Oxygen delivery does not limit cardiac performance during high work states

This study tested the hypothesis that the loss of myocardial high-energy ph osphates (HEP), which occurs during high cardiac work states [J. Zhang, D. J. Duncker, Y. Xu, Y. Zhang, G. Path, H. Merkle, K. Hendrich, A. H. L. From , R. Bache, and K. Ugurbil. Am. J. Physiol. 268: (Heart Circ. Physiol. 37): H1891-H1905, 1995], is not the result of insufficient intracellular O-2 av ailability. To evaluate the state of myocardial oxygenation, the proximal h istidine signal of deoxymyoglobin (Mb-delta) was determined with H-1 nuclea r magnetic resonance spectroscopy (MRS), whereas HEP were examined with P-3 1 MRS. Normal dogs (n = 11) were studied under basal conditions and during combined infusion of dobutamine and dopamine (20 mu g.kg(-1).min(-1) iv eac h), which increased rate-pressure products to >50,000 mmHg.beats.min(-1). C reatine phosphate (CP) was expressed as CP/ATP, and myocardial myoglobin de saturation was normalized to the Mb-delta resonance present during total co ronary artery occlusion. This Mb-delta resonance appeared at 71 parts per m illion downfield from the water resonance. CP/ATP decreased from 2.22 +/- 0 .12 during the basal state to 1.83 +/- 0.09 during the high work state (P < 0.01), whereas Delta P-i/CP increased from 0 to 0.21 +/- 0.04 (P < 0.01). Despite these HEP changes, Mb-delta remained undetectable. In contrast, whe n a coronary stenosis was applied to produce a similar decrease in CP/ATP, Mb-delta reached 0.38 +/- 0.10 of the value present during total coronary o cclusion. These data demonstrate that Mb-6 is readily detected in vivo duri ng limitation of coronary blood flow sufficient to cause a decrease of myoc ardial CP/ATP. However, similar HEP changes that occur at high work states in the absence of coronary occlusion are not associated with a detectable M b-delta resonance. The findings support the hypothesis that the myocardial HEP changes observed at high work states are not due to inadequate O-2 avai lability to the mitochondria and emphasize the limitations of interpreting HEP alterations in the absence of knowing the level of myocyte oxygenation.