Elevation of jugular venous superoxide anion radical is associated with early inflammation, oxidative stress, and endothelial injury in forebrain ischemia-reperfusion rats.

A novel electrochemical sensor was used in this study to determine the correlations between jugular venous O(2)(-) and HMGB1, malondialdehyde (MDA), and intercellular adhesion molecule-1 (ICAM-1) in rats with forebrain ischemia/reperfusion (FBI/R). Twenty-one male rats were divided into a Sham group, a hemorrhagic shock/reperfusion (HS/R) group, and a forebrain ischemia/reperfusion (FBI/R) group. The O(2)(-) sensor in the jugular vein detected the current derived from O(2)(-) generation (abbreviated as "O(2)(-) current"), which was integrated as the partial value of quantified electricity during ischemia (Q(I)) and after reperfusion (Q(R)). The plasma O(2)(-) current showed a gradual increase during forebrain ischemia in the HS/R and the FBI/R groups. The current showed a marked increase immediately after reperfusion and continued for more than 60 min in the FBI/R group. In the HS/R group, the current was gradually attenuated to the baseline level. Brain and plasma HMGB1 increased significantly in the FBI/R group compared with those in the Sham and the HS/R groups, and both brain and plasma HMGB1 correlated significantly with the sum of Q(I) and Q(R) (total Q). Brain and plasma MDA and plasma soluble ICAM-1 also correlated significantly with total Q. Here, we report the correlation between O(2)(-) and HMGB1, MDA, and sICAM-1 in rats with cerebral ischemia-reperfusion, using a novel electrochemical sensor. These data indicated that excessive production of O(2)(-) after ischemia-reperfusion was associated with early inflammation, oxidative stress, and endothelial activation in the brain and plasma, which might enhance the ischemia-reperfusion injury.