TY - JOUR
T1 - Effect of status epilepticus on hypoxic-ischemic brain damage in the immature rat
AU - Cataltepe, Oguz
AU - Vannucci, Robert C.
AU - Heitjan, Daniel F.
AU - Towfighi, Javad
PY - 1995/8
Y1 - 1995/8
N2 - 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 sie/.ures 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 seizure 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 III 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.
AB - 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 sie/.ures 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 seizure 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 III 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.
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U2 - 10.1203/00006450-199508000-00019
DO - 10.1203/00006450-199508000-00019
M3 - Article
C2 - 7478824
AN - SCOPUS:0029082598
SN - 0031-3998
VL - 38
SP - 251
EP - 257
JO - Pediatric Research
JF - Pediatric Research
IS - 2
ER -