IT IS WELL established that the arterial carbon dioxide tension (Pco2) is an important factor controlling cerebral vascular resistance (CVR) and cerebral blood flow (CBF) in healthy animals and man. An acute rise in Pco2 causes a decrease in CVR which increases the CBF, and a fall in Pco2 has the opposite effect. However, during sustained alteration of Pco2, the CBF and absolute carbon dioxide tension often fail to correlate closely, and much recent evidence summarized by Lassen1 suggests that alterations of the pH of the brain's extracellular space mediate the cerebral vascular response to carbon dioxide and that brain interstitial fluid pH is the major regulator of CBF. The pH hypothesis is physiologically attractive, but evidence against it comes from a series of experiments in several laboratories in which prolonged passive hyperventilation of animals2-5 and man6 producing sustained, constant arterial hypocapnia
Raichle ME, Posner JB, Plum F. Cerebral Blood Flow During. Arch Neurol. 1970;23(5):394–403. doi:10.1001/archneur.1970.00480290014002
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