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Raichle ME, Posner JB, Plum F. 
“Cerebral blood flow during and after hyperventilation”. 
Arch Neurol. 1970 Nov;23(5):394-403.
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 animalsz.5 and man6 producing sustained, constant arterial hypocapnia lowered the CBF to a level which did not alter with time. Since there is abundant evidence that despite the constant hypocapnia prolonged hyperventilation produces first a rise and then a fall in brain interstitial pH,z-4 the CBF should first fall and then gradually rise toward normal if the hypothesis was correct that interstitial pH controls CBF. The present studies reexamine the effects on CBF of prolonged hyperventilation. We studied both awake men and anesthetized animals with results that support the pH hypothesis and offer an explanation for the contrary experimental results.

Key Words: carbogen
Notes # : carbogen
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