Oxygen supply and oxidative phosphorylation limitation in rat myocardium in situ

Ulrike Kreutzer, Yousry Mekhamer, Youngran Chung, Thomas Jue

Research output: Contribution to journalArticlepeer-review

26 Scopus citations


The 1H-NMR signal of the proximal histidyl-NδH of deoxymyoglobin is detectable in the in situ rat myocardium and can reflect the intracellular Po2. Under basal normoxic conditions, the cellular Po2 is sufficient to saturate myoglobin (Mb). No proximal histidyl signal of Mb is detectable. On ligation of the left anterior descending coronary artery, the Mb signal at 78 parts/million (ppm) appears, along with a peak shoulder assigned to the corresponding signal of Hb. During dopamine infusion up to 80 μg·kg-1·min-1, both the heart rate-pressure product (RPP) and myocardial oxygen consumption (MVo2) increase by about a factor of 2. Coronary flow increases by 84%, and O2 extraction (arteriovenous O2 difference) rises by 31%. Despite the increased respiration and work, no deoxymyoglobin signal is detected, implying that the intracellular O2 level still saturates MbO2, well above the Po2 at 50% saturation of Mb. The phosphocreatine (PCr) level decreases, however, during dopamine stimulation, and the ratio of the change in Pi over PCr (ΔPi/PCr) increases by 0.19. Infusion of either pyruvate, as the primary substrate, or dichloroacetate, a pyruvate dehydrogenase activator, abolishes the change in ΔPi/PCr. Intracellular O2 supply does not limit MVo2, and the role of ADP in regulating respiration in rat myocardium in vivo remains an open question.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number5 49-5
StatePublished - May 2001


  • Bioenergetics
  • Heart
  • Myoglobin
  • Nuclear magnetic resonance
  • Respiration

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)


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