U. Kreutzer et T. Jue, CRITICAL INTRACELLULAR O-2 IN MYOCARDIUM AS DETERMINED BY H-1 NUCLEAR-MAGNETIC-RESONANCE SIGNAL OF MYOGLOBIN, American journal of physiology. Heart and circulatory physiology, 37(4), 1995, pp. 1675-1681
The H-1 nuclear magnetic resonance (NMR) signal of tissue myoglobin ha
s provided an opportunity to determine the critical O-2 level in salin
e-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 un
til the cellular PO2 reaches 2 mmHg. The ATP signal intensity dips onl
y 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, sta
rting with alterations in the lactate formation rate and RPP, indicate
s that NADH, rather than ADP, signals tissue hypoxia. Moreover, the st
udy suggests that the O-2 gradient from capillary to cell is larger th
an that from cytosol to mitochondria.