Improvement of myocardial oxygenation is a major goal in the treatment of ischaemic heart disease. Propranolol, 0-1 mg/kg intravenously, was administered to 20 patients with acute myocardial infarction without clinical evidence of left ventricular failure. The most important haemodynamic response was a substantial decrease in myocardial contractility. This was reflected by a fall in cardiac index (average of 0-4 l/min/M2, P less than 0-001) and of arterial mean pressure (average of 16 mmHg, P less than 0-001) with little change in systemic vascular resistance. Heart rate, not strikingly increased at the control state in the majority of patients, decreased an average of 7 beats/minute (P less than 0-001). Pulmonary wedge pressure varied; it decreased in 6 patients with high values (greater than 15 mmHg) prior to propranolol. These changes in wedge pressure in the presence of decreased contractility are probably related to improved left ventricular compliance, produced by propranolol. Propranolol markedly improved myocardial metabolism. Arterial-coronary sinus oxygen difference decreased an average of 0-72 ml/100 ml (P less than 0-001). Myocardial lactate production shifted to extraction (average of -8% to 14%) or the rate of lactate extraction increased (average of 20% to 29%). Coronary blood flow decreased an average of 13 ml/100 g/min (P less than 0-001). The finding, that myocardial metabolism improved, suggests that decrease in coronary blood flow was mediated by reduced myocardial oxygen requirements. None of the 20 patients developed left ventricular failure or other complications related to beta-adrenergic blockade. Severe chest pain, unresponsive to conventional therapy in four patients, was relieved by propranolol. These findings demonstrate that acutely administered propranolol improves myocardila oxygenation in patients with uncomplicated acute infarction without endangering perfusion of other vital organs.