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

颅脑损伤是法医学领域中常见的一种损伤类型。液压冲击模型是公认的创伤性颅脑损伤的实验模型。创伤性脑损伤后可伴有继发性或迟发性脑水肿，这些脑水肿过程也被认为参与了创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）是创伤性脑损伤的代谢后遗症和器官死亡的重要介质。为了研究TNF α和LT在大鼠创伤性脑损伤后的作用，通过液压冲击损伤装置产生1000 mmHg的中度脑损伤。结果表明：撞击后24小时，撞击部位、海马和浅侧枕旁皮质出现水肿，48小时后水肿减轻，提示撞击后早期脑组织（包括胶质细胞）直接合成TNF-α，导致撞击部位微血管损伤。在撞击后24小时，经常观察到白细胞浸润到远撞击点。此外，目前的免疫电镜研究表明，LT的反应是检测到白细胞和胶质细胞在遥远的影响网站。这些数据表明，由于TNF α引起的这些血管源性损伤诱导脑缺血，并且缺血性损伤促进LT合成。LT对脑组织具有强的细胞毒活性，我们想提及的是，LT是导致中度脑损伤后液体水肿性脑水肿形成的辅助因子之一。

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.