1. The effect of adenosine on left ventricular contractility and developed tension was studied in the anaesthetized intact dog. Normal and propranolol-treated animals were used. Adenosine was infused through a catheter into one of the two main branches of the left coronary artery, usually the circumflex branch. The rate of infusion was 150 x 10(-9)M/min. The infusion was maintained during 50 min.2. In both series of animals, no change was observed in the heart rate, aortic pressure, left ventricular end-diastolic pressure, time from onset of left ventricular contraction to peak dP/dt, peak dP/dt and left ventricular tension-time index. It is concluded that a regional increase in adenosine concentration in the left ventricular wall has no inotropic effect when the adrenergic mechanisms are normal or depressed.3. The myocardial blood flow response to adenosine was determined at the 10th, 30th and 50th min of the infusion by the radioactive inert gas method. At the 10th min of the infusion, the myocardial blood flow averaged three times the control value in both series of dogs. Thereafter, the flow response remained stable in the normal dogs but declined at the 50th min of the infusion in the propranolol-treated animals. It is suggested that autoregulation of the coronary circulation in response to overperfusion of the myocardium at constant cardiac work may be enhanced at the lower myocardial oxygen requirements of the propranolol-treated dogs while, in the normal animals, it was insufficient to overcome the potent coronary dilator action of adenosine.

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In closed-chest anaesthetized dogs, aminophylline was infused into the left circumflex coronary artery at a rate of 250 mug/min. When the heart rate was lower than 100 beats/min, infusion did not modify the left circumflex coronary blood flow and resistance. When the heart rate was elevated to an average of 153 +/- 6 beats/min by right atrial pacing, infusion inhibited the increase in left circumflex coronary blood flow and decrease in coronary resistance. The pacing-induced increment in coronary blood flow was reduced by an average of 64% and the flow deficit was associated with a lowering of the coronary sinus blood oxygen tension. Since aminophylline is known to inhibit the coronary dilator action of exogenous adenosine, the results support the concept that adenosine resulting from the breakdown of adenine nucleotides is a mediator of the metabolic regulation of coronary blood flow.