Abstract
Cerebral ischemia was induced in anesthetized rats by occluding both common carotid arteries; the vertebral arteries had been permanently occluded one day earlier. The levels of lipid-soluble antioxidants (alpha-tocopherol, reduced ubiquinones), free fatty acids and energy metabolites were measured in forebrain tissue after 30 min of ischemia, and after 15 min or 30 min of postischemic recirculation. Alpha-tocopherol decreased by 7% at the end of ischemia and decreased further during postischemic recirculation, indicating that free radical reactions were initiated during ischemia. All measured saturated, mono- and polyunsaturated free fatty acids accumulated markedly during ischemia. However, particularly rapid decrements were observed in polyunsaturated free fatty acids (arachidonic and docosahexaenoic acids) during an initial 15-min period of recirculation, while other free fatty acids gradually returned toward their preischemic levels after 30 min of recirculation. Both reduced and oxidized ubiquinone-9 tended to increase at the end of ischemia. During recirculation, reduced ubiquinone-9 declined below control by 20–24%,accompanied by a rise in the oxidized form. Profiles of free fatty acids and the changes in ubiquinones were compatible with the postischemic occurrence of lipid peroxidation. High energy phosphates were nearly depleted by ischemia, and recovery of adenosine triphosphate was limited to 73% of control after 30 min of recirculation. The results are compatible with the view that free radical reactions are initiated during ischemia, and that overt peroxidative processes become manifest during reflow when cerebral tissue is reoxygenated. Lipid peroxidation by free radical reactions may be a factor restricting postischemic recovery of energy metabolism, and lipid-soluble antioxidants may act to mitigate the extent of eventual brain damage.
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