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Departments of Medicine and Radiology and Center for Magnetic Resonance Research, University of Minnesota Health Sciences Center and Minneapolis Veterans Affairs Medical Center, Minneapolis, Minnesota 55455
This study was performed to determine
the myocyte PO2 required to sustain normal
high-energy phosphate (HEP) levels in the in vivo heart. In 10 normal
dogs, myocyte PO2 values were calculated from
the myocardial deoxymyoglobin resonance (Mb-
) intensity determined
with 1H-NMR spectroscopy during sequential flow reductions
produced by a hydraulic occluder that decreased coronary perfusion
pressure to ~60, 50, and 40 mmHg and, finally, during total
occlusion. Myocardial blood flow was measured with microspheres, and
HEP levels were determined with 31P magnetic resonance
spectroscopy. During control conditions, Mb-
was undetectable.
Myocardial blood flow was 1.11 ± 0.06 ml · min
1 · g
1 during basal
conditions and decreased with sequential graded occlusions to 0.78 ± 0.05, 0.58 ± 0.03, and 0.38 ± 0.04 ml · min
1 · g
1,
respectively; blood flow during total occlusion was 0.07 ± 0.02 ml · min
1 · g
1. Reductions
of blood flow caused progressive increases of Mb-
, which were
associated with decreases of phosphocreatine (PCr), ATP, and the
PCr-to-ATP ratio, as well as progressive increases of the
Pi-to-PCr ratio. There was a strong linear correlation between normalized blood flow and Mb-
(R2 = 0.89, P < 0.01).
Reductions of HEP and PO2 were also highly correlated (although nonlinearly); with the assumption that myoglobin was 90% saturated with O2 during basal conditions and 5%
saturated during total coronary occlusion, the intracellular
PO2 values for 20% reductions of PCr and ATP
were ~4.4 and ~0.9 mmHg, respectively. The data indicate that
O2 availability plays an increasing role in regulation of
oxidative phosphorylation when mean intracellular PO2 values fall below 5 mmHg in the in vivo heart.
myocardium; blood flow; myoglobin oxygen saturation; ischemia
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