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II. The Intravascular Effect

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

Arch Neurol. 1967;17(4):337-341.

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

IN a previous report¹ we demonstrated that carbon dioxide (CO₂) may increase cerebral blood flow (CBF) when supplied to the brain via the subarachnoid space (SAS) while the arterial carbon dioxide tension (Paco₂) is kept at a low level, suggesting that the effect of CO₂ on CBF may not necessarily be mediated by its effect on the smooth muscle of the cerebral arterial wall, but perhaps by another mechanism, such as mediation through a chemoreceptor reflex mechanism.

Reviewing previous pertinent work, it was somewhat surprising to discover that no direct demonstration of the effect of CO₂ on the smooth muscle of the cerebral arterial wall had been described. The only direct investigation, frequently quoted in various reviews dealing with this subject, is the work of Cow² in 1911 who observed that isolated segments of the carotid artery dilate when CO₂ is added . . . [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 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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