The role of chemical mediator on the occurrence of brain edema after traumatic head injury

外伤性脑损伤是法医学领域的常见案例。流体冲击模型是目前公认的颅脑外伤实验模型。外伤性脑损伤伴发继发性或迟发性脑水肿，这些水肿过程也被认为参与了外伤性脑损伤的发病机制。最近的证据表明，肿瘤坏死因子- α (TNF α)和白三烯（LT）是创伤性颅脑损伤代谢后遗症和器官死亡的重要介质。为探讨大鼠创伤性颅脑损伤后TNF - α和LT的作用，采用液体冲击损伤装置造成1000mmHg中度颅脑损伤。撞击后24小时，在撞击部位、海马和浅表副神经皮层发生了液体性脑水肿，并在撞击后48小时通过MRI减轻了这些水肿。我们目前的研究表明，在遥远的撞击部位观察到的微血管损伤可能是由包括神经胶质细胞在内的脑组织在撞击后早期直接合成的TNF -诱导的。在撞击后24h，白细胞频繁浸润到远处的撞击部位。除此之外，目前的免疫电镜研究表明，LT的反应在远处的撞击部位被检测到白细胞和胶质细胞。这些数据表明，这些由TNF α引起的血管源性损伤诱导了脑缺血，缺血损伤促进了LT的合成。LT对脑组织具有强大的细胞毒活性，我们想提到的是，LT是中度脑损伤后液体性撞击性脑水肿形成的一个辅助因素。

Traumatic head injury is frequently occurred in the field of forensics. Fluid percussion models are well-recognized experimental models of traumatic heads injury. Traumatic head injury is accompanied by the secondary or delayd brain edema and these edema process are also believed to participate in the pathogenesis of traumatic head injury. Recent evidence suggest tumor necrosis factor-alpha (TNF alpha) and leukotriene (LT) is important mediator of the metabolic sequelae and organ demise of traumatic head injury. To investigate the role of TNF alpha and LT after traumatic head injury in rats, moderate brain injury of 1000mmHg was generated by an fluid percussion injury device. Fluid percussive brain edema occurred at 24hr after impact in the areas of the impact site, hippocampus and superficial parasagital cortex, and reduced these edema at 48hr after impact by the use of MRI.Our present study suggests that microvascular damages which observed in the remote impact sites may be induced by TNF alpha which is synthesized directly early times after impact by brain tissues including glial cells. The leukocyte infiltration into remote impact sites were frequently observed at 24hr after impact. Add to this fact, present immunoelectron microscopical study indicates that the reactions of LT were detected leukocyte and glia cells in the remote impact sites. This data suggest that these vasogenic damages owing to TNF alpha induce brain ischemia, and the ischemic insult promoting LT synthesis. LT possesses potent cytotoxic activity against brain tissues and we would like to mention that LT is one cofactor contributing to the fluid percussive brain edema formation after moderate brain injury.