Myocardial oxygenation and high-energy phosphate levels during graded coronary hypoperfusion

This study was performed to determine the myocyte PO2 required to sustain n ormal high-energy phosphate (HEP) levels in the in vivo heart. In 10 normal dogs, myocyte PO2 values were calculated from the myocardial deoxymyoglobi n resonance (Mb-delta) intensity determined with H-1-NMR spectroscopy durin g sequential flow reductions produced by a hydraulic occluder that decrease d coronary perfusion pressure to similar to 60, 50, and 40 mmHg and, finall y, during total occlusion. Myocardial blood flow was measured with microsph eres, and HEP levels were determined with P-31 magnetic resonance spectrosc opy. During control conditions, Mb-delta was undetectable. Myocardial blood flow was 1.11 +/- 0.06 ml.min(-1).g(-1) during basal conditions and decrea sed 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 occlu sion was 0.07 +/- 0.02 ml.min(-1).g(-1). Reductions of blood flow caused pr ogressive increases of Mb-delta, which were associated with decreases of ph osphocreatine (PCr), ATP, and the PCr-to-ATP ratio, as well as progressive increases of the P-i-to-PCr ratio. There was a strong linear correlation be tween normalized blood flow and Mb-delta (R-2 = 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 O-2 during basal conditio ns and 5% saturated during total coronary occlusion, the intracellular PO2 values for 20% reductions of PCr and ATP were <similar to>4.4 and similar t o0.9 mmHg, respectively. The data indicate that O-2 availability plays an i ncreasing role in regulation of oxidative phosphorylation when mean intrace llular PO2 values fall below 5 mmHg in the in vivo heart.