ALTHOUGH many laboratories have confirmed Kety and Schmidt's1 finding that a rise in the arterial blood carbon dioxide tension (Paco2) increases the cerebral blood flow (CBF) while a fall in Paco2 decreases it, the mechanism mediating this response is unknown. Carbon dioxide diffuses rapidly across the blood-brain barrier and, theoretically, this blood gas could exert direct action on structures lying in any layer of the vessel wall or even on a pH sensitive receptor lying outside the vessel itself, in the adjacent brain extracellular space. An alternate proposal has been that carbon dioxide alters the pH of a brainstem regulatory center, which in turn produces reflex cerebral vasodilatation or constriction in a manner analogous to the control of pulmonary ventilation.
Lassen2 has summarized the evidence that brain extracellular pH is the main factor controlling CBF: in severe diabetic acidosis, CBF is increased above normal