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-δ) 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-δ 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-δ, which were associated with decreases of phosphocreatine (PCr), ATP, and the PCr-to-ATP ratio, as well as progressive ir creases of the Pi-to-PCr ratio. There was a strong linear correlation between normalized blood flow and Mb-δ (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% salurated 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 availabiliy plays an increasing role in regulation of oxidative phosphorylation when mean intracellular Po2 values fall below 5 mmHg in the in vive heart.
|Original language||English (US)|
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|Issue number||1 49-1|
|State||Published - 2001|
- Blood flow
- Myoglobin oxygen saturation