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In the immature brain, postischemic metabolism may be influenced beneficially by the effect of inducing hypercarbia or hypothermia. With use of  31 P nuclear magnetic resonance spectroscopy, intracellular pH (pH i ) and cellular energy metabolites in ex vivo neonatal rat cerebral cortex were measured before, during, and after substrate and oxygen deprivation in in vitro ischemia. Early postischemic hypothermia (fall in temperature −3.2 ± 1.0°C) delayed the normalization of pH i  after ischemia by inducing an acid shift in pH i  ( P &lt; 0.01). Postischemic hypercarbia (Krebs—Henseleit bicarbonate buffer equilibrated with 10% carbon dioxide in oxygen) and hypothermia induced separate, but potentially additive, reversible decreases in pH i , each of approximately −0.16 pH unit ( P &lt; 0.05). When these postischemic perturbations were applied in isolation, there was significant improvement of ∼20% in the recovery of β-ATP ( P &lt; 0.05). In combination, however, hypercarbia and hypothermia worsened recovery in ATP by ∼20% ( P &lt; 0.05). In control tissue, which had not been exposed to ischemia, ATP content was also significantly reduced by co-administration of the two treatments ( P &lt; 0.05), an effect that persisted even after discontinuing the perturbing conditions. Therefore, in this vascular-independent neonatal preparation, early postischemic modulation of metabolism by hypercarbia or hypothermia appears to confer improved bioenergetic recovery, but only if they are not administered together.

Hypercarbia and Mild Hypothermia, Only When Not Combined, Improve Postischemic Bioenergetic Recovery in Neonatal Rat Brain Slices