Total circulatory arrest (TCA) with hypothermia in open heart surgery is associated with a risk for brain ischemia. We studied cerebral energy metabolism in 8 patients (0.02-1.17 yr) undergoing TCA (7-56 min) by measuring degradation products of ATP, ie. hypoxanthine (HX) and xanthine (X), in simultaneously collected v. jugularis bulb and arterial samples. Before TCA the gradient of HX across the cerebral circulation (v. jugularis bulb - artery) was 0.32 ± 0.53 and that of X was 0.28 ± 0.40 μmol/l. After reconstitution of cerebral circulation (=reperfusion) the gradient remained unchanged at 2, 7 and 15 min, whereas significant (p<0.05) increases were found at 30 min (HX: 2.67 ± 1.27 μmol/l), 60 min (HX: 3.44 ± 1.08, X:1.76 ± 0.39), and 120 min (HX: 1.83 ± 1.21, X: 0.95 ± 0.50). At 6 and 10 h after reperfusion the gradients had disappeared. During rewarming (≅30 min after reperfusion) correlations existed between nasopharyngeal temperature and gradients of HX(R=0.50, p=0.006) and X (R=0.43, p=0.018). During 2 h after reperfusion an inverse correlation was found between HX gradient and hemoglobin oxygen saturation in jugular bulb (R=0.36, p=0.029). TCA causes a cerebral energy debt that increases in parallel with rise in body temperature and culminates at the end of the rewarming period. The magnitude of the energy debt may be indicative of cerebral ischemia and damage.