A. Nakai et al., Developmental changes in tolerance to transient intrauterine ischemia in rat cerebral mitochondria, AM J OBST G, 184(4), 2001, pp. 731-735
OBJECTIVE: Mitochondfial respiratory activities were measured in neonatal r
at 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 al
pha -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 investi
gation 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-buty
l-nitrone treatment investigation, term fetuses were exposed to ischemia wi
th alpha -phenyl-N-tert-butyl-nitrone (n = 8). All subjects underwent cesar
ean 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 ische
mia 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. Th
e neonatal mitochondrial deterioration caused by term ischemia was prevente
d 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 tra
nsient intrauterine ischemia and suggest that oxygen-derived free radicals
may play a crucial role in the development of neonatal neurologic deficit.