Cerebral neuroprotection and ketamine

摘要: Ketamine is said to increase intracranial pressure (ICP), cerebral blood flow (CBF) and metabolic rate for oxygen (CMRO2) hence be unsuitable neuroanaesthesia. This may require reconsideration in the light of neuroprotective properties mediated by interaction ketamine with N-methyl-D-aspartate receptor (NMDA). Meta-analysis published experimental rodent studies yields contradictory conclusions. does not provide neuroprotection against hypoxic hypoxaemia or focal ischaemia. During complete forebrain ischaemia 10 min duration, offers some degree protection only if administered before (i.e. prophylactically) after therapeutically) a transient ischaemic episode. In head injury, protective therapeutically within 2 h trauma. case incomplete ischaemia, provides both during Clinical primate are available; extrapolation results derived from requires caution has limitations. With respect pharmacodynamic action providing neuroprotection, NMDA-receptor antagonism just one several mechanisms; others include scavenging free radicals, central sympatholytic effect augmentation dopamine metabolism caudate. The suitability neuroanaesthesia, which must also take account its effects on ICP, CBF CMRO2, is--for time being--questionable.