Cerebral glucose metabolism (CMRglu) is decreased during acute and prolonged hypercapnic acidosis and during prolonged metabolic (HCl) acidosis; it is increased in acute (hypocapnic) metabolic acidosis and is not changed in acute isocapnic metabolic acidosis. The alteration in CMRglu can be explained by the changes occurring in intracerebral pH under these experimental conditions. In pontine gray matter, n. tractus solitarii, and n. ambiguus, three structures participating in the neuronal regulation of ventilation, local CMRglu is increased in all acidotic groups, suggesting coupling of function and metabolism at the local level during acidosis-induced hyperventilation.

The effect of ventriculocisternal perfusion with mock CSF with alkaline or acidic pH on the local CMRglu (LCMRglu) in the caudatoputamen was studied in artificially ventilated and relaxed rats. In control rats both lateral cerebral ventricles were perfused with mock CSF at pH 7.4. In the experimental series one cerebral ventricle was infused with normal mock CSF while the other was infused with mock CSF in which the pH was decreased or increased by changing [HCO-3]. LCMRglu was depressed in acidotic brain tissue while it was strongly increased in alkalotic brain tissue. The importance of these alterations in brain glucose metabolism for the homeostatic regulation of brain pH is discussed.

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