Nitrite oxidation of myoglobin in perfused myocardium: Implications for energy coupling in respiration

Research output: Contribution to journalArticle

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. P(i), 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 languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume271
Issue number3 40-3
StatePublished - Sep 1996

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Myoglobin
Nitrites
Myocardium
Respiration
Metmyoglobin
Oxygen Consumption
Magnetic Resonance Spectroscopy
Pressure
Phosphocreatine
Reperfusion
Pulse
Lactic Acid
Buffers
Oxidoreductases
Perfusion
Adenosine Triphosphate
Phosphates
Oxygen

Keywords

  • bioenergetics
  • nuclear magnetic resonance
  • oxidative phosphorylation

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

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title = "Nitrite oxidation of myoglobin in perfused myocardium: Implications for energy coupling in respiration",
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. P(i), 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.",
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author = "Youngran Chung and Dejun Xu and Thomas Jue",
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month = "9",
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T2 - Implications for energy coupling in respiration

AU - Chung, Youngran

AU - Xu, Dejun

AU - Jue, Thomas

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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. P(i), 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. P(i), 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.

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