Brain blood flow regulation of the cardiovascular center

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In urethane-anesthetized, paralyzed and artificially ventilated rats, the neurons in the rostral ventrolateral pressor area(VLPA), origin of the sympathetic nerve activities in the brain stem, were chemically stimulated by microinjection of L-glutamate and the spinal cord blood flow(SCBF) was determined using labeled microspheres. The local SCBFs were significantly decreased and local spinal cord vascular resistances(SCVRs) were significantly increased in all spinal cord regions by unilateral chemical stimulation of the VLPA(n=12). During the chemical stimulation of the VLPA, SCBF increased in response to the changes in arterial PaCO_2, indicating that the reactivity of the spinal cord vasculature was intact(n=5). Microinjections of L-glutamate into an area adjacent to the VLPA had no effect on spinal cord circulation(n=5). These results suggest that the neurons within the VLPA may play a role in the control of spinal cord circulation.Microinjection of L-glutamate(1.7 nmol) into the ventrolateral medullary depressor area(VLDA) produced a significant(P<0.01) decrease in cerebral blood flow(CBF) and a significant(P<0.01) increase in cerebrovascular resistance(CVR) in the cerebral cortex ipsilateral to the stimulated VLDA side(n=9). Cervical sympathectomy blocked the decrease in CBF and increase in CVR elicited by chemical stimulation of the VLDA (n=10). Depression of the VLPA neurons induced by microinjection of muscimol into the VLPA blocked the CBF decrease and CVR increase responses following chemical stimulation of VLDA(n=11). These results suggest that a vasoconstrictor pathway to control cerebral vessels involves an excitatory projection from the VLDA to the VLPA and the changes in cerebral circulation are mediated by the cervical sympathetic nerves.