猫脑外伤后脑静脉6-keto-PGF_(1α)和TXB_2的变化及消炎痛对其的作用

INFLUENCE OF INDOMETHAC IN ON 6-keto-PGF_(1α) AND TXB_2 IN CEREBRAL VEINS OF CATS WITH HEAD INJURY

目的 :观察脑损伤后早期前列腺素的变化及消炎痛对其的作用。方法 :将 3 6只杂种猫 ,随机分为 A,B,C3组 ,每组 12只。A组为正常对照组 ,B组为损伤组 ,C组为损伤加消炎痛组。脑创伤按分级机械脑损伤实验动物模型制作 ,取中度脑损伤水平进行研究。伤后 6h测定脑静脉血中前列腺环素 (PGI2 )和血栓素 (TXA2 )的最终分解产物 6- keto- PGF1α和 TXB2 、脑组织总超氧化物歧化酶 (SOD)及脑含水量。结果 :猫脑外伤后早期脑静脉中 6- keto- PGF1α和 TXB2 均明显增加 ,6- keto- PGF1α增幅大于 TXB2 ,TXB2 / 6- keto- PGF1α倒置 ,脑含水量增加 ,同时脑组织总 SOD明显降低 (P <0 .0 1) ;C组 (与 B组比较 ) 6- keto- PGF1α和 TXB2 明显降低 ,与 A组接近 ,而总 SOD则有增加 (P <0 .0 1) ,脑含水量略降低 (P >0 .0 5 )。结论 :猫脑损伤后早期 PGI2和 TXA2 增加 ,并伴随自由基产生 ,由此加重脑损害。消炎痛通过调节脑损伤后 PGT2 / TXA2 失衡 ,减少自由基产生 。

Objective:To investigate the effects of indomethacin on 6 keto PGF1α and TXB 2 in cerebral veins of cats with head injury at early stage. Methods:36 cats were divided into three groups at randoml(12 cats in each group): Group A: the normal control group. Group B: head injury group. Group C: head injury treated with indomethacin, which were administered intravenously in dose of 3 mg/kg body weight at thirtith minute after head injury. The 6 keto PGF 1α and TXB 2 in cerebral venous of cats,total SOD and water content in brain tissues were measured at 6th hour after head injury. Results:The 6 keto PGF 1α ,TXB 2 and brain water content in group B were all significantly higher than those in the normal group A(P<0.01), and the 6 keto PGF 1α increased more than TXB 2, so having a decreased value of T/K.The total SOD in group B was significantly lower than those in the normal group (P<0.01) .After treatment with indomethacin (group C), the 6 keto PGF 1α and TXB 2 were significantly lower, and the total SOD was higher than those in group B (P<0.01), but the brain water content was reduced a little comparing to group B. Conclusion:There are increases of PGI 2 ,TXA 2, free radicals and water contents in brain of cats with head injury at 6th hour post injury. Indomethacin treatment at the early stage of brain injury could be helpful for alleviating secondary brain damage by attenuating PGI 2 ,TXA 2,and free radicals reaction in injured brain.