[Neurochemical changes associated with ischemic-reperfusion injury of the CNS]

Ischaemia-reperfusion injury of the central nervous system is the third leading cause of death in the European countries. Since nerve cells are exclusively dependent on glucose oxidation, reduction of the glucose and oxygen delivery to the neurons affect all cellular metabolic pathways. Decrease of ATP production and its concentration as well as activation of ionic gradients, seems to be a primary process. Several degrading cellular enzymes, as lipases, phospholipases, proteases and endonucleases, are activated, in contrast to the severe inhibition of protein and phospholipid synthesis. Signal transduction pathways, playing a role in the regulation of cellular metabolism, are depressed due to the energy deprivation. After certain time of ischaemia, reperfusion does not lead to restoration of normal cell metabolism and intracellular situation could be even worsen, depending on the neuron type and duration of ischaemic period. Inhibition of glucose oxidation, decrease of ATP concentration, inhibition of proteosynthesis and signal transduction disturbances were observed during the period of reperfusion. Despite of proteosynthesis inhibition, several proteins, especially transcription and growth factors are overproduced. The loss of intracellular homeostasis, as the consequence of the above mentioned processes, could lead to neuronal death.