The Annals of Thoracic Surgery, Vol 41, 407-412, Copyright © 1986 by The Society of Thoracic Surgeons
Oxygen utilization during isovolumic pressure-volume loading: effects of prolonged extracorporeal circulation and cardioplegic arrest
I Krukenkamp, N Silverman, D Sorlie, A Pridjian, H Feinberg and S Levitsky
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.
