IN A series of papers in this journal last year Shalit and his co-workers discussed "Carbon Dioxide and Cerebral Circulatory Control." From three series of experiments on anesthetized dogs they concluded that the well-known CO2 effect on the cerebral blood flow (CBF increases when the arterial CO2 pressure [Pco2] increases) was due to receptors sensitive to CO2 and not to pH,1 that changes in the arterial Pco2 had no direct effect on the cerebral vessels,2 and that destruction in the upper part of the medulla, pons, and the lower part of mesencephalon abolished the CBF response to changes in the arterial Pco2.3 These experiments suggest the existence of a CO2-sensitive center in the brain stem regulating the cerebral vascular resistance in the hemispheres via a neurogenic mechanism.
Two different problems are involved in this hypothesis: is the CO