Oxygen radicals in brain injury.

Abstract

Experimental fluid percussion brain injury in anesthetized cats causes vascular injury characterized by sustained arteriolar dilation, abnormal reactivity to vasoconstrictor and vasodilator interventions, focal endothelial lesions, and reduction of the oxygen consumption of the vessel wall. These abnormalities are minimized or completely inhibited by pretreatment with cyclooxygenase inhibitors or with oxygen radical scavengers. They were therefore ascribed to oxygen radicals generated in the course of accelerated arachidonate metabolism via cyclooxygenase. Following this type of brain injury, there is an increase in the activity of phospholipase c in the brain and a transient increase in brain concentration of prostaglandins. Superoxide anion radical was detected in the extracellular space of the brain both immediately following brain injury as well as one hour afterwards as the superoxide dismutase inhibitable portion of nitroblue tetrazolium reduction. The sustained dilation and abnormal reactivity of cerebral arterioles following brain injury were also reversed by superoxide dismutase and catalase applied on the brain surface 30 minutes after injury. These results suggest that treatment with oxygen radical scavengers might be effective in inhibiting or reversing some of the effects of brain injury, even though the intervention with the therapeutic agents occurs sometime after the injury has taken place.