Summary: In the periphery of ischemic brain lesions, transient spreading depression-like direct current (DC) deflections occur that may be of pathophysiological im portance for determining the volume of the ischemic in farct. The effect of these deflections on cerebral blood flow, tissue oxygen tension, and electrophysiology was studied in rats submitted to intraluminal thread occlusion of the middle cerebral artery (MCA) and compared with the changes following potassium chloride (KCl)-induced spreading depression of intact animals, Immediately after MCA occlusion, cortical laser-Doppler flow (LDF) in the periphery of the MCA territory sharply decreased to 35 ± 14% of control (mean ± SD; p < 0,05), tissue P02 de clined from 28 ± 4 to 21 ± 3 mm Hg (p < 0.05), and EEG power fell to -80% of control. During 7-h occlusion, 3-11 DC deflections with a mean duration of 5.2 ± 4.8 min occurred at irregular intervals, and EEG power gradually During the last years, several laboratories have been able to show that glutamate antagonists reduce the volume of ischemic infarcts (Ozyurt et aI. , 1988; Park et aI., 1988; Dirnagl et aI., 1990). The thera peutical effect could not be attributed to increased cerebral blood flow (Park et aI., 1989; Iijima et aI., 1992), indicating that molecular mechanisms are in volved. This observation is widely held to support an excitotoxic mechanism of brain infarcts in anal ogy to glutamate toxicity in vitro (Choi, 1985) and the phenomenon of delayed neuronal death in se lectively vulnerable brain regions following a period of global ischemia (Suzuki et aI., 1983). The com-