Nitric oxide changes in adult rat brain after transient global ischemia

Nitric oxide (NO), has recently emerged as an important mediator of cellular events which impacts the pathophysiology of cerebral ischemia. Using electrochemical microsensors, we measured the cortical NO concentration within ischemic tissue before and during 3 min. of airway occlusion (asphyxia) and during reperfusion in adult rats (n=6). Baseline concentrations of NO were 1.89/spl plusmn/0.33 /spl mu/M. The maximum concentrations of NO during asphyxia and on reperfusion were 5.15/spl plusmn/0.45 /spl mu/M and 6.50/spl plusmn/0.24 /spl mu/M, respectively. A novel method (cepstral distance) was used to quantify changes in EEG due to brain injury. Our data indicates that excess NO is released in the brain after the onset of ischemia. Its restoration to baseline appears to impact recovery of the brain's electrical function as measured by EEG. Animals (n=2) in which NO did not return to baseline value had isoelectric EEG and showed no sign of recovery.