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 Paco2is thought to be a result of the direct action of the gas on the smooth muscle in the cerebral arterial wall.1-3The observation of Cow in 19114that isolated strips of carotid artery immersed in Ringer's solution dilate when CO2is 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)