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Am J Physiol Regul Integr Comp Physiol 279: R9-R16, 2000;
0363-6119/00 $5.00
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Vol. 279, Issue 1, R9-R16, July 2000

Critical oxygen tension in rat brain: a combined 31P-NMR and EPR oximetry study

Ellis L. Rolett1, Ali Azzawi2, Ke Jian Liu2, Martin N. Yongbi2, Harold M. Swartz2, and Jeff F. Dunn2

Departments of 1 Medicine and 2 Radiology, Nuclear Magnetic Resonance and Electron Paramagnetic Resonance Research Centers, Dartmouth-Hitchcock Medical Center, Hanover, New Hampshire 03755

The relationship between cerebral interstitial oxygen tension (PtO2) and cellular energetics was investigated in mechanically ventilated, anesthetized rats during progressive acute hypoxia to determine whether there is a "critical" brain PtO2 for maintaining steady-state aerobic metabolism. Cerebral PtO2, measured by electron paramagnetic resonance oximetry, decreased proportionately to inspired oxygen fraction. 31P-nuclear magnetic resonance measurements revealed no changes in Pi, phosphocreatine (PCr)/Pi ratio, or intracellular pH when arterial blood oxygen tension (PaO2) was reduced from 145.1 ± 11.7 to 56.5 ± 4.4 mmHg (means ± SE). Intracellular acidosis, a sharp rise in Pi, and a decline in the PCr/Pi ratio developed when PaO2 was reduced further to 40.7 ± 2.3 mmHg. The corresponding PtO2 values were 15.1 ± 1.8, 8.8 ± 0.4, and 6.8 ± 0.3 mmHg. We conclude that over a range of decreasing oxygen tensions, cerebral oxidative metabolism is not sensitive to oxygen concentration. Oxygen becomes a regulatory substrate, however, when PtO2 is decreased to a critical level.

hypoxia; electron paramagnetic resonance; nuclear magnetic resonance spectroscopy; energy metabolism; pH


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