Critical intracellular O₂ in myocardium as determined by ¹H nuclear magnetic resonance signal of myoglobin

The ¹H nuclear magnetic resonance (NMR) signal of tissue myoglobin has provided an opportunity to determine the critical O₂ 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, O₂ consumption and the ³¹P-NMR signal of phosphocreatine level remain relatively constant until the cellular PO₂ reaches 2 mmHg. The ATP signal intensity dips only when cellular O₂ reaches 0.8 mmHg, while pH remains unchanged at 7.2. The sequential nature of the cellular response to limiting O₂, 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 O₂ gradient from capillary to cell is larger than that from cytosol to mitochondria.