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Konstantin-A. Hossmann, MD; Paul Kleihues, MD

Arch Neurol. 1973;29(6):375-384.

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

The susceptibility of the brain to anoxia is considered to be the limiting factor for resuscitation after transient circulatory arrest, both in clinical and experimental conditions.^1,2 In the classic experiments of Weinberger et al,³ Kabat et al,⁴ Grenell,⁵ Hirsch et al,⁶ and others, the upper limit for full recovery was found to be three to four minutes of cardiocirculatory arrest, and eight to ten minutes of isolated cerebrovascular arrest.

The high sensitivity of the central nervous tissue to ischemia has been attributed to low reserves in substrates suitable for anaerobic energy metabolism, because a close correlation was found between the depletion of energy-rich phosphates and the irreversibility of brain damage.⁷ This concept, however, is difficult to reconcile with more recent demonstrations of the recovery of various neuronal functions after time intervals which by far exceed the limit of energy depletion. Examples are the return . . . [Full Text PDF of this Article]

Author Affiliations
Cologne, West Germany

From the Max-Planck-Institut für Hirnforschung, Cologne, West Germany.

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 Max-Planck-Institut für Hirnforschung, 5 Köln-Merheim, Ostmerheimerstrasse 200, West Germany (Dr. Hossmann).

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