THE ELECTROCONVULSIVE THRESHOLD AND CEREBRAL METABOLISM DURING STARVATION IN THE ADULT RAT
| Autor: | Arthur L. Prensky, Kenneth L. Malas, Mary P. Leckie, Darryl C. DeVivo |
|---|---|
| Rok vydání: | 1974 |
| Předmět: |
Starvation
medicine.medical_specialty business.industry Sodium medicine.medical_treatment Potassium chemistry.chemical_element Ouabain Endocrinology chemistry Internal medicine Pediatrics Perinatology and Child Health Ketone bodies medicine Glycolysis medicine.symptom Energy charge business Ketogenic diet medicine.drug |
| Zdroj: | Pediatric Research. 8:463-463 |
| ISSN: | 1530-0447 0031-3998 |
| DOI: | 10.1203/00006450-197404000-00736 |
| Popis: | Brief fasting raises the convulsive threshold in the human. This clinical observation led to the use of a ketogenic diet in epilepsy. To study the mechanism underlying this observation, the electroconvulsive threshold (ECT) of adult rats was determined before fasting and at 24, 48 and 72 hours after food deprivation. The ECT was unchanged at 24 hours, rising at 48 hours (p < .05) and 72 hours (p < .01). During starvation blood glucose levels fell and blood ketone bodies rose with similar changes, respectively, in brain tissue. Brain sodium levels were slightly higher at 24 and 72 hours and unchanged at 48 hours whereas brain potassium levels gradually rose at 48 hours (p < .10) and at 72 hours (p < .025). Brain water content was relatively constant. Ouabain sensitive and insensitive ATPase activity remained unchanged. Glucose-6-phosphate levels rose at 48 and 72 hours whereas malate fell progressively throughout fasting. Lactate and pyruvate levels fell initially then rose and the L/P ratio fell steadily from 12.7 to 10.9. The adenylate pool and Pi remained constant but the cerebral energy charge potential and the phosphorylation state rose at 48 and 72 hours (p < .05). The cerebral energy reserve remained constant. These observed changes are felt to be the consequence of increasing utilization of ketone bodies for cerebral oxidative metabolism with a secondary depression in glycolysis. The rise in brain potassium may reflect this increased utilization of anions and explain the rise in the electroconvulsive threshold. |
| Databáze: | OpenAIRE |
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