The experiments performed here are currently based on the hypothesis that oxygen radicals generated as a result of central nervous systems (CNS) injury and/or ischemia contribute to pathogenesis, at least in part, by altering endothelial membrane integrity. Due to the limited availability of cultured cerebrovascular endothelial cells (EC) which constitute the blood-brain barrier (BBB), only a minimal number of experiments were able to be performed under this project title. However, these experiments demonstrated that oxygen free radicals such as superoxide anion (.O2-) and hydroxyl (OH-) generated by EC may be responsible for alterations in BBB permeability known to occur in neuropathologic disorders such as stroke.
