The effect of preasphyxia blood glucose concentration on postasphyxia (PA) cerebral hemodynamics was examined in 21 newborn lambs. Glucose was unregulated in one group (n=7), and controlled throughout the study by glucose clamp in hyperglycemic (n=7) and hypoglycemic (n=7) groups. Cerebral blood flow, determined using radiolabelled microspheres, and arterial and sagittal sinus O2contents were measured at control, 5 min, 1, 2, and 4 h after resuscitation from an asphyxial insult. Preasphyxia blood glucoses were 6.48 ± 0.55 mM (mean ± SEM), 12.08 ± 0.80, and 2.66 ± 0.14 in the three study groups. In all three groups, 5 min PA cerebral blood flow was significantly increased from control. In the late period after asphyxia, the unregulated group had decreased cerebral blood flow compared with control, 53.2 ± 3.8 mL·100 g-1·min-1, mean ± SEM,P<0.01; 49.6 ± 2.0,P<0.005; 53.4 ± 3.0,P<0.01, at 1, 2, and 4 h PA, respectively,versus85.7 ± 6.9 at control, whereas both the hyper- and hypoglycemic groups did not differ significantly from control measurements. Cerebral oxygen consumption (CMRO2) was significantly decreased in all three groups 5 min PA and remained decreased in the late period after asphyxia in both the unregulated and hypoglycemic groups. In the unregulated group, CMRO2was 191 ± 14 μM·100 g-1·min-1, mean ± SEM,P<0.05; 200 ± 4; and 181 ± 10,P<0.05 at 1, 2, and 4 h, respectively, PA versus 251 ± 12 at control. In the hypoglycemic group, CMRO2was 170 ± 9 μM·100 g-1·min-1, mean ± SEM,P< 0.05; 174 ± 14,P<0.05; and 183 ± 17 at 1, 2, and 4 h PA, respectively,versus231 ± 15 at control. CMRO2did not differ from control in the hyperglycemic group at 1, 2, and 4 h PA. In our newborn lamb postasphyxia model, CMRO2was best maintained PA when the lambs were hyperglycemic before asphyxia and throughout the recovery period. To the extent that more rapid recovery of CMRO2postasphyxia is a favorable outcome, these data may have implications for clinical management.