The effect of ischemia and recirculation, hypoxia and recovery on anti-oxidant factors and β-adrenoceptor density: Is the damage in the erythrocytes a reflection of brain damage caused by complete cerebral ischemia and by hypoxia?

Abstract

This investigation was focussed on the gravity of tissue injury caused by complete ischemia (for five min) and hypoxia (for three weeks) in the cerebral cortex (homogenate) and the erythrocyte lysate or the erythrocyte membrane of the rat in order to investigate if the changes that occur in brain tissue are reflected in the erythrocyte. To this end, glutathione (GSH), superoxide dismutase (SOD) and catalase were measured, also alterations in β-adrenoceptor density under these two conditions were examined. It was found that in ischemia partial parallellism in changes that occur in the central nervous system (cerebral cortex) and the erythrocyte exists. The SOD activity became higher and the β-adrenoceptor density (measured as specific (−)-[ 125I] iodocyanopindolol binding) was decreased in both tissues. However after the hypoxic condition we established a decrease in the number of β-adrenoceptors in the cerebral cortex but an increase in β-adrenoceptor density in the erythrocyte.