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I. The Extravascular Effect

M. N. Shalit, MD; S. Shimojyo, MD; O. M. Reinmuth, MD

Arch Neurol. 1967;17(3):298-303.

	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 response of cerebral circulation to changes in arterial carbon dioxide tension (Paco₂) is well known and has been confirmed in numerous experiments and clinical observations. Nonetheless, the mechanism of the action of this gas is not completely understood although certain theories are presently generally accepted.

The dilation of the cerebral vessels following an increase of Paco₂ is thought to be a result of the direct action of the gas on the smooth muscle in the cerebral arterial wall._1-3 The observation of Cow in 1911⁴ that isolated strips of carotid artery immersed in Ringer's solution dilate when CO₂ is dissolved in the medium is the principal justification for this theory.

The possibility of a neural regulatory mechanism for the cerebral circulation has been widely assumed to be negligible or nonexistent because of failure of autonomic denervation or stimulation to affect cerebral blood flow (CBF) . . . [Full Text PDF of this Article]

Author Affiliations
Miami, Fla

From the Department of Neurology, University of Miami School of Medicine, Miami, Fla. The present address of Dr. Shalit is Department of Neurosurgery, Hadassah University Hospital, Jerusalem, Israel.

Footnotes
Submitted for publication March 30, 1967; accepted May 6.

Read before the American Heart Association, New York, Oct 22, 1966, and in part before the Third International Symposium on Cerebral Circulation Research, Salzburg, Austria, Oct 20, 1966.

Reprint requests to Department of Neurology, University of Miami School of Medicine, Box 875, Biscayne Annex, Miami, Fla 33152 (Dr. Reinmuth).

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