Neurogenic cerebral vasodilation from electrical stimulation of the cerebellum in the monkey.

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Abstract
The effect of stimulation of fastigial nucleus (FN) on cerebral blood flow (CBF) was examined in anesthetized, paralyzed monkeys. CBF was measured with a flow transducer chemically implanted on the left common carotid artery. The left external carotid artery and its branches were ligated. Electrical stimulation of the fastigal nucleus produced rapid (within two seconds) increases in arterial pressure (AP) and heart rate. Mean carotid blood flow (MCBF) rose 77% (+/- 40% SEM) above control and followed the increases in mean arterial pressure (MAP). Calculated cerebrovascular resistance decreased immediately by 27% (+/- 14% SEM) below control. The increases in MCBF were not caused by a passively responding cerebrovascular bed (CVB) resulting from the stimulation or trauma to the vessels. Cerebral metabolism was not altered during stimulation as determined from the arteriovenous oxygen content difference. CBF autoregulation was still present with stimulation of the fastigial nucleus. The autoregulatory curve was shifted to a higher flow level. During the initial MAP changes in sympathectomized animals, MCBF increased to a greater extent than in the innervated animals, suggesting the presence of two neurogenic vasodilatory systems. It appears that electrical stimulation of the fastigial nucleus inhibits sympathetic tone and increases parasympathetic activity to the CVB, resulting in vasodilation and an increase in MCBF.