Oxygen utilization during isovolumic pressure-volume loading: effects of prolonged extracorporeal circulation and cardioplegic arrest.

In canine hearts supported by cardiopulmonary bypass, isovolumic peak developed pressure (PDP, mm Hg) and myocardial oxygen consumption (MVO2, ml O2 X 10(-2)/beat/100 gm left ventricular [LV] weight) were determined at 5-ml increments of LV balloon inflation before and after either 2 hours of potassium cardioplegic arrest (ischemia, N = 7) or a comparable period of normothermic perfusion without ischemia (control, N = 6). The sensitivity of MVO2 as a marker of ischemic injury was compared with preservation of both adenosine triphosphate (ATP) stores and systolic pump function. Over a physiological range of end-diastolic volumes (5 to 35 ml) and end-diastolic pressures (0 to 18 mm Hg), the Frank-Starling curves were not depressed following both cardioplegic arrest and prolonged nonischemic perfusion. Although ATP stores decreased by 26% and 22% (ischemia and control groups, respectively; not significant), these levels did not distinguish the effects of cardioplegic arrest from prolonged perfusion. At the preinterventional measurement in both groups, PDP between 50 and 200 correlated with MVO2 from 3.0 to 10.0 (r = +0.84). Following cardioplegic arrest, postischemic MVO2 increased 137 +/- 6% when measured over the PDP range of 75 to 200 mm Hg (p less than 0.01). This change was not evident at a PDP of less than 75, in the empty beating heart, or in control hearts subjected to nonischemic extracorporeal perfusion. These data suggest that increased utilization of oxygen to develop physiological pressures may be a more sensitive indicator of ischemic injury than shifts in the pressure-volume relationship or depletion of adenine nucleotide stores.