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  Vol. 29 No. 6, December 1973 TABLE OF CONTENTS
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  PAPERS 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
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Metabolic Alterations in Brain During Anoxic-Anoxia and Subsequent Recovery

Lester R. Drewes, PhD; David D. Gilboe, PhD; A. Lorris Betz

Arch Neurol. 1973;29(6):385-390.

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

Until a few years ago, it was generally thought that irreversible brain damage would result from any condition that produced a profound cerebral anoxia of greater than eight to ten minutes' duration. This conclusion was based on observations made by physicians during clinical emergencies and by investigators using experimental models in which the onset, degree, and duration of anoxia could be controlled.1-6 Most techniques for producing anoxia in the intact animal also produce ischemia and there is some evidence to suggest that cerebral anoxia is exacerbated by ischemia.7 However, the results of recent studies with totally ischemic brain tissue suggest that many of the variables measured approach normal after reoxygenation. This has led some workers to question whether cerebral anoxia actually causes irreversible brain damage within so short a period as ten minutes.8-11

If proper protocols are to be established for the treatment of cardiac arrests and . . . [Full Text PDF of this Article]


Author Affiliations

Madison, Wis

From the departments of neurosurgery (Dr. Drewes and Gilboe) and physiology (Mr. Betz), University of Wisconsin, Madison.


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 Department of Neurosurgery, University of Wisconsin, Madison, WI 53706 (Dr. Gilboe).



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