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Bo K. Siesjö, MD; Bengt Ljunggren, MD

Arch Neurol. 1973;29(6):400-407.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

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 . . . [Full Text PDF of this Article]

Author Affiliations
Lund, Sweden

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

Footnotes
Read before the symposium held at New York Hospital—Cornell Medical Center: The Threshold and Mechanisms of Anoxic-Ischemic Brain Injury, New York, June 10, 1973.

Reprint requests to Brain Research Laboratory, E-blocket, University Hospital, Lund, Sweden (Dr. Siesjö).

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