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The effect of sympathetic stimulation on cerebral blood flow was investigated in dogs anesthetized with chloralose. A preparation has been developed for the moment-to-moment measurement of cerebral venous outflow with an electromagnetic flow transducer. The brain's arterial supply was left undisturbed. The sympathetic innervation of the cerebral vessels was stimulated at the stellate ganglion (3-9 v, 3 msec, and 1, 3, 6, 10, and 15 Hz for 60 or 90 seconds). Stimulation at 15 Hz resulted in an average decrease in cerebral blood flow of 79.7%. During stimulation the arterial oxygen tension decreased from 93.2 to 84.9 mm Hg, the arterial carbon dioxide tension increased from 32.9 to 34.6 mm Hg, and arterial pH fell from 7.392 to 7.378. These changes in blood gas variables all opposed the observed vasoconstriction. Interactions between intracranial pressure and sympathetic cerebral vasoconstriction were evaluated by measuring cerebrospinal fluid pressure and cerebral venous outflow pressure. Stimulation of the left sympathetic stellate ganglion produced a 64% decrease in cerebral blood flow and an 8 mm Hg increase in intracranial pressure. Infusion of saline into the cisterna magna, raising intracranial pressure to 47 mm Hg, produced a 3% decrease in cerebral blood flow. Opening the cerebrospinal fluid space and thus fixing intracranial pressure at zero (atmospheric pressure) did not alter the cerebral blood flow response to sympathetic stimulation. It was concluded that stimulation of the sympathetic stellate ganglion resulted in cerebral vasoconstriction which was independent of changes in arterial P CO 2 , Po 2 , and pH and was also independent of changes in cerebrospinal fluid pressure.
D’Alecy et al. (Tue,) studied this question.