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

Abstract

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.