[Cerebral edema: intra-cellular or extra-cellular mechanisms?].
Many cerebral pathological processes are attended by edema defined as an increase in brain volume associated with an increase in brain water and sodium contents. The aggravation of lesions induced by this edema warrants a pharmacological and therapeutic approach based on a detailed knowledge of its physiopathological mechanisms. Experimental models and in vitro studies have shown that the fundamental mechanisms leading to edema are: cold, acute hypoxia, ischaemia, arachidonic acid, toxic substances and plasma hypo-osmolarity. To the various types of edema described (vasogenic, cytotoxic, hydrocephalic) correspond different mechanisms. Vasogenic edema essentially depends on osmotic and hydrodynamic factors; cytotoxic edema results from perturbations in energy-dependent cellular osmoregulation. The underlying biochemical disorders have now been demonstrated, mostly in ischaemic edema; they include, during the revascularization phase, disruption of the blood-brain barrier (vasogenic component) and changes in ion concentrations, neurotransmitters and energetic mechanisms. Key factors in the development of edema are cyclic AMP, serotonin and Na-K-ATPase.
D000818:Animals; D001812:Blood-Brain Barrier; D001834:Body Water / Q000378:metabolism; D001929:Brain Edema / Q000145:classification / Q000209:etiology* / Q000378:metabolism; D002118:Calcium / Q000378:metabolism; D002712:Chlorides / Q000378:metabolism; D000242:Cyclic AMP / Q000378:metabolism; D006801:Humans; D007511:Ischemia / Q000150:complications; D009995:Osmosis; D011188:Potassium / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism
D002712:Chlorides; D000242:Cyclic AMP; D000254:Sodium-Potassium-Exchanging ATPase; D011188:Potassium; D002118:Calcium
L'oedème cérébral: mécanisme intra-cellulaire ou extra-cellulaire?