[Physiopathology of cerebral ischemia]

This article reviews the most currently used experimental models of cerebral ischaemia. Mechanisms involved in ischaemic neuronal death are considered at the tissue, cellular and molecular levels. The various steps of the excitotoxic cascade induced by anoxic depolarization in conditions of energy failure are analyzed, from excessive glutamate release to intracellular calcium accumulation, massive calcium-dependent enzyme activation, and the formation of oxygen radicals. Apoptotic neuronal death is also discussed, which leads one to distinguish between genes whose expression is beneficial or deleterious in ischaemic conditions. Finally, the putative causes of contradictory results obtained from pharmacological studies in animals and humans are discussed.