Myocardial oxygen consumption: the role of wall force and shortening.
The relationship between the force in the left ventricular wall during systole and myocardial O2 consumption (MVO2) was determined. In addition, the relative influence of the load imposed during shortening and fiber shortening on MVO2 was assessed. For this purpose, 14 servo-regulated, paced, isolated canine hearts were used and the steady-state response in total coronary flow and arteriovenous oxygen difference was measured. For both the isovolumetrically beating and the ejecting ventricle, statistically significant linear relations were observed between MVO2 and the integral of systolic force. These relations were not significantly different from one another, indicating that shortening was not a determinant of MVO2. Moreover, when ejecting an isolumetric beats of equivalent developed force were compared, a difference in MVO2 (deltaMVO2) was found. deltaMVO2 was a function of the force integral difference between these contractions and not fiber shortening. Thus, under the conditions of this experiment, the integral of systolic force that includes developed force and shortening load is the predominant factor regulating MVO2 for any given contractile state, whereas the influence of fiber shortening is negligible.
D000818:Animals; D001794:Blood Pressure; D003331:Coronary Vessels; D004285:Dogs; D006352:Heart Ventricles; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism*; D010100:Oxygen / Q000097:blood; D010101:Oxygen Consumption; D010477:Perfusion; D011312:Pressure
D010100:Oxygen