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urbil, andDepartments of Medicine, Biochemistry, Radiology, and the Center for Magnetic Resonance Research, University of Minnesota Health Sciences Center, Minneapolis 55455; and Department of Veterans Affairs Medical Center, Minneapolis, Minnesota 55417
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. U
urbil. 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-
) 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-
resonance present during total coronary artery occlusion. This Mb-
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
Pi/CP increased from 0 to 0.21 ± 0.04 (P < 0.01). Despite these HEP changes, Mb-
remained undetectable. In
contrast, when a coronary stenosis was applied to produce a similar
decrease in CP/ATP, Mb-
reached 0.38 ± 0.10 of the value present
during total coronary occlusion. These data demonstrate that Mb-
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-
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.
deoxymyoglobin; high-energy phosphates; intense catecholamine stimulation; myocardium
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