The mitochondrial respiratory activities and energy metabolism in the fetal rat brain were measured at the end of 30 minutes of intrauterine ischemia and after 2 and 4 hours of recirculation. The transient ischemia was associated with a delayed deterioration of cellular bioenergetic state and mitochondrial activities. The deterioration was not prevented by a free radical scavenger, 3-methyl-1-phenyl-2-pyrazolin-5-one (MCI-186), given immediately after recirculation.