Anoxic Injury of Endothelial Cells Increases Production of Nitric Oxide and Hydroxyl Radicals

摘要: Abstract Reactive oxygen radicals have been implicated as mediators of anoxic injury in brain, but the cellular source these is unknown. In periphery, there evidence that endothelial cells play a fundamental role tissue injury. The objective present study was to examine response rat brain anoxia/reoxygenation vitro . results demonstrate produce hydroxyl and increased nitric oxide synthase activity after production cerebral does not appear be mediated by an increase either inducible or constitutive synthase. radical trap α-phenyl- tert -butyl nitrone blocked free production, oxide. These data suggest microcirculation may important site ischemic stroke.