Oxygen delivery does not limit cardiac performance during high work states

This study tested the hypothesis that the loss of myocardial high- energy phosphates (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 O₂ availability. To evaluate the state of myocardial oxygenation, the proximal histidine signal of deoxymyoglobin (Mb-δ) was determined with ¹H nuclear magnetic resonance spectroscopy (MRS), whereas HEP were examined with ³¹P MRS. Normal dogs (n = 11) were studied under basal conditions and during combined infusion of dobutamine and dopamine (20 μg · kg^-1 · min^-1 iv each), which increased rate-pressure products to >50,000 mmHg · beats · min^-1. Creatine phosphate (CP) was expressed as CP/ATP, and myocardial myoglobin desaturation was normalized to the Mb-δ resonance present during total coronary artery occlusion. This Mb-δ resonance appeared at 71 parts per million 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 ΔP(i)/CP increased from 0 to 0.21 ± 0.04 (P < 0.01). Despite these HEP changes, Mb-δ remained undetectable. In contrast, when a coronary stenosis was applied to produce a similar decrease in CP/ATP, Mb-δ reached 0.38 ± 0.10 of the value present during total coronary occlusion. These data demonstrate that Mb-δ is readily detected in vivo during limitation of coronary blood flow sufficient to cause a decrease of myocardial CP/ATP. However, similar HEP changes that occur at high work states in the absence of coronary occlusion are not associated with a detectable Mb-δ resonance. The findings support the hypothesis that the myocardial HEP changes observed at high work states are not due to inadequate O₂ availability to the mitochondria and emphasize the limitations of interpreting HEP alterations in the absence of knowing the level of myocyte oxygenation.