Velocity of contraction as a determinant of myocardial oxygen consumption.

SONNENBLICK, EDMUND H., JOHN Ross, JR., JAMES W. COVELL, GERARD A. KAISER, AND EUGENE BRAUNWALD. Velocity of contraction US a determinant of rnyocardial oxygen consumption. Am, J, Physiol. 2og(5) : 919-927. Ig65.-In 12 dogs on rightheart bypass with heart rate, stroke volume, and aortic pressure constant, the velocity of contraction was augmented comparably by three fundamentally distinct interventions in the same heart: I) sustained postextrasystolic potentiation produced by paired, electrical stimulation; 2) norepinephrine infusion; and 3) calcium infusion. In each instance the correlation between velocity of contraction and Mqoz was striking. During paired stimulation, maximum rate of left ventricular ejection increased by an average of 50.3 y. AZ 3.8a/, (SE of mean) above control, Mvoz .increased by I .g6 & o. IO ml/r oo g per min (39.8 y0 rt I .6 y0 above control), while the tension-time index (TTI) fell I 2.4% & I. I %. With norepinephrine, and with calcium, left ventricular ejection rates were increased 52.9 A 3.2 y0 and 55.1 ZIZ 3.2 %, respectively, and Mvoz was augmented 2.03 A 0.08 ml/roe g per min and I .87 + 0.04 ml/100 g per min, while the TTI decreased 15.9 + 0.6 y0 and 12.4 =t 2.4%. Since Mvog always increased substantially while TTI fell, tension cannot be considered to be the sole determinant of MGoz. Since comparable increases in velocity of contraction produced by different interventions were associated with similar large augmentations of MVoz, it appears that the velocity of contraction is an important determinant of Mvoz. Furthermore, it is likely that the so-called 02 wasting effect exerted by norepinephrine on myocardial metabolism may be explained largely by an increased velocity of contraction.