Effets du vieillissement et de divers agents pharmacologiques sur le métabolisme énergétique cérébral au cours de la récupération post-hypoglycémique chez le rat

Severe acute hypoglycaemia with isoelectric electroencephalogram induces a major deterioration of the energy state and amino acid contents of the brain. During post-hypoglycaemia recovery of adult animals, brain glucose concentrations return to normal values, whereas glycogen turnover remains low as aspartate and pyruvate concentrations increase. ATP levels rise, but the adenine-nucleotide pool remains small despite return to normal of ADP and AMP. Brain phosphocreatine levels return to normal values, with reciprocal changes in creatine content. In adult rats one also notes during recovery an increase in brain glutamine and glutamate, whereas the gamma-aminobutyrate returns to normal. Finally, ammonium and aspartate remain below, and alanine remains above normal values. Aging has no effect on cerebral metabolic disturbances induced by hypoglycaemia, but it influences the cerebral metabolic restoration processes that develop during post-hypoglycaemia recovery. The restitution of cerebral metabolites is weaker in mature and senescent rats than in adult rats. In the oldest rats, in particular, the concentrations of most of the amino acids and of adenyl nucleotides remain largely abnormal. The effects of dihydroergocristine, erbunamonine, raubasine, almitrine and of the almitrine-raubasine combination on post-hypoglycaemia recovery were evaluated in adult, mature and senescent rats. During recovery these pharmacological agents exert different effects on glycolytic metabolites, amino acids and energy-rich phosphates