Insulin-induced hypoglycemic coma and regional cerebral energy metabolism.
Swiss-Albino female mice weighing 20 g were rendered hypoglycemic by injecting insulin (2 units/kg). Animals were sacrificed at 40 min (pre-coma), 2 h (coma) and 4.5 h (recovery) after insulin injection by rapid submersion in liquid N2. Following sectioning at 20 micrometer, samples from the ascending reticular activating system and the inferior colliculus were freeze-dried and assayed for glucose, lactate, ATP and phosphocreatine (PCr). There was a preferential effect of hypoglycemia on ATP and PCr in cells of the ascending reticular activating system. ATP was depleted 30%, and PCr 55% in the pre-coma stage. ATP and PCr in cells from the inferior colliculus were not decreased. This selective effect on cells of the ascending reticular activating system followed by coma suggests that the coma per se may not represent total failure of the organism, but rather a compensatory mechanism designed to permit the animal to correct its compromised energy status.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000378:metabolism*; D004734:Energy Metabolism / Q000187:drug effects*; D005260:Female; D005947:Glucose / Q000378:metabolism; D007003:Hypoglycemia / Q000378:metabolism*; D007328:Insulin / Q000494:pharmacology*; D007331:Insulin Coma / Q000378:metabolism*; D007700:Kinetics; D007773:Lactates / Q000378:metabolism; D051379:Mice; D009928:Organ Specificity; D010725:Phosphocreatine / Q000378:metabolism
D007328:Insulin; D007773:Lactates; D010725:Phosphocreatine; D000255:Adenosine Triphosphate; D005947:Glucose