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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.

Vesicles in a highly enriched sarcolemma preparation from canine ventricle were found to develop membrane potentials in response to outwardly directed potassium and inwardly directed sodium concentration gradients. The magnitude of the potential measured by the fluorescent dye diS-C3-(5) suggested a sodium-to-potassium permeability ratio between 0.2 and 1.0 which is one to two orders of magnitude greater than values obtained for the myocardial cell. Radiotracer techniques were employed to evaluate the permeability coefficients of the isolated cardiac sarcolemma membrane for sodium and potassium under equilibrium conditions (i.e., equal salt concentrations in the intravesicular and extravesicular spaces). The uptake of sodium and potassium was best described by two exponential processes which followed an increment of uptake that occurred prior to the earliest assay time (i.e., 17 sec). The compartment sizes were linear, nonsaturable functions of the cation activity. Evaluation of the rate coefficients of cation uptake by the two exponential processes versus cation activity revealed that sodium influx via the slow process and potassium influx via the fast process varied linearly with cation activity, suggesting that the permeability coefficients were concentration independent for these compartments. Conversely, sodium influx via the fast process exhibited a nonlinear increase with increasing sodium activity, and potassium influx via the slow process appeared to saturate with increasing potassium activity. In general, the permeabilities of the sarcolemma-enriched preparation for sodium and potassium were of equal magnitude. The permeability coefficients were lower than that for the potassium coefficient reported for cardiac cells but are in the range of that reported for sodium.