Key result
L-propranolol prolongs AV nodal refractoriness and sinus node recovery in dogs, distinguishing it from quinidine.
Why the study?
The electrophysiological effects of quinidine and propranolol isomers need differentiation between beta-blockade and membrane-stabilizing effects.
Do quinidine and propranolol isomers have different electrophysiological effects in anesthetized dogs?
Do quinidine and propranolol isomers have different electrophysiological effects in anesthetized dogs?
Answers are grounded in this paper and cite their sources.
The electrophysiological effects of propranolol isomers are related to beta-blockade and differ significantly from the membrane-stabilizing effects of quinidine.
Electrophysiological properties of quinidine and the two isomers of propranolol were compared in pentobarbital-anesthetized dogs using His bundle recordings and programmed stimulation in order to differentiate the effects resulting from beta-blockade from those related to nonspecific membrane-stabilizing effects. Quinidine in the plasma concentration range of 2.7-20 microM/liter resulted in concentration-dependent increases in atrionodal and His-Purkinje system conduction times and in the atrial effective refractory period. Quinidine did not produce any significant concentration-dependent change in atrioventricular (AV) nodal and ventricular refractory periods, sinus node automaticity, or QTc interval duration. Propranolol isomers in concentration range of 0.03-0.85 microM/liter produced a concentration-dependent increase in atrionodal conduction time but exerted no significant effect on His-Purkinje conduction time, QTc duration, or ventricular refractory period. Both isomers increased the atrial effective refractory period, but with slopes of concentration-response regression lines which were significantly different from those of quinidine. Only l-propranolol produced concentration-dependent increases in AV nodal refractory period, Wenckebach cycle length, and sinus node recovery time. These results suggest that the electrophysiological effects of propranolol isomers are related to beta-blockade and are significantly different from those resulting from the membrane-stabilizing effect of quinidine.
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Jaillon et al. (1981) studied this question. Quinidine and propranolol isomers was evaluated on Electrophysiological properties including atrionodal and His-Purkinje conduction times and refractory periods. In anesthetized dogs, l-propranolol produced concentration-dependent increases in AV nodal refractory period and sinus node recovery time, distinguishing its beta-blocking effects from quinidine.
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