Summary:The present experiments were undertaken to determine if loss of vascular autoregulation during severe hypoglycemia shows regional differences that could help to explain the localization of hypoglycemic cell damage. Artificially ventilated rats (70% NzO) were subjected to a 30-min insulin-induced hypoglycemic coma (with ces sation of EEG activity), with mean arterial blood pressure being maintained at 140, 120, 100, and 80 mm Hg, After 30 min of hypoglycemia, local cerebral blood flow (CBF) in 25 brain structures was measured autoradiographically with a [14C]iodoantipyrine technique. Since local CBF values did not differ between the 120 and the 100 mm Hg groups, the animal s of these groups were pooled (110 mm Hg group). The results showed that at a blood pressure of 140 mm Hg, CBF was increased in 22 of 25 structures analysed, the maximal values approximating 300% of control. At 110 mm Hg, cerebral cortical structures hadThe mechanisms leading to hypoglycemic cell damage have not been adequately clarified, and it is not known why such damage often shows a pref erential localization to certain vulnerable brain structures such as the hippocampus, the caudopu tamen, and the neocortex (Meyer, 1963; Siesj6 et aI., 1982). The primary pathophysiological event in hypoglycemia is a reduction in glucose supply to the brain without a corresponding decrease in ox ygen delivery (Kety et aI., 1948;Eisenberg and Seltzer, 1962; Della Porta et aI., 1964; Pappen heimer and Setchell, 1973). In the experimental set ting, the adequacy of cerebral oxygen supply is re flected in a shift of cellular redox systems in the direction of oxidation (Lewis et aI., 1974a; Norberg and Siesj6, 1976). As a result of this mismatch be-