Limitation of Myocardial Function by Reduced Coronary Blood Flow during Isoproterenol Action

Abstract

The interpolated decrease in heart force or isometric systolic tension that occurs during isoproterenol stimulation has been examined in terms of changes in coronary flow and myocardial metabolism. In 67 open-chest dogs under pentobarbital anesthesia, determinations were made of lactate, pyruvate, Po 2 and Pco 2 in arterial and coronary sinus blood; coronary flow was measured with an electromagnetic flow transducer and ventricular force with a strain gauge arch. Although the characteristic, uncomplicated effect of isoproterenol is a marked increase in coronary flow and contractile force, this is briefly interrupted by a sharp decrease in these functions, and the decrease is associated with evidence of anaerobic metabolism. This decrease is concomitant with decreased coronary perfusion pressure and is intensified by sustained infusion of isoproterenol or by lowered oxygen concentrations in the inspired air. The stage of depressed function is counteracted by mechanical maintenance of high aortic pressure or by slow, controlled heart rate. When uncontrolled, tachycardia due to isoproterenol continues without phasic interruption. The intermediate period of depressed function is interpreted in terms of sharply decreased oxygen delivery when both cardiac rate and force are increased. The hemodynamic and metabolic values for these acutely occurring, reversible extremes have been specified.