Abstract
We have been studying the long-standing problem of how contractile state affects myocardial oxygen consumption (VO2), using the new concept that the total mechanical energy generated by contraction can be quantified by the systolic pressure-volume (P-V) area (PVA). PVA is the specific area in a P-V diagram under the end-systolic P-V relation and the systolic P-V trajectory. Experimental data in dog hearts show that PVA correlates linearly and closely with PVA in a given contractile state whereas the VO2-PVA relation shifts upward in a parallel manner by positive inotropic agents including some new cardiotonic agents. The component of VO2 for PVA remains proportional to PVA whereas the component of VO2 for excitation-contraction coupling changes with contractile state in general. The effects of contractile state on various cardiac efficiencies are also discussed using the concept of PVA.
