Objective: Mitochondfial respiratory activities were measured in neonatal rat brain to compare the influence of transient intrauterine ischemia in the preterm fetus with that in the term fetus and to evaluate the effect of alpha-phenyl-N -tert-butyl-nitrone treatment.
Study design: Intrauterine ischemia was induced by a 30-minute occlusion of the right uterine artery. The control group consisted of term fetuses (20 days old) exposed to normoxia (n = 8) and ischemia (n = 8). For the investigation into maturity effect, preterm fetuses (14 days old) were exposed to normoxia (n = 8) or ischemia (n = 8), and for the alpha-phenyl-N -tert-butyl-nitrone treatment investigation, term fetuses were exposed to ischemia with alpha-phenyl-N -tert-butyl-nitrone (n = 8). All subjects underwent cesarean delivery at 21 days of gestation, and the mitochondrial respiration was measured polarographically 1 hour after delivery.
Results: In the control group the neonatal cortical tissue exposed to ischemia showed a significant decrease in mitochondrial activities compared with those in normoxic control animals. In the preterm group the mitochondrial activities of ischemic fetuses were maintained close to normoxic levels. The neonatal mitochondrial deterioration caused by term ischemia was prevented by alpha-phenyl-N -tert-butyl-nitrone.
Conclusion: The results indicate that preterm fetuses are more capable than term fetuses of maintaining mitochondrial function under conditions of transient intrauterine ischemia and suggest that oxygen derived free radicals may play a crucial role in the development of neonatal neurologic deficit.