| Literature DB >> 20974112 |
Alessandro Viggiano1, Emanuela Viggiano, Ilaria Valentino, Marcellino Monda, Andrea Viggiano, Bruno De Luca.
Abstract
Cortical spreading depression (CSD) is a reversible electrophysiological phenomenon that is not associated with tissue damage under normal blood supply. The induction of CSD during ischemia causes an increase in tissue damage, while pre-conditioning with CSD decreases the damage induced by a subsequent episode of ischemia. The mechanisms underlying these effects are not clear. Because the production of reactive oxygen species (ROS) is involved in tissue damage during ischemia-reperfusion, the aim of the present study was to evaluate the effects of CSD on superoxide production (O(2)(-)), on hydrogen peroxide (H(2)O(2)) production and on superoxide dismutase (SOD) activity in the cerebral cortex. CSD was induced by KCl application on the cortical surface in rats. O(2)(-) production was evaluated using dihydroethidium (DHE) that is oxidized to the fluorescent dye ethidium (HEt) by O(2)(-). The extracellular level of H(2)O(2) was evaluated by microdialysis sampling and HPLC analysis. SOD activity was evaluated with a histochemical assay. The results showed an increase in H(2)O(2) production, an increase in SOD activity and a decrease in O(2)(-) concentration 1h after CSD induction. Copyright ÂEntities:
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Year: 2010 PMID: 20974112 DOI: 10.1016/j.brainres.2010.10.062
Source DB: PubMed Journal: Brain Res ISSN: 0006-8993 Impact factor: 3.252