Summary:We investigated, using laser-Doppler flow me try, whether nitric oxide (NO)-and/or indomethacin (lND)-sensitive mechanisms mediate the elevations of re gional cerebral blood flow (rCBF) elicited by electrical stimulation of the rostral ventrolateral medulla (RVL) in the anesthetized spinalized rat. Stimulation of the RVL for 10 s caused increased rCBF in the frontal cortex by 31 % (n = 46), peaking at 22 s and persisting for up to 8 min. Intravenous L-nitro-�-arginine (NNA) dose depen dently and reversibly increased arterial pressure and re duced basal and evoked rCBF to 74 and 54% of the con trol, respectively (p < 0.05; n = 7). Superfused over the cortex, NNA dose dependently reduced only the evoked elevations of rCBF, to .�9% of the control (p < 0.05; n = 6). Intravenous IND decreased the basal rCBF dose de pendently and decreased the elevations evoked from the Electrical or chemical stimulation of the rostral ventrolateral medulla (RVL) increases regional ce rebral blood flow (rCBF) in rat cerebral cortex (Saeki et aI., 1989; Underwood et aI., 1992) without parallel changes in regional cerebral glucose utiliza tion (Underwood et aI., 1992). The mechanism by which the afferent neural signal is transduced into vasodilation is unknown. The fact that a brief stim ulus train can elevate rCBF for minutes (Saeki et Received January 19, 1993; final revision received September 23, 1993; accepted September 30, 1993. Address correspondence and reprint requests to Dr. E. V.
492RVL by 38% (p < 0.05), but IND was without effect when superfused. Combined, the effects of intravenous NNA and IND summated, reducing rCBF by 70%. However, when NNA and IND were superfused together, the inhi bition of the evoked vasodilation was comparable to that elicited by NNA alone. We conclude that the elevation in reBF elicited from the RVL is partially mediated by (a) NO synthesized locally in the cortex in response to an afferent neural signal and (b) an IND-sensitive mecha nism, probably a product of cyclooxygenase, located in larger cerebral arteries, in response to a retrograde vas cular signal resulting from increased blood flow within the brain. Key Words: Nitric oxide-Prostanoids-Regional cerebral blood flow-Vasopressin-Ventrolateral me dulla.aI. , 1989; Golanov et aI., 1991) suggests that the vascular response may result from repetitive action of local neurons and/or release of diffusible media tors.In the present study we investigated whether two classes of vasoactive molecules are potential candi dates. One, nitric oxide (NO), is continuously syn thesized from L-arginine in brain and cerebral ves sels by the action of the constitutive form of nitric oxide synthase (NOS) (Palmer et aI., 1988; Bredt et aI., 1990; Moncada et aI., 1991; Murphy et aI., 1991). NO not only tonically dilates cerebral vessels (Kovach et aI., 1992) but also may participate in the vasodilation elicited by electrical stimulation of the cerebellar fastigial nucleus (ladecola, 1992). The other consists of those products of arachidonic acid met...