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We used our recently developed method for the simultaneous measurement of the local CMRglc (LCMRglc) and composite tissue pH to evaluate the response to unilateral carotid ligation and moderate hypoxia [40.1 +/- 4.8 (SD) mm Hg]. The LCMRglc and tissue pH were measured simultaneously in brain slices using [14C]2-deoxy-D-glucose and [14C]5,5-dimethyl-2,4-oxazolidinedione. The ipsilateral LCMRglc was increased significantly in the caudate-putamen and medical thalamus and was surrounded by a much more extensive zone of acidosis, as shown by significant reductions in the tissue pH, which was affected in parietal cortex, caudate-putamen, lateral septal nucleus, medial geniculate, Ammon's horn, and nucleus reticularis of substantia nigra. In regions with an elevated LCMRglc and acidosis, anaerobic glycolysis combined with ATP hydrolysis are likely to co-exist. In regions characterized by normal glucose metabolism and acidosis, we hypothesize that a direct effect of hypoxia on the sodium/hydrogen ion antiporter may lead to secondary acidosis. Disturbed acid-base balance during hypoxia may have an adverse effect on cerebral function and cause clinical symptoms.

Effects of Moderate Hypoxemia and Unilateral Carotid Ligation on Cerebral Glucose Metabolism and Acid-Base Balance in the Rat