Neuroprotective effects of anaesthetic agents.

During cerebral ischaemia, energetic failure of injured cells together with excessive release of glutamate the most common excitatory amino acid in th e brain, lead to excitotoxicity and immediate or delayed neuronal death. Th ere is strong experimental evidence to support the neuroprotective role pla yed by anaesthetic agents. Hence, barbiturates, volatile anesthetics or ket amine exhibit significant protective effects against ischaemic injury in nu merous experimental models of ischaemia in vitro or in vivo. The neurobiolo gical substrate of this action is probably a reduction of the activity of g lutamate receptors (N-methyl-D-aspartate and kainate), and/or downstream bi ochemical events. Reduction of cerebral metabolism by these agents seems no t to be their primary neuroprotective mechanism. However, no data are avail able at the present time to support any clinical benefit of these actions i n neurosurgical patients, head trauma in contrast to mild hypothermia or ce rebrovascular disease. Future research should develop models as close as po ssible to the clinical situation to examine further pathophysiological hypo theses and clinical implications. (C) 1999 Elsevier, Paris.