CELLULAR-RESPONSE TO REPERFUSED OXYGEN IN THE POSTISCHEMIC MYOCARDIUM

Perfused rat heart experiments focused on determining the critical O-2 level in postischemic myocardium. After a 20-min global ischemia, rep erfusion began with O-2-saturated saline buffer reflowing at different rates (0.5-12 ml/min). The H-1 nuclear magnetic resonance (NMR) signa l of the Val Ell myoglobin (Mb) gave an index of the intracellular oxy genation, whereas the P-31-NMR spectra reflected the high-energy phosp hate and pH status. At the same time, physiological monitors recorded both contractile function and O-2 consumption. Biochemical analysis de termined the lactate concentration. Within 6-12 min of reperfusion, th e O-2 reached a new steady state, which depended directly on the flow rate. Below 12 ml/min reflow, the postischemic O-2 level was consisten tly lower than the corresponding control values. Phosphocreatine, P-i, pH, myocardial O-2 consumption, and lactate formation rate exhibited a similar linear relationship with MbO(2) saturation in both the contr ol and postischemic myocardium. It appears that neither the cellular e nergy production nor the steep intracellular O-2 gradient has changed substantially in the postischemic myocardium.