ABSTRACT
During normal heart function, the mitochondrial adenosine triphosphate synthase makes approximately 95% of all of the adenosine triphosphate consumed by the organ; the remaining relatively small amount of adenosine triphosphate is made by aerobic glycolysis. In sharp contrast to the situation in normally perfused myocardium, in totally ischemic quiescent heart muscle, the mitochondrial adenosine triphosphate synthase not only ceases to make adenosine triphosphate, but is thermodynamically poised to go in the reverse direction. Species that exhibit the ischemia-induced inhibition of the mitochondrial ATPase have conscious heart rates of approximately 200 beats per minute or less and contain predominantly the slow isoform of the myosin ATPase. Lactate accumulation in ischemic dog heart, a slow heart-rate heart, is relatively gradual and essentially linear for at least the first 80 min of zero-flow ischemia in canine myocardium and is essentially unaffected by oligomycin pretreatment.
