Nitrite oxidation of myoglobin in perfused myocardium: implication
for energy coupling in respiration.
Chung, Youngran, Dejun Xu, and Thomas Jue.
Biological Chemistry Department, University of California Davis,
Davis, CA 95616-8635
APStracts 3:0127H, 1996.
Nitrite oxidation of oxymyoglobin in perfused rat myocardium under
non-limiting oxygen produces a detectable 1H NMR metMb signal at -3.9
ppm. When the myocardium is perfused with < 10 mM nitrite, the
1H NMR MbO2 ( CH3 Val E11 signal does not change intensity, and the
metMb reporter signal at -3.9 ppm is undetectable. However the rate
pressure product (RPP) decreases 26% from the control level. PCr,
MVO2, Pi, ATP, and pH remain constant. With > 10 mM infused
nitrite, Mb oxidation becomes apparent. As the MbO2 ( CH3 Val E11
signal intensity decreases, the metMb signal intensity at -3.9 ppm
increases. At the same time the 31P high energy phosphate signals,
RPP, and lactate formation exhibit significant alterations. MVO2,
however, remains constant. The data indicate that Mb oxidation does
not limit myocardial respiration, but does reduce energy production.
Pulse-recovery experiments further demonstrate that a transient
perfusion with 2 mM infused nitrite depresses the contractile
function, which does not recover during reperfusion with oxygenated,
nitrite free buffer. The findings support the view that either Mb
mediates energy coupling or nitrite directly uncouples energy
production in myocardium. They also reveal a glimpse of the
intracellular reductase activity that maintains the Mb in the Fe (II)
state.
Received 2 June 1995; accepted in final form 14 March 1996.
APS Manuscript Number H510-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 1 April 96