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.