Abstract
Nitrite oxidation of oxymyoglobin in perfused rat myocardium under nonlimiting oxygen produces a detectable 1H nuclear magnetic resonance metmyoglobin (metMb) signal at -3.9 ppm. When the myocardium is perfused with <10 mM nitrite, the 1H nuclear magnetic resonance MbO2 γ CH3 Val E11 signal does not change intensity and the metMb reporter signal at -3.9 ppm is undetectable. However the rate pressure product decreases by 26% from the control level. Phosphocreatine, myocardial oxygen consumption, Pi, ATP, and pH remain constant. With >10 mM infused nitrite, myoglobin (Mb) oxidation becomes apparent. As the MbO2 γ 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, rate pressure product, and lactate formation exhibit significant alterations. Myocardial oxygen consumption, 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.
| Original language | English (US) |
|---|---|
| Journal | American Journal of Physiology - Heart and Circulatory Physiology |
| Volume | 40 |
| Issue number | 3 |
| State | Published - Sep 1996 |
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Keywords
- Bioenergetics
- Nuclear magnetic resonance
- Oxidative phosphorylation
ASJC Scopus subject areas
- Physiology
Cite this
Nitrite oxidation of myoglobin in perfused myocardium : Implications for energy coupling in respiration. / Chung, Youngran; Xu, Dejun; Jue, Thomas.
In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 40, No. 3, 09.1996.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Nitrite oxidation of myoglobin in perfused myocardium
T2 - Implications for energy coupling in respiration
AU - Chung, Youngran
AU - Xu, Dejun
AU - Jue, Thomas
PY - 1996/9
Y1 - 1996/9
N2 - Nitrite oxidation of oxymyoglobin in perfused rat myocardium under nonlimiting oxygen produces a detectable 1H nuclear magnetic resonance metmyoglobin (metMb) signal at -3.9 ppm. When the myocardium is perfused with <10 mM nitrite, the 1H nuclear magnetic resonance MbO2 γ CH3 Val E11 signal does not change intensity and the metMb reporter signal at -3.9 ppm is undetectable. However the rate pressure product decreases by 26% from the control level. Phosphocreatine, myocardial oxygen consumption, Pi, ATP, and pH remain constant. With >10 mM infused nitrite, myoglobin (Mb) oxidation becomes apparent. As the MbO2 γ 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, rate pressure product, and lactate formation exhibit significant alterations. Myocardial oxygen consumption, 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.
AB - Nitrite oxidation of oxymyoglobin in perfused rat myocardium under nonlimiting oxygen produces a detectable 1H nuclear magnetic resonance metmyoglobin (metMb) signal at -3.9 ppm. When the myocardium is perfused with <10 mM nitrite, the 1H nuclear magnetic resonance MbO2 γ CH3 Val E11 signal does not change intensity and the metMb reporter signal at -3.9 ppm is undetectable. However the rate pressure product decreases by 26% from the control level. Phosphocreatine, myocardial oxygen consumption, Pi, ATP, and pH remain constant. With >10 mM infused nitrite, myoglobin (Mb) oxidation becomes apparent. As the MbO2 γ 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, rate pressure product, and lactate formation exhibit significant alterations. Myocardial oxygen consumption, 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.
KW - Bioenergetics
KW - Nuclear magnetic resonance
KW - Oxidative phosphorylation
UR - http://www.scopus.com/inward/record.url?scp=33750685374&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=33750685374&partnerID=8YFLogxK
M3 - Article
C2 - 8853356
AN - SCOPUS:33750685374
VL - 40
JO - American Journal of Physiology - Renal Fluid and Electrolyte Physiology
JF - American Journal of Physiology - Renal Fluid and Electrolyte Physiology
SN - 1931-857X
IS - 3
ER -