CRITICAL INTRACELLULAR O-2 IN MYOCARDIUM AS DETERMINED BY H-1 NUCLEAR-MAGNETIC-RESONANCE SIGNAL OF MYOGLOBIN

The H-1 nuclear magnetic resonance (NMR) signal of tissue myoglobin has provided an opportunity to determine the critical O-2 level in saline-perfused myocardium at room temperature. Above the intracellular PO2 of 4 mmHg, the myocardium exhibits no sign of hypoxia. At 4 mmHg, the rate pressure product (RPP) decreases, and the lactate formation rate, measured enzymatically, increases. However, O-2 consumption and the P-31-NMR signal of phosphocreatine level remain relatively constant until the cellular PO2 reaches 2 mmHg. The ATP signal intensity dips only when cellular O-2 reaches 0.8 mmHg, while pH remains unchanged at 7.2. The sequential nature of the cellular response to limiting O-2, starting with alterations in the lactate formation rate and RPP, indicates that NADH, rather than ADP, signals tissue hypoxia. Moreover, the study suggests that the O-2 gradient from capillary to cell is larger than that from cytosol to mitochondria.