Rats were subjected to severe incomplete cerebral ischemia followed by recirculation. The levels of several of the cyclooxygenase products of arachidonic acid were measured at 5 and 15 minutes of ischemia and at 30 minutes of recirculation following 15 minutes of ischemia, PGE2 accumulated during the first 5 min. of ischemia and its level declined at 15 min. and returned to control level at 30 min. of recirculation. TXB2, on the other hand, increased during the whole time course of the experiment and at the end of the post ischemic period its level was 5 times higher than control. Treatment of the animals with indomethacin (4 mg/Kg, i.v.) prior to ischemia reduced the levels of these products without altering the pattern of their changes. During the ischemic period the EEG was isoelectric and the mean recovery time of electrical cortical activity after 15 min. of ischemia was 10.4 +/- 3.5 min. in the control rats. The rats which received indomethacin recovered faster (43. +/- 0.9 min) and were more resistant to the induction of ischemia. We suggest that the reversibility of cortical activity may be correlated to the accumulation of TXB2 during ischemia and recirculation, and inhibition of its synthesis might improve the post-ischemic reflow.