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June 1942

REGULATION OF CEREBRAL CARBON DIOXIDE

Author Affiliations

BOSTON; NEW HAVEN, CONN.

From the Neurological Unit of the Boston City Hospital, the Department of Neurology of the Harvard Medical School and the Laboratory of Physiology of Yale University School of Medicine.

Arch NeurPsych. 1942;47(6):879-889. doi:10.1001/archneurpsyc.1942.02290060017001
Abstract

Students of cerebral function have, in general, paid too little attention to carbon dioxide. Procedures which alter the tension of carbon dioxide in the brain have a pronounced effect on cerebral function1 and on the electrical activity of the cortex.2 As shown by some of these experiments, extreme shifts in the carbon dioxide tension of the brain are disadvantageous. Therefore, a mechanism which would provide for the homeostasis of carbon dioxide would be advantageous. Such a mechanism appears to reside in the response of cerebral blood vessels to changes in alveolar or arterial carbon dioxide.

An increase of carbon dioxide tension in the cerebral blood vessels causes dilatation of the cerebral arterioles, and a decrease causes constriction. In contrast, a maximal increase of oxygen tension produces only feeble constriction, and an extreme decrease in oxygen tension causes only moderate dilatation. These facts have been abundantly proved both for

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