Lactate accumulation during moderate hypoxic hypoxia in neocortical rat brain.

Neocortical metabolism was studied during moderate hypoxic hypoxia, reoxygenation, and postmortem periods in anesthetized normocapnic rats using 1H nuclear magnetic resonance (NMR) spectroscopic imaging. Rats were prepared with unilateral common carotid occlusion to determine the ipsilateral metabolic effects of inadequate cerebral blood flow (CBF) response to hypoxia. No difference in brain metabolism between the two hemispheres was found during the control period. Hypoxic hypoxia (PaO2 = 54.1 +/- 5.8 mm Hg) resulted in a significant rise in neocortical lactate peak in both hemispheres, with an additional marked rise in the clamped side compared to the unclamped side (53 +/- 27 vs. 22 +/- 13% of postmortem value, p < 0.001). These lactate changes were not reversible within 30 min of reoxygenation in the clamped hemisphere. No changes in neocortical lactate peak were observed while elevating arterial lactate via intravenous lactate infusion without hypoxia. In addition, hypoxic hypoxia resulted in an apparent decrease in neocortical water and N-acetyl aspartate (NAA) signals, which were related to a shortening in T2 relaxation times. It is concluded that neocortical lactate is an early metabolic indicator during moderate hypoxic hypoxia in normocapnic conditions.