Myocardial Oxygen Consumption After Reversible Ischemia

There is a marked dissociation between return of contractile function and oxidative metabolism in stunned myocardium. Initial observations in isovolumically contracting hearts demonstrated that postischemically, the MVO2 to generate a given peak-developed pressure was augmented compared to preischemia. This metabolic inefficiency was independent of coronary hyperemia and myocellular oxygen extraction and not evident in the vented, empty beating state. In an ejecting heart model, the highly linear relationship between external mechanical work (integrated area of dynamic pressure-volume loops) increased non-working oxygen needs not to the efficiency of ejecting a given stroke volume. More sophisticated mathematical modeling to further compartmentalize chemomechanical transduction in the globally stunned heart has confirmed deranged energetics, but ascribing specific work components to inefficient oxygen need is predicated on the biological validity of each model. The findings in regionally stunned myocardium are more uniform, demonstrating paradoxically normal oxygen consumption despite persistent systolic bulging or markedly decreased systolic shortening. The relatively increased MVO2 in stunned hearts is not due to uncoupling of oxidative phosphorylation, but inefficient cellular ATP utilization.