. The present experiments demonstrated that in animals in which a large dose of DCI did not increase the adrenaline threshold for bigeminy, previously ineffective mechanical elevation of the blood pressure induced bigeminy. Neither methoxamine nor DCI alone caused bigeminal rhythm, but their combination effectively induced bigeminy of long duration. These results are interpreted to indicate that apparent failure of DCI to block adrenaline-induced bigeminy is not due to inability to antagonize this cardiac action, but is due to a combination of the intrinsic cardiac sympathomimetic activity of DCI with an increase in blood pressure induced by the subsequent injection of adrenaline.
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Sutter et al. (1961) studied this question.
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