In physiological conditions blood glucose concenration (80-90 mg/dl) is maintained through highly regulated systemic mechanisms. Disruption of, these mechanisms leads to hypoglycemia, whose decreases to levels lower to 20 mg/dl blocks the electrical activity of the brain. This condition is known as hypoglycemic coma and can be overcome by intravenous administration of glucose. Subsequently to the hypoglycemic episode, it occurs brain damage determined by the high dependency of brain on glucose blood supply, which is the main energy source necessary for its normal functioning. Many neuronal functions are compromised during energy failure such as the maintenance of ionic gradients, the release and reuptake of neurotransmitters, the intracellular buffering of calcium, and the mitochondrial function. Excitotoxical glutamate activity in hypoglycemic neuronal damage is well documented, and a role of oxidative stress in this process has recently raised. The contribution of these processes to hypolgycemic brain damage is the main subject of this review. ©INNN, 2005.
Última actualización: 06/12/2021