Electrophysiologic effects of prazosin during acute myocardial ischemia

Prazosin, 100 micrograms/kg, had no effect on baseline refractoriness or intraventricular conduction in anesthetized dogs. During 1 h of coronary artery occlusion followed by reperfusion, prazosin significantly blunted the shortening of the ventricular effective refractory periods within ischemic myocardial region relative to vehicle-treated animals. Prazosin treatment also prevented the delayed conduction of paced ventricular complexes entering and exiting the ischemic zone. These effects may be associated with the blockade of alpha 1-adrenoceptor activation during the acute phase of myocardial ischemia.