Myocardial Oxygen Consumption in Acute Experimental Cardiac Depression
Myocardial oxygen consumption (MV·o2) during drug-induced cardiac depression was measured in 8 anesthetized, open chest dogs in which myocardial wall tension was controlled. The right side of the heart was bypassed and myocardial contractility was reduced with procaine HCl, propranolol, or pronethalol. MV·o2 consistently fell during cardiac depression (avg = 1.52 ml/min per 100 g left ventricle or - 11.6%). These reductions occurred despite small increases in developed tension. Changes in the tension-time index, contractile element work, and contractile element power did not correlate invariably with ΔMV·o2, while reductions in velocity of the contractile elements at isotension, maximum left ventricular dp/dt, and the extent of shortening of the contractile elements and circumferential fibers were associated in every experiment with the reductions in MV·o2. The finding that negative inotropic influences are associated with a reduction in myocardial energy utilization, when considered with earlier observations showing that positive inotropic influences induce an augmentation of MV·o2, provides evidence that the inotropic state and its mechanical correlates are coupled with myocardial energy utilization by a mechanism that is independent of tension development.
- Accepted June 8, 1967.
- © 1967 American Heart Association, Inc.