[Cell membrane alterations during situations of acute stress to the cerebral parenchyma. Mechanisms, consequences and therapeutic perspectives].

Marked alterations to phospholipid structures of the different cell membranes can be clearly demonstrated on experimental models during acute or subacute cerebral aggression . Tissues surrounding hematomas, traumatic lesions, infective zones and certain tumors undergo autocatalytic peroxidation which attacks fatty acid chains that include double bonds. Intracellular invasion of ischemic foci by calcium, related to the energy deficit, activates phospholipases which liberate the same fatty acids. These lipidic disorders greatly alter membrane functions, particularly inactivating protein enzymes essential for maintenance of ionic gradients. Certain degradation products liberated disorganize other cell functions. The edema and microcirculation disorders that are characteristic of these focal lesions and are responsible for their invasive nature appear finally to be the consequences of membrane damage. The extent of membrane injury can be limited by various treatments, each possessing their time constant and specificity of biochemical action: the barbiturates could "protect", the corticoids "stabilize" and the metabolic precursors of the phospholipids "restore" membranes attacked in this way.