Abstract: AIM:METHODS: The acute complete cerebrali schemia model and the ischemia-reperfusion model were made by eluding four-vessel, both bilateral carotid an dvertebral arteries, and removing the occlusion of bilateral caroli at the end of 30 minutes ischemia. Control group(A) was intravenously infused. 9% saline (1 ml· kg^-1 before ischemia and before reperfusion, but XNJI group(B) were inlused XNJI (1 ml· kg^-1) The contents and of 6-KETO-PGF_1a in both plasma and braintissue were separalely measured with radioimmunoassayIe ore isehemia. 30 min after ischemia and 30 min, 1 h and 2 h after reperfusion. Cerebral ultrastruc true changes were observed at the end of experiment.RESULTS: Forthe XNJI group, compared with control group, TXB₂ > content and the radio of TXB2/6-KETO-PGFLA in both plasma and brain tissue decreased (P < 0.05). The observation of the pathologic changes of ultrastruc true in rain tissue showed that the injury was relieved in XN JI group.CONCLUSION: XNJI can effectively decrease the radio of TXB2/6-KETO-PGF_1a, by decreasing the synthesis of TXBand accelerating the growing of 6-KETO-PGF_1a, and it maybe another mechanism in protecting the brain from ischemia and reperfusion injury.

Key words: Xingnaojing injection (XNJI), erebralischemia-reperfusion injury (CIRI), the metabolism ofarachidonic acid: thromboxance B, (TXB, ) 6-keto-PGF_1α