Developmental changes in tolerance to transient intrauterine ischemia in rat cerebral mitochondria

Citation
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
Citations number
23
Categorie Soggetti
Reproductive Medicine","da verificare
Journal title
AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
ISSN journal
00029378 → ACNP
Volume
184
Issue
4
Year of publication
2001
Pages
731 - 735
Database
ISI
SICI code
0002-9378(200103)184:4<731:DCITTT>2.0.ZU;2-J
Abstract
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.