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Jerome B. Posner, MD; Fred Plum, MD; Dominic Zee, MA

Arch Neurol. 1969;20(6):664-667.

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

ALTHOUGH many laboratories have confirmed Kety and Schmidt's¹ finding that a rise in the arterial blood carbon dioxide tension (Paco₂) increases the cerebral blood flow (CBF) while a fall in Paco₂ decreases it, the mechanism mediating this response is unknown. Carbon dioxide diffuses rapidly across the blood-brain barrier and, theoretically, this blood gas could exert direct action on structures lying in any layer of the vessel wall or even on a pH sensitive receptor lying outside the vessel itself, in the adjacent brain extracellular space. An alternate proposal has been that carbon dioxide alters the pH of a brainstem regulatory center, which in turn produces reflex cerebral vasodilatation or constriction in a manner analogous to the control of pulmonary ventilation.

Lassen² has summarized the evidence that brain extracellular pH is the main factor controlling CBF: in severe diabetic acidosis, CBF is increased above normal . . . [Full Text PDF of this Article]

Author Affiliations
New York

From the Department of Neurology, Cornell University Medical College, New York.

Footnotes
Submitted for publication Jan 4, 1969; accepted Jan 20.

Reprint requests to Department of Neurology, 525 E 68th St, New York 10021 (Dr. Posner).

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