It is now well recognized that the central events resulting in cellular injury following periods of tissue ischaemia occur primarily on re-oxygenation. This injury is inflammatory in nature and is mediated in large part through the generation of reactive and toxic metabolites of oxygen. Therapeutic strategies based on anti-oxidant administration have shown great promise in experimental models of traumatic brain injury and cerebral ischaemia-reperfusion; however, these treatments have not yet translated into the significant improvements in clinical outcome that were expected. Issues of patient selection, endpoint evaluation and the temporal relationship of brain injury and drug delivery contribute to the difficulty in extrapolating what appear to be proved scientific concepts in the experimental setting to useful treatment strategies in the clinical arena. However, efforts in this field are ongoing, and eventual clinical advances will doubtless be based on basic scientific investigation in the pre-clinical and experimental setting.
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Siddiqi et al. (1996) studied this question.
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