Focal brain ischemia was induced in rats by inserting a silicone rubber cylinder attached to a nylon surgical thread from the common carotid artery into the middle cerebral artery bifurcation. Reperfusion was achieved by removing the cylinder. In the ischemic area, free fatty acids were measured. Arachidonic acid lipoxygenase metabolites: leukotriene C4 (LTC4), and cyclooxygenase metabolites: thromboxane B2 (TXB2), prostaglandin E2 (PGE2) and 6-keto-prostaglandin-F1 alpha (6-keto-PGF1 alpha) were measured during ischemia and after reperfusion. There were five ischemia groups. The rats in these groups were killed 1, 2, 3, 4 or 6 hours after occlusion. In the reperfusion group, rats exposed to 1, 2, 3 and 4 hours of ischemia were killed 5, 4, 3 and 2 hours after reperfusion, respectively. The free fatty acids, which had increased due to occlusion, decreased after reperfusion from 1 hour of ischemia. With 2 or more hours of ischemia, however, the free fatty acids increased after reperfusion, indicating cell membrane destruction. Eicosanoids showed almost the same changes in all groups. The eicosanoid level was high only after 1 hour of ischemia and it stayed low if the ischemia time exceeded 2 hours and after reperfusion. Therefore, we suggested that eicosanoids are not a main cause of tissue damage in the ischemic area after 2 or more hours of ischemia.