LACTATE ACCUMULATION DURING MODERATE HYPOXIC HYPOXIA IN NEOCORTICAL RAT-BRAIN

Neocortical metabolism was studied during moderate hypoxic hypoxia, re oxygenation, and postmortem periods in anesthetized normocapnic rats u sing H-1 nuclear magnetic resonance (NMR) spectroscopic imaging. Rats were prepared with unilateral common carotid occlusion to determine th e ipsilateral metabolic effects of inadequate cerebral blood flow (CBF ) response to hypoxia. No difference in brain metabolism between the t wo hemispheres was found during the control period. Hypoxic hypoxia (P (a)o(2) = 54.1 +/- 5.8 mm Hg) resulted in a significant rise in neocor tical 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 no t 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 neocorti cal water and N-acetyl aspartate (NAA) signals, which were related to a shortening in T-2 relaxation times. It is concluded that neocortical lactate is an early metabolic indicator during moderate hypoxic hypox ia in normocapnic conditions.