Corticosterone-aggravated ischemic neuronal damage in vitro is relieved by vanadate.
Preischemic hyperglycemia-aggravated neuronal damage has been postulated to occur via enhanced lactic acidosis. We have hypothesized that preischemic glucose loading induces a short-lived elevation in glucocorticoid release which, when combined with ischemia, aggravates the postischemic outcome. This study tested this hypothesis in rat hippocampal slices exposed to 4 min in vitro ischemia of which 58% exhibited recovery of neuronal function. However, when corticosterone (CT) was present during ischemia, the recovery of neuronal function decreased in a concentration-dependent manner. At 5 microM, CT reduced the recovery rate to 40% while only 10% of slices recovered when exposed to 20 microM CT. Insulin could not block the effect of CT; however, vanadate improved the postischemic recovery of CT-treated (20 microM) slices to 43%. These results indicate that acute, short exposure to CT can significantly exacerbate postischemic outcome and that vanadate can antagonize CT action.
Payne
R S
RS
Brain Attack Research Laboratory, Department of Anesthesiology, University of Louisville School of Medicine, Louisville, KY 40292, USA.
Schurr
A
A
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000009:adverse effects*; D002545:Brain Ischemia / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology*; D015687:Cell Hypoxia / Q000187:drug effects; D003345:Corticosterone / Q000009:adverse effects*; D004305:Dose-Response Relationship, Drug; D005947:Glucose / Q000172:deficiency; D006624:Hippocampus / Q000187:drug effects*; D066298:In Vitro Techniques; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D014638:Vanadates / Q000627:therapeutic use*
D000893:Anti-Inflammatory Agents; D014638:Vanadates; D005947:Glucose; D003345:Corticosterone