THE CEREBRAL VASCULAR RESPONSE TO REDUCTION IN ARTERIAL CARBON DIOXIDE TENSION*

Abstract

Studies using the nitrous oxide technique in 6 adult males revealed no alteration in cerebral oxygen consumption (CMR02) during voluntary hyperventilation. With CMRO2 constant, cerebral blood flow (CBF) varies as the reciprocal of the cerebral arteriovenous oxygen difference. This function, 1/(A-V)O2 was measured by continuous oximetry in 19 experiments on 11 normal subjects and correlated with arterial CO2 tension (PaCO2)- After a threshold of about 2 mm Hg, further reduction in PaCO2 induced cerebral vaso-constriction, but with a decreasing responsiveness of the cerebral vessels as severe hypocapnia developed. The mean curve is described by the following formula: y= 77.6 + (-29.1) (x - 0.918) where y = CBF expressed as per cent of control and x = log (-[DELTA] PaCO2)- The importance of hypocapnia and its associated cerebral vasoconstriction in response to alterations in perfusion pressure and in particular in diseases associated with hyperventilation may now be better assessed. Cerebral tissue anoxia and deterioration in mental function which have been shown to result from hyperventilation are probably related to the cerebral vasoconstriction induced by hypocapnia.