THE PHOSPHOCREATINE OVERSHOOT OCCURS INDEPENDENT OF MYOCARDIAL WORK

Although the exact mechanism(s) responsible for the phosphocreatine/AT P overshoot have not been completely elucidated, our data demonstrate that the overshoot does not stem from reduced myocardial work, and con sequently, reduced utilization of phosphocreatine (PCr). Additionally, we highlight a basic difference in the physiologic responses of skele tal and cardial muscle to work demands. By understanding the bioenerge tic derangements which accompany reperfusion injury, one may hope to b etter salvage post-ischemic myocardium.