Brain lipid peroxidation and antioxidant levels in fetal lambs 72 hours after asphyxia by partial umbilical cord occlusion.

OBJECTIVES: The purpose of this study was to explain the role of oxidative stress in the pathogenesis of brain damage caused by intrauterine fetal asphyxia. STUDY
DESIGN: Six chronically instrumented near-term fetal lambs were subjected to asphyxia by partial umbilical cord occlusion for approximately 60 minutes until fetal arterial pH diminished to less than 6.9 and base excess to less than -20 mEq. Another six fetuses surgically prepared but not occluded were used as control. Fetuses were killed after 72 hours and eight different brain regions (frontal and parietal gray matter, frontal and parietal white matter, basal ganglia, thalamus, hippocampus, and cerebellum) were dissected and assayed for thiobarbituric acid reactive substances, glutathione, and superoxide dismutase.
RESULTS: Thiobarbituric acid reactive substance levels in asphyxiated animals were elevated in frontal and parietal white matter, basal ganglia, and thalamus compared with those in controls. The concentrations of superoxide dismutase in the asphyxiated group were also higher in frontal and parietal white matter, basal ganglia, and cerebellum compared with those in the control group. Between the two groups, however, glutathione concentrations did not differ significantly.
CONCLUSION: These results suggest that oxidative stress may be a major contributing factor to the development of brain damage in intrauterine fetal asphyxia.