ABSTRACT. Ventilated piglets were studied before, during (15 min), and after (90 min) hemorrhagic hypotension to correlate a 60% reduction in cerebral blood flow with cerebral energy state using radiolabeled microspheres (n = 12) and in vivo 31P nuclear magnetic resonance spectroscopy (n = 11). Cerebral blood flow (ml. min-I .I00 g-') decreased during hypotension (98 f 28 to 41 f 28, p < 0.05), increased at 5 min postreperfusion (131 f 53, p < 0.05), and returned to control values by 90 min postreperfusion. Cerebral O2 uptake was reduced during partial ischemia, remained depressed 5 rnin postreperfusion, and increased to within 20% of control values at 90 rnin postreperfusion. Relative to control, hypotension was associated with decreased ( p < 0.05) phosphocreatine (62 f 11%), phosphocreatine/inorganic phosphate ratio (41 2 lo%), and nucleoside triphosphate (82 2 12%) while inorganic phosphate increased (155 f 32%,p < 0.05). During ischemia intracellular pH dropped from 7.06 f 0.07 to 6.59 f 0.31 ( p < 0.05) and the cerebral arteriovenous difference of glucose increased. Phosphorylated metabolites returned to within 10% of control 15 rnin after blood reinfusion and remained constant thereafter. Based on calculations of ATP synthesis and utilization rates during control and hypotension, we speculate that the rate of energy utilization of the brain during ischemia is reduced 18-49% relative to the control utilization rate. (Pediatr Res 23: 206-211,1988 Cerebral metabolic effects of partial ischemia are pertinent to multiple problems in sick human neonates. Events such as asphyxia, tension pneumothorax, intracranial hemorrhage, and hypovolemia may result in alterations in cerebral perfusion pressure with or without changes in blood O2 tension. Although scant data are available concerning CBF measurements in sick human neonates (1-4), partial cerebral ischemia may be of greater clinical concern than complete cerebral ischemia in view of the prevalence of events contributing to the former compared to the latter. Despite this, relatively little research has been done on perinatal brain ischemia and the most frequently used animal model has been complete cerebral ischemia via decapitation (5-7).Inasmuch as partial ischemia encompasses a spectrum of cerebral perfusion pressure and CBF, multiple investigations in adult animals have examined the reduction in CBF necessary to alter energy metabolism. Siesjo and Zwetnow (8) used hypovolemic hypotension in adult rats and reported unaltered brain ATP and PCr when MABP >40 mm Hg. Although CBF was not measured, the results were attributed to maintenance of CBF at the lower limit of autoregulation. Similarly, reduction in cerebral perfusion pressure by increased CSF pressure was associated with unaltered adenine nucleotides until cerebral perfusion pressure <30 mm Hg (9). Further investigations of adult rats by Eklof and Siesjo (10) revealed that 50-60% decreases in CBF were necessary to decrease cerebral ATP. Welsh et al.(1 1) suggested that in adult animals there is a criti...