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The hemodynamic effects of sulfinpyrazone were investigated in 12 anesthetized dogs. Bolus injections into a coronary artery (1--500 mg) and a femoral artery (10--300 mg) and intravenous infusions (10 and 20 mg/min up to 500 mg) were given. After intracoronary injection, coronary dilatation occurred for over 20 min without major changes in cardiac muscle function. Femoral vasodilatation was also induced by local injection. Slow intravenous infusion resulted in inconsistent changes of coronary blood flow. However, in one instance, coronary dilatation was observed at a plasma level of 27.8 microgram/ml, which is comparable with that reached in man after standard oral dosage. Thus, sulfinpyrazone has coronary vasodilator effects which may have relevance to patient therapy.

This paper describes a method for determining whether beta-blocking agents reduce myocardial oxygen consumption by a direct action on the myocardium in addition to that reduction produced by changes in cardiac mechanical function. Measurements of myocardial oxygen consumption were made in anaesthetized dogs . Changes in heart rate were produced by atropine and by ventricular pacing. Alterations in ventricular loading were achieved by balloon inflations in the descending aorta and by infusions of nitroprusside and dextran. Measurements under these conditions were repeated after beta-blockade. Analysis required the separation of the part of reduced myocardial oxygen consumption resulting from the mechanical effects of beta-blockade from any possible additional direct effect on the myocardium. There was no evidence for a significant direct effect. The average overall reduction in myocardial oxygen consumption after beta-blockade was 18% but the estimated reduction not accountable to mechanical effects was only 2% (range, 95% probability, -7% to 3%).

Measurements have been made of pressure and blood velocity in venae cavae and aorta in a patient with severe cardiac tamponade in whom there was pulsus paradoxus. The characteristic pressure changes of pulsus paradoxus were associated with variations in peak blood velocity in the ascending aorta and stroke output. Maximum filling of the right side of the heart occurred during inspiration, and was associated in time with minimum left ventricular stroke volume. These findings point to competition for space by the ventricles in the distended pericardial sac as being the major factor in the production of pulsus paradoxus.