Mild brain ischemia increases cerebral lipid peroxidation and activates leukocytes in the peripheral blood of rats.

This study evaluated local and systemic leukocyte changes, respectively in the jugular and femoral veins, after an acute reduction of cerebral blood flow (oligoemia) in rats submitted either to permanent bilateral carotid occlusion (BCO) (no. = 36) for 5 hours or to sham operation (no. = 33). In a subgroup of rats (no. = 13) the extent of neural damage was histologically assessed. As a marker of biochemical brain changes the entity of the iron-ascorbate induced lipid peroxidation of synaptosomes was assessed in vitro by measuring malondialdehyde (MDA) reactive products. Five hours after surgery, the percentage of aggregated leukocytes and of activated neutrophils reducing the NBT were significantly higher in BCO rats (p < 0.05). However, leukocyte changes did not differ significantly between the jugular and the femoral districts. The brains of BCO rats showed tiny foci of neuronal necrosis. Synaptosomes obtained from the BCO animals showed a small but highly significant increase of MDA production (p < 0.01). Long-lasting brain oligoemia increases the production of lipid peroxidative metabolites, and causes the occurrence of tiny foci of neuronal necrosis in different brain regions. The lack of a significant gradient in aggregated leukocytes and activated neutrophils between the jugular and femoral venous districts demonstrates that leukocytes are stimulated in the peripheral blood by even mild biochemical and morphological brain damage.