Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
6265601 | Brain Research | 2009 | 11 Pages |
A novel electrochemical sensor was used in this study to determine the correlations between jugular venous O2â 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 O2â sensor in the jugular vein detected the current derived from O2â generation (abbreviated as “O2â current”), which was integrated as the partial value of quantified electricity during ischemia (QI) and after reperfusion (QR). The plasma O2â 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 60Â 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 QI and QR (total Q). Brain and plasma MDA and plasma soluble ICAM-1 also correlated significantly with total Q. Here, we report the correlation between O2â and HMGB1, MDA, and sICAM-1 in rats with cerebral ischemia-reperfusion, using a novel electrochemical sensor. These data indicated that excessive production of O2â 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.