diphenylhexatriene and Ischemic-Attack--Transient

Light-microscopical studies revealed that oligemic hypoxia for 24 and 60 min as produced by bilateral clamping of the carotid arteries (BCCA) in normotension does not produce neuronal cell necrosis in the vast majority of rat brain. Less than 5% of cases showed a pattern of mild selective neuronal necrosis as would be expected in ischemia. However, significant changes in both lipid peroxidation (as measured by MDA formation) and membrane anisotropy (measured by DPH or TMA-DPH, respectively, as a fluorescence probe) in cortical and striatal, but not in hippocampal, membrane fractions could be measured in ex vivo studies. Twenty-four and 60 min of BCCA without reperfusion decreased lipid peroxidation in the cerebral cortex but not in the striatum. BCCA, either for 24 or 60 min, and 60 min of reperfusion produced no changes in lipid peroxidation in either structure. However, 24 and 60 min of BCCA followed by 14 days of reperfusion led to a significant increase in MDA formation in the striatum, while lipid peroxidation in the cortex was only increased after 60 min of BCCA. Cortical as well as striatal membrane anisotropy increased significantly 14 days later in rats submitted to BCCA for 24 or 60 min. The study shows an increased lipid peroxidation 2 weeks after a transient reduction in cerebral blood flow although no neuronal necrosis could be observed in general.

Topics: Animals; Brain; Cell Membrane; Cerebral Cortex; Corpus Striatum; Diphenylhexatriene; Fluorescence Polarization; Fluorescent Dyes; Ischemic Attack, Transient; Lipid Peroxidation; Male; Malondialdehyde; Rats; Rats, Wistar; Time Factors