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作者通过大鼠脑落体致伤模型,放免法检测伤后早期鼠脑皮质血栓素B_2(TXB_2)与6-酮-前列环素F_(1α)(6-酮)含量,同时对重型颅脑伤患者20例作脑脊液(CSF)TXB_2测定,以探讨TXA_2及PGI_2代谢失衡与继发性脑损害的关系,以及川芎嗪对TXA_2,PGI_2代谢的影响.结果如下:伤后3 h内,大鼠挫伤脑皮质TXB_2及6-酮含量逐渐增高(P<0.01);TXB_2/6-酮(T/K)值亦呈上升趋势,与继发性脑损害加重相一致,川芎嗪可抑制TXB_2生成(P<0.01),减轻继发性脑损害.CSF中TXB_2在伤后7d均增高(P<0.01),以伤后3 d为甚,与创伤性脑水肿的发生、发展过程相符.提示脑损伤后,脑内TXA_2及PGI_2的失衡代谢是加重继发性脑损害的重要因素.
The authors used a rat brain injury model to determine the content of TXB_2 and 6-keto-prostaglandin F_(1α) (6-keto) in rat brain cortex at the early post-injury period by radioimmunoassay. Twenty cases of cerebrospinal fluid (CSF) TXB 2 were measured to investigate the relationship between metabolic imbalance of TXA 2 and PGI 2 and secondary brain damage, and the effects of tetramethylpyrazine on the metabolism of TXA 2 and PGI 2 . The results were as follows: Within 3 h after injury, the rat contused brain Cortex TXB_2 and 6-keto levels increased gradually (P<0.01); TXB_2/6-ketone (T/K) values also showed an upward trend. Consistent with the increase in secondary brain damage, tetramethylpyrazine inhibited TXB_2 production (P< 0.01), to reduce the secondary brain damage. TXB 2 in CSF increased in the 7th day after injury (P <0.01), especially 3 days after the injury, and coincided with the occurrence and development of traumatic brain edema, suggesting that after brain injury, The imbalance metabolism of TXA_2 and PGI_2 in the brain is an important factor in aggravating secondary brain damage.