• J Mantz.
• Service d'anesthésie et de réanimation chirurgicale et inserm U 408, hôpital Bichat, Paris, France.
• Ann Fr Anesth Reanim. 1999 May 1; 18 (5): 588-92.

AbstractDuring cerebral ischaemia, energetic failure of injured cells together with excessive release of glutamate the most common excitatory amino acid in the brain, lead to excitotoxicity and immediate or delayed neuronal death. There is strong experimental evidence to support the neuroprotective role played by anaesthetic agents. Hence, barbiturates, volatile anesthetics or ketamine exhibit significant protective effects against ischaemic injury in numerous experimental models of ischaemia in vitro or in vivo. The neurobiological substrate of this action is probably a reduction of the activity of glutamate receptors (N-methyl-D-aspartate and kainate), and/or downstream biochemical events. Reduction of cerebral metabolism by these agents seems not to be their primary neuroprotective mechanism. However, no data are available at the present time to support any clinical benefit of these actions in neurosurgical patients, head trauma in contrast to mild hypothermia or cerebrovascular disease. Future research should develop models as close as possible to the clinical situation to examine further pathophysiological hypotheses and clinical implications.

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