Objective: Recirculation following transient intrauterine ischemia has previously been found to cause partial recovery and secondary deterioration of cellular bioenergetic states in the fetal rat brain. Our objective was to assess whether secondary bioenergetic failure is due to mitochondrial dysfunction.
Study design: Cerebral cortical tissues were obtained from 20-day-old fetal rats at the end of 30 minutes of intrauterine ischemia (n = 6) and after 1 hour (n = 6), 2 hours (n = 6), and 4 hours (n = 6) of recirculation. Mitochondrial respiratory activities were measured polarographically using homogenates.
Results: Mitochondrial activities decreased to 45% of sham-operated controls at the end of ischemia. Recirculation (1 hour) brought about partial recovery, but continued reflow (2 hours and 4 hours) was associated with a secondary deterioration of mitochondrial activities.
Conclusion: The results indicate that although during the early time period after ischemia mitochondrial respiratory capacity is restored, secondary mitochondrial dysfunction develops in the immature rat brain.