Positive inotropic agents (epinephrine or calcium) increased ventricular oxygen consumption primarily by increasing energy utilization associated with excitation-contraction coupling.
Do positive inotropic agents (epinephrine or calcium) alter the relationship between oxygen consumption and systolic pressure-volume area in canine left ventricles?
In canine hearts, positive inotropes increase oxygen consumption primarily through increased energy utilization for excitation-contraction coupling, rather than altering mechanical efficiency.
We analyzed the effect of positive inotropic agents on the relation between left ventricular oxygen consumption and the systolic pressure-volume area. Pressure-volume area is a measure of total mechanical energy for ventricular contraction, and is a specific area in the ventricular pressure-volume diagram circumscribed by the end-systolic and end-diastolic pressure-volume relation curves and the systolic segment of the pressure-volume trajectory. Either epinephrine (1 microgram/kg per min, iv) or calcium ion (0.03 mEq/kg per min, iv) was administered to canine excised cross-circulated hearts. These agents increased an index of ventricular contractility, Emax, or the slope of the end-systolic pressure-volume line, by 70%. The regression lines of ventricular oxygen consumption on pressure-volume area in control and in enhanced contractile states were of the same formula: ventricular oxygen consumption (ml O2/beat per 100 g) equals A times pressure-volume area (mm Hg ml/beat per 100 g) plus a constant B. Coefficient A remained unchanged at 1.8 X 10(-5) ml oxygen/(mm Hg ml), but constant B increased from 0.03 ml oxygen/beat per 100 g by more than 50% with either agent. The reciprocal of A reflects the energy conversion efficiency for the total mechanical energy, and this efficiency remained near 36%. The increase in B was equal to the directly measured increment in ventricular oxygen consumption for mechanically unloaded contraction. The basal metabolism remained unchanged. We conclude that the augmented oxygen consumption under the acutely enhanced contractile state with either epinephrine or calcium was caused primarily by an increased energy utilization associated with the excitation-contraction coupling.
Suga et al. (1983) studied Ventricular contractility. Epinephrine or calcium ion vs. Control was evaluated on Relation between left ventricular oxygen consumption and the systolic pressure-volume area. Positive inotropic agents (epinephrine or calcium) increased ventricular oxygen consumption primarily by increasing energy utilization associated with excitation-contraction coupling.