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December 1973

Cerebral Energy Reserves After Prolonged Hypoxia and Ischemia

Author Affiliations

Lund, Sweden
From the Brain Research Laboratory, Eblocket, University Hospital, Lund, Sweden.

Arch Neurol. 1973;29(6):400-407. doi:10.1001/archneur.1973.00490300062008

This presentation is intended to summarize information obtained on the energy state of the brain in hypoxia (low arterial oxygen pressure [Po2]) and in ischemia (interruption of the cerebral circulation). The discussion is directed to the following questions: (1) At what arterial and cerebral venous Po2 levels are there changes indicating a derangement of cerebral energy metabolism? (2) What is the metabolic picture in complete ischemia, and when does energy depletion occur? (3) Is there complete restitution of energy metabolism even after prolonged ischemia, or are there postischemic changes indicative of a permanent biochemical lesion? (4) Can the biochemical data reveal the presence of unperfused areas?

The results were obtained on lightly anesthetized and artificially ventilated rats in which body temperature, arterial blood pressure, and arterial Po2, carbon dioxide pressure (Pco2), and pH were monitored. Cerebral metabolites were analyzed after freezing the tissue in situ, using the

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