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October 1967

Carbon Dioxide and Cerebral Circulatory ControlII. The Intravascular Effect

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.

Arch Neurol. 1967;17(4):337-341. doi:10.1001/archneur.1967.00470280003001
Abstract

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

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