Twelve rabbits were submitted to 20-min global cerebral ischemia. Half of them were treated continuously with prostacyclin (PGI2) for 3 min before and during ischemia, and for 15 min after it. Untreated animals were not given PGI2 medication. The cases treated with PGI2 were found to have recovered bioelectric activity of the brain in half the time that its return took in the untreated cases. In the group that received PGI2, the ischemic ultrastructural changes in the cytoplasm of neuroglial cells were abolished, however, PGI2 did not prevent pathological damage in the neuroglial nuclei after ischemia. These damages were manifested in numerous vesicular structures, nuclear inclusions and chromatin clumping and margination. The vesicular structures were enclosed in a single smooth membrane without contact with the nuclear envelope. It is suggested that the vesicular structures may form as the result of disturbances in the water-electrolyte exchange between the cytoplasm and karyoplasm of neuroglial cells. The inclusions consisted of filaments and/or membranes. The amassing in the karyoplasm of vesicular structures and intranuclear inclusions with chromatin clumping and margination probably leads later to the death of the neuroglial cells after total cerebral ischemia. Hence, the described data indicate that the curative effects of PGI2 are directed only to early changes in the neuroglial cells cytoplasm and reflect a transient facilitation of functional recovery and/or metabolism rather then permanent brain protection after complete cerebral ischemia.