Status epilepticus in immature rats. Protective effects of glucose on survival and brain development.
The role of glucose metabolism in alleviating the complications of status epilepticus (SE) was investigated in developing rats. Pretreatment with glucose reduced mortality from SE by 90% in rats under 1 week of age, 80% in 10-day-old rats, 50% in 15- to 20-day-olds, and not at all in adults. In 4-day-old animals, brain DNA synthesis during seizures, and in survivors, brain weight, DNA, RNA, protein, and cholesterol contents at 7 days of age were reduced less in glucose-treated than in saline-treated littermates. In the saline group, seizures caused a progressive fall in brain glucose level but no fall in blood glucose level, suggesting that glucose transport from blood to brain could not keep pace with glycolytic demands. In glucose-treated rats, blood and brain glucose concentrations remained elevated throughout the convulsive period. There was no reduction of brain adenosine triphosphate levels in either group. Thus, the protection by glucose appears to be related to its roles as a carbon source rather than an energy source. It is concluded that in immature animals, depletion of brain glucose can occur in the absence of hypoglycemia, and may be an important and potentially treatable complication of status epilepticus.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000367:Age Factors; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001921:Brain / Q000254:growth & development* / Q000378:metabolism; D004247:DNA / Q000096:biosynthesis; D005947:Glucose / Q000378:metabolism / Q000627:therapeutic use*; D007773:Lactates / Q000378:metabolism; D010101:Oxygen Consumption; D051381:Rats; D012640:Seizures / Q000188:drug therapy* / Q000401:mortality / Q000503:physiopathology
D001786:Blood Glucose; D007773:Lactates; D000255:Adenosine Triphosphate; D004247:DNA; D005947:Glucose