Yr. Chung et al., NITRITE OXIDATION OF MYOGLOBIN IN PERFUSED MYOCARDIUM - IMPLICATIONS FOR ENERGY COUPLING IN RESPIRATION, American journal of physiology. Heart and circulatory physiology, 40(3), 1996, pp. 1166-1173
Nitrite oxidation of oxymyoglobin in perfused rat myocardium under non
limiting oxygen produces a detectable H-1 nuclear magnetic resonance m
etmyoglobin (metMb) signal at -3.9 ppm. When the myocardium is perfuse
d with <10 mM nitrite, the H-1 nuclear magnetic resonance MbO(2) gamma
CH3 Val E11 signal does not change intensity and the metMb reporter s
ignal at -3.9 ppm is undetectable. However the rate pressure product d
ecreases by 26% from the control level. Phosphocreatine, myocardial ox
ygen consumption, P-i, ATP, and pH remain constant. With >10 mM infuse
d nitrite, myoglobin (Mb) oxidation becomes apparent. As the MbO(2) ga
mma CH3 Val E11 signal intensity decreases, the metMb signal intensity
at -3.9 ppm increases. At the same time the P-31 high-energy phosphat
e signals, rate pressure product, and lactate formation exhibit signif
icant alterations. Myocardial oxygen consumption, however, remains con
stant. The data indicate that Mb oxidation does not limit myocardial r
espiration but does reduce energy production. Pulse-recovery experimen
ts further demonstrate that a transient perfusion with 2 mM infused ni
trite depresses the contractile function, which does not recover durin
g reperfusion with oxygenated, nitrite-free buffer. The findings suppo
rt the view that either Mb mediates energy coupling or nitrite directl
y uncouples energy production in myocardium. They also reveal a glimps
e of the intracellular reductase activity that maintains the Mb in the
Fe (II) state.