脑损伤周边部位花生四烯酸代谢的实验研究

Arachidonic acid metabolism at the periphery of the injured zone after an experimental head trauma

由自由落体装置造成脑皮质损伤模型。Ｗｉｓｔａｒ大鼠被分成对照组，伤后１５分钟、１小时、２小时、２４小时、４天、２周等七组。断头处死大鼠，迅速取出整个脑组织，从损伤周边部位及对侧大脑半球相应的部位取出脑皮质，制成皮质切片于Ｋｒｅｂｓ－Ｒｉｎｇｅｒ氏液内孵育１．５小时。头部外伤导致脑水肿，伤侧大脑半球脑水肿高峰于伤后２４小时出现。ＴＸＢ２、６－Ｋｅｔｏ－ＰＧＦ１α、ＬＴＢ４的合成随时间呈显著性改变：伤后１５分钟ＴＸＢ２、ＬＴＢ４的合成已明显增加，６－Ｋｅｔｏ－ＰＧＦ１α的合成在伤后２４小时达高峰。结果提示，伤后脑水肿的产生可能和ＴＸＢ２与６－Ｋｅｔｏ－ＰＧＦ１α的比值增加和ＬＴＢ４的增高有关。而伤后晚期其比值又有所下降，这种不均衡性明显有助于脑血管扩张，使损伤周边区域脑血流得到改善。ＴＸＢ２与６－Ｋｅｔｏ－ＰＧＦ１α的比值下降对脑组织有保护作用，这也可能是损伤周边部位的一种修复机制。

Head trauma was induced in Wistar rats by a weight-drop device falling over the exposed dura of the left hemisphere. They were divided into seven groups. All of these rats survived until their planned sacrifice for 15 minutes, 1 hour, 2 hours, 24 hours, 4 days or 2 weeks respectively after trauma. They were then decapitated and their brains were rapidly removed (<1min). Cerebral cortex from the periphery and corresponding zone in the contralateral hemisphere was taken. Cortical slices were taken from the same sites and incubated in Krebs-Ringer solution for 1.5 hours. Head trauma induced edema, which was maximal at 24 hour after head trauma in the left injured hemisphere. Differential patterns of temperal changes of TXB 2, 6-Keto-PGF 1α , LTB 4 were evident in the contused hemisphere, TXB 2 and LTB 4 synthesis occurred at 15 min and the maximal synthesis of 6-Keto-PGF 1α at 24h after head trauma. The experiment indicates that the production of edema after brain injury may be related to the increased ratio between TXB 2 and 6-Keto-PGF 1α and the increase of LTB 4. In the later period of injury the sustained imbalance was apparently in favor of the vasodilation and improved blood supply for the region. The decreased ratio between TXB 2 and 6-Keto-PGF 1α had a protective effect on brain, which might be a part of the mechanism repairing the periphery of the injured zone.