Effect of insulin hypoglycemia upon cerebral energy metabolism and EEG activity in the rat.
Anesthetized ventilated rats were subjected to insulin-induced hypoglycemia (50 units/kg i.v.) while EEG, ECG, mean arterial pressure, blood gases, arterial pH and rectal temperature were controlled. Animals were sacrificed by rapid transcalvarial freezing of the brain in situ. Glucose, pyruvate and lactate were measured in blood, CSF and cortical tissue, in which additionally glycogen, phosphocreatine, ATP, ADP, AMP, aketoglutarate (aKG), glutamate, oxalacetate, aspartate, ammonia and water content were estimated. ATP/ADP ratio, energy charge (ECh) energy reserve, NADH/NAD+ quotient and intracellular pH were calculated. ECh does not correlate with either dysfunction of carbohydrate depletion, but declines in a threshold fashion when tissue glucose has fallen by over 97% and glycogen by over 60%. The EEG correlates with the degree and duration of carbohydrate depletion in cortical tissue. An isoelectric EEG occurs pari passu with the fall of the ECh. Increase in ammonia and decrease in aKG and Glut are supportive evidence of intrinsic substrate. Lactate decrease during hypoglymecia is not reversed by super-imposed hyqoxia.
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001831:Body Temperature; D001921:Brain / Q000187:drug effects* / Q000378:metabolism; D002245:Carbon Dioxide / Q000097:blood; D004569:Electroencephalography; D004734:Energy Metabolism / Q000187:drug effects*; D005947:Glucose / Q000134:cerebrospinal fluid / Q000378:metabolism; D007003:Hypoglycemia / Q000139:chemically induced* / Q000378:metabolism; D000860:Hypoxia / Q000378:metabolism; D007328:Insulin / Q000494:pharmacology*; D008297:Male; D010710:Phosphates / Q000378:metabolism; D051381:Rats; D013997:Time Factors
D001786:Blood Glucose; D007328:Insulin; D010710:Phosphates; D002245:Carbon Dioxide; D005947:Glucose