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用四血管阻断法造成大鼠全脑缺血。脑缺血３０ｍｉｎ后再恢复双侧颈总动脉血流３０ｍｉｎ，此时大鼠体内ＰＬＡ＿２活性、ＴＸＢ＿２／６一ｋｅｔｏ一ＰＧＦ＿（１α）比值和ＥＴ、ＬＰＯ含量明显增高，大脑神经细胞和血脑屏障明显损害；预防用氯喹或ＳＯＤ治疗后，上述物质的增多受到抑制，神经细胞和血脑屏障损害也明显减轻。ＰＬＡ＿２、ＴＸＡ＿２／ＰＧＩ＿２、内皮素、自由基与脑组织损伤密切相关。脑缺血再灌注时，ＰＬＡ＿２、ＴＸＡ＿２／ＰＧＩ＿２、ＥＴ、自由基间存在相互作用，并可测定血浆中ＴＸＢ＿２、６一ｋｅｔｏ－ＰＧＦ＿（１α）、ＥＴ、ＬＰＯ浓度反映脑组织内的含量。
Four-vessel occlusion was used to induce global cerebral ischemia in rats. After 30min of cerebral ischemia, the common carotid artery blood flow was recovered for 30min. The PLA2 activity, TXB_2 / 6-keto-PGF_ (1α) ratio and ET and LPO contents were significantly increased in the rats. Cerebral nerve cells and blood- Obvious damage; Prevention with chloroquine or SOD treatment, the increase of these substances is inhibited, nerve cells and blood-brain barrier damage was also significantly reduced. PLA_2, TXA_2 / PGI_2, ET and free radicals are closely related to brain injury. There was interaction between PLA_2, TXA_2 / PGI_2, ET and free radicals during cerebral ischemia-reperfusion. The concentration of TXB_2.6-keto-PGF_ (1α), ET and LPO in plasma could be measured to reflect the content of brain tissue.