Upgrading acellular to sanguineous cardioplegic efficacy

To determine which biochemical entity of the red cell is responsible for preventing augmented postischemic myocardial oxygen consumption (MVO2), 28 canine hearts instrumented with ultrasonic dimension crystals underwent simultaneous determination of stroke work (SW) and MVO2 during incremental volume loading on right heart bypass before and 30 min after 2 hr of 10 degrees C cardioplegic arrest with unmodified oxygenated crystalloid cardioplegia (OC), OC with histidine of equal buffering capacity as 18% hematocrit blood (OC + H), or OC with 200 units/ml of superoxide dismutase and catalase (OC + SOD/C). In all groups, the slope of the linear SW vs end-diastolic volume relationship, Mw, and the slope of the linear SW vs MVO2 relationship, Me, were unchanged after cardioplegic arrest. The intercept of the SW vs MVO2 relationship, Eo, was augmented an average of 22.2% in the OC group, but both OC + H and OC + SOD/C prevented this subtle expression of ischemic injury. The characteristic of the red cell most likely responsible for the myoprotective efficacy of blood cardioplegia is buffering capacity; however, since the effects of tissue acidosis are partially mediated by free radicals, the use of free radical scavengers can also ameliorate ischemic damage incurred during cardioplegic arrest.