Yr. Chung et T. Jue, CELLULAR-RESPONSE TO REPERFUSED OXYGEN IN THE POSTISCHEMIC MYOCARDIUM, American journal of physiology. Heart and circulatory physiology, 40(2), 1996, pp. 687-695
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.