Central nervous system trauma and stroke. II. Physiological and pharmacological evidence for involvement of oxygen radicals and lipid peroxidation

The previous article outlined the biochemical basis and evidence for the occurrence of oxygen radical generation and lipid peroxidation during the acute phase of central nervous system (CNS) trauma or stroke (ischemic and hemorrhagic). The identification of oxygen radicals and lipid peroxidation as important pathophyiological mediators of trauma or stroke-induced neural degeneration, rather than simply epiphenomena, depends upon the successful demonstration of their association with actual secondary physiological and structural degenerative events. Moreover, their significance in the pathophysiology of CNS trauma or stroke must be supported by experimental observations that pharmacological antagonism of either oxygen radical generation and/or lipid peroxidation results in a therapeutic effect (i.e., interruption of seconadry nervous tissue degeneration). Indeed, recent investigations have provided compelling evidence for the view that oxygen radical-mediated processes play a key pathophysiological role during the acute phase of CNS trauma or stroke. Furthermore, their pharmacological manipulation may serve as an avenue for the therapeutic attempts aimed at limiting neural degeneration and improving neurological recovery.