Seven-day postnatal rats were subjected to unilateral common carotid artery ligation, 3 h after which they were subjected to hypoxia with 8% oxygen at 37°C for 2 h. Thereafter, they received multiple s.c. injection(s) of bicuculline (6 mg/kg) adequate to produce behaviorally apparent siezures lasting greater than 1 h (status epilepticus). Repeated episodes of status epilepticus at 2, 6, and 12 h of recovery from hypoxia-ischemia (III) produced a mortality rate of 53%. Among the survivors, there was no statistically significant difference in the extent of brain damage between convulsing and nonconvulsing HI controls, analyzed at 30 d of age. Histopathologic examination for acute lesions also indicated no difference in the severity of brain damage between dead and surviving rat pups subjected to status epilepticus, indicating that mortality was not related to the severity of prior HI brain damage. Those immature rats that died during status epilepticus exhibited lower blood glucose concentrations (1.75 ± 0.35 mmol/L) compared with surviving, convulsing animals (4.25 ± 0.51 mmol/L;p- 0.016). Glucose supplementation (0.1 mL of 50% glucose) early during status epilepticus improved survival and significantly prolonged scizure activity (90 ± 14 min) compared with nonglucose treated, convulsing littermates (47 ± 10 min;p- 0.02). Glucose supplementation did not increase the extent of brain damage despite improved survival and increased duration of seizure activity. The findings indicate that even repetitive episodes of status epilepticus in immature rats previously subjected to cerebral HI do not accentuate brain damage despite a substantial mortality. Hypoglycemia contributes to death arising from status epilepticus, and both survival and seizures can be prolonged by glucose supplementation without risk of increasing the severity of any existing brain damage.