Hyperglycemia does not augment neuronal damage in experimental status epilepticus.
The neuronal regions affected and the neuropathologic features of ischemia and status epilepticus are similar. Experimentally, elevated plasma glucose levels, increasing brain lactate, are associated with more severe neuropathologic damage from cerebral ischemia. We therefore studied the cytologic features and cerebral content of lactate and glucose in the selectively vulnerable neurons of rat hippocampus after 2 hours of L-allylglycine-induced status epilepticus in rats with mean plasma glucose concentrations of 65, 250, and 480 mg/100 ml. Brain lactate concentration was elevated in status and maximal in the high-glucose group, but the maximum levels (8 mumol/g) were less than those thought to augment cell death in ischemia. Using multiple linear regressions, only time-in-status predicted neuropathologic damage.
D000818:Animals; D001921:Brain / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D006943:Hyperglycemia / Q000150:complications* / Q000378:metabolism; D007773:Lactates / Q000378:metabolism; D019344:Lactic Acid; D008297:Male; D009474:Neurons / Q000473:pathology*; D051381:Rats; D011919:Rats, Inbred Strains; D013226:Status Epilepticus / Q000150:complications* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology
D007773:Lactates; D019344:Lactic Acid; D005947:Glucose