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  Vol. 12 No. 3, March 1965 TABLE OF CONTENTS
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Hyperventilation in Awake and Anesthetized Man

Effects on Cerebral Blood Flow and Cerebral Metabolism

LAWRENCE C. McHENRY, JR., MD; HARVEY C. SLOCUM, MD; HOLLIS E. BIVENS, MD; HUBERT A. MAYES, MD; GEORGE J. HAYES, MD

Arch Neurol. 1965;12(3):270-277.

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 EFFECTS of hyperventilation on cerebral blood flow are well known, but the changes in cerebral metabolism associated with hypocapnia are in some dispute. Kety and Schmidt,1,2 using the nitrous oxide technique, originally showed that there was a diminution of cerebral blood flow but no change in cerebral oxygen consumption with passive hyperventilation. The measurement of cerebral cortical oxygen tension with the oxygen electrode, however, has given different results. Sugioka and Davis3 reported "a marked drop in cerebral oxygen tension as the result of hyperventilation" and postulated that cerebral hypoxia may be caused by hyperventilation and that the use of hyperventilation in anesthesia and resuscitation may be dangerous. In another study based on polarographic oxygen electrode, Meyer and Gotoh4 showed that hyperventilation caused vasoconstriction up to 50% and a marked reduction in cortical pO2. Meyer concluded that hyperventilation causes progressive vasoconstriction of small cerebral arterioles and . . . [Full Text PDF of this Article]


Author Affiliations

WASHINGTON, DC

From the Department of Neurophysiology, Walter Reed Army Institute of Research, and the departments of anesthesiology and neurosurgery, Walter Reed General Hospital, Walter Reed Army Medical Center.


Footnotes

Submitted for publication Aug 13, 1964; accepted Nov 17.

Read by title before the annual meeting of the American Neurological Association, June 1964.

Reprint requests to Department of Neurology, Jefferson Medical College, Philadelphia, Pa 19107 (Dr. McHenry).



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