Summary:We examined the effects of electrical stimu lation of a restricted area of the dorsal medullary reticular formation (DMRF) on regional cerebral blood flow (CBF) in anesthetized (by chloralose), paralyzed (by curare) rats. CBP was measured in tissue samples by the Kety prin ciple, with 14C-iodoantipyrine as indicator. Stimulation of DMRF elicited a widespread, significant increase in CBP in 12 of 13 areas. The increase in flow was greatest in cerebral cortex, up to 240% of control. However, it was also substantially increased in selected regions of telen cephalon, diencephalon, mesencephalon, and lower brainstem, but not cerebellum. In contrast, electricalIt has been believed for many years that the brainstem may control cerebral circulation. The ev idence has been derived largely from studies that have assessed the effects on cerebral blood flow (CBF) of locally altering neuronal activity by focal electrical stimulation (Reis, 1979). Such studies have demonstrated that modification of brainstem func tion may, in fact, alter CBF, thereby suggesting that the CNS can regulate its own circulation through intrinsic neuronal systems.These investigations, however, left two issues un resolved. First, since CBF was measured either across the entire brain (Langfitt and Kassell, 1968; Meyer et aI., 1969 Meyer et aI., , 1971Lang and Zimmer, 1974) or only qualitatively estimated from restricted brain regions, usually cerebral cortex (lngvar, 1958;Molnar and Szanto, 1964; Vern et aI., 1981; Reis et aI., 1982), they did not establish whether the evoked changes in flow were localized or global. Second,
270stimulation of the midline (interstitial nucleus of the me dial longitudinal fasciculus) I mm medial to the DMRF did not change CBF. The increase in CBP evoked by DMRF stimulation persisted after transection of the spinal cord at CI or cervical sympathetic trunk. We conclude that excitation of neurons originating in or passing through the DMRF can elicit a potent and virtually global increase of CBF. The effect appears to be mediated by intrinsic pathways of the central nervous system.