Critical intracellular O2 in myocardium as determined by 1H nuclear magnetic resonance signal of myoglobin

U. Kreutzer, Thomas Jue

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73 Citations (Scopus)

Abstract

The 1H nuclear magnetic resonance (NMR) signal of tissue myoglobin has provided an opportunity to determine the critical O2 level in saline- perfused myocardium at room temperature. Above the intracellular PO2 of 4 mmHg, the myocardium exhibits no sign of hypoxia. At 4 mmHg, the rate pressure product (RPP) decreases, and the lactate formation rate, measured enzymatically, increases. However, O2 consumption and the 31P-NMR signal of phosphocreatine level remain relatively constant until the cellular PO2 reaches 2 mmHg. The ATP signal intensity dips only when cellular O2 reaches 0.8 mmHg, while pH remains unchanged at 7.2. The sequential nature of the cellular response to limiting O2, starting with alterations in the lactate formation rate and RPP, indicates that NADH, rather than ADP, signals tissue hypoxia. Moreover, the study suggests that the O2 gradient from capillary to cell is larger than that from cytosol to mitochondria.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume268
Issue number4 37-4
StatePublished - 1995

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Myoglobin
Lactic Acid
Myocardium
Magnetic Resonance Spectroscopy
Pressure
Phosphocreatine
NAD
Cytosol
Adenosine Diphosphate
Mitochondria
Adenosine Triphosphate
Temperature
Hypoxia

Keywords

  • bioenergetics
  • heart
  • oxidative phosphorylation

ASJC Scopus subject areas

  • Physiology
  • Medicine(all)

Cite this

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AB - The 1H nuclear magnetic resonance (NMR) signal of tissue myoglobin has provided an opportunity to determine the critical O2 level in saline- perfused myocardium at room temperature. Above the intracellular PO2 of 4 mmHg, the myocardium exhibits no sign of hypoxia. At 4 mmHg, the rate pressure product (RPP) decreases, and the lactate formation rate, measured enzymatically, increases. However, O2 consumption and the 31P-NMR signal of phosphocreatine level remain relatively constant until the cellular PO2 reaches 2 mmHg. The ATP signal intensity dips only when cellular O2 reaches 0.8 mmHg, while pH remains unchanged at 7.2. The sequential nature of the cellular response to limiting O2, starting with alterations in the lactate formation rate and RPP, indicates that NADH, rather than ADP, signals tissue hypoxia. Moreover, the study suggests that the O2 gradient from capillary to cell is larger than that from cytosol to mitochondria.

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