Observations on the Extrinsic Neural Control of Cerebral Blood Flow in the Baboon
Cerebral blood flow was measured using 133xenon in forty-five baboons lightly anesthetized with pentobarbital. Blood flow varied between 62 and 82 ml/100g/min in gray matter and between 15 and 21 ml/100g/min in white matter. Hypercapnia and hypoxia caused a rise in blood flow and a fall in vascular resistance. Blood flow was independent of mean arterial blood pressure over the range 60 to 130 mm Hg. Section of the cervical sympathetic nerve enhanced the vascular response to CO2. Stimulation of the sympathetic nerve caused a reduction in blood flow in proportion to the initial blood flow. Similarly, after sympathectomy, blood flow was uniformly higher than control over the range of Pao2 tested (35 to 450 mm Hg). After sympathectomy, blood flow was little different from control at low blood pressure but was higher within the physiological range and blood flow then fell steadily as pressure was reduced. When the carotid, vagus, and aortic nerves were cut in the neck, the blood flow response to hypoxia and hypercapnia was reduced, and when the aortic or vagus nerves were stimulated centrally, blood flow increased independently of PaCO2. Section of the seventh cranial nerve caused small and variable changes in blood flow, but if the vagus nerves had previously been sectioned, stimulation of the seventh cranial nerve caused an increase in blood flow in some of the tests. These results indicate that cerebral blood vessels are under reflex control. Possible receptors and pathways involved are discussed.
- Received January 27, 1969.
- Accepted May 14, 1969.
- © 1969 American Heart Association, Inc.