Electrophysiological and antiarrhythmic effects of propranolol in canine acute myocardial ischemia

To correlate the antiarrhythmic and electrophysiological effects of propranolol in acute myocardial ischemia, the authors examined the effects of temporary (15 minute) ligations of the left anterior descending coronary artery in studies on 15 dogs. The authors recorded bipolar electrograms and monophasic action potentials from the ischemic and normal zones and measured the intervals from the onset of QRS in a standard electrocardiogram lead to the major deflection of electrograms recorded from the ischemic and normal zones. They also determined monophasic action potential duration (APD) and effective refractory period (ERP). Data for control ligations were compared to those during which propranolol, 40 μg/kg, was administered intravenously immediately after ligation. Propranolol reduced the mean number of ventricular beats per minute (from 15 to 6) (P <0.01). Propranolol slowed conduction in the ischemic zone (by 10 msec at peak effect, P <0.01) and had no or only a very slight effect (by 1 msec at 15 minutes, P <0.05) on conduction in the normal zone. Propranolol also prolonged APD in the ischemic (32 msec) and normal (14 msec) zones (P <0.01), prolonged ERP in the ischemic (41 msec) and normal (20 msec) zones (P <0.01), and reduced the APD/ERP ratio in the ischemic (1.62 to 1.47) (P <0.01) and normal (1.62 to 1.55) (P <0.05) zones. During the control ligation, APD in the ischemic zone was 25 msec shorter than in the normal zone (P <0.01), but with propranolol the difference was not significant. The effects of propranolol in slowing conduction in the ischemic zone, in prolonging refractoriness, in reducing APD/ERP, and in reducing the disparity in APD between ischemic and normal zones may explain its demonstrated antiarrhythmic effects in acute myocardial ischemia.