In seven dogs with long-standing left ventricular dysfunction induced 16 weeks earlier by repetitive transmyocardial direct current (DC) shock, the acute hemodynamic effect of the α1-adrenoceptor antagonist urapidil was studied. Left ventricular end-diastolic pressure (LVEDP) was significantly increased from preshock levels at the time of study and cardiac output was reduced. Plasma norepinephrine was significantly increased from control levels and was not altered by urapidil infusion. The mean arterial pressure fell in response to α1-blockade from 111 to 85 mm Hg, the LVEDP fell from 16 to 9 mm Hg, and cardiac output increased from 2.90 to 3.70 L/min (all p < 0.01). Regional blood flows measured by microsphere injection revealed an increase in blood flow to skeletal muscle, which had not been significantly decreased by the left ventricular dysfunction in this model, and further decreases in splanchnic flow, which was already depressed compared with that in normal dogs. Therefore acute α-adrenoceptor blockade improves central hemodynamics in experimental heart failure but does not normalize the resting blood flow maldistribution in this model.