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

化学介质在颅脑外伤后脑水肿发生中的作用

• 批准号: 07457120
• 负责人: TANAKA Noriyuki
• 金额: $ 2.11万
• 依托单位: University of Occupational and Environmental Health
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (B)
• 财政年份: 1995
• 资助国家: 日本
• 起止时间: 1995 至 1996
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-07457120/
• 关键词: Traumatic brain edema; Fluid percussion device; MRI; Chemical mediator; Leukotriene; Tumor necrosis factor-alpha; Blood brain barrier; Fluid percussion; 脳血管関門(BBB)

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.

外伤性颅脑损伤在法医学领域经常发生。流体冲击模型是公认的颅脑外伤实验模型。颅脑外伤伴有继发性或迟发性脑水肿，这些水肿过程也被认为参与了颅脑外伤的发病机制。最近的证据表明肿瘤坏死因子-α (TNF α) 和白三烯 (LT) 是颅脑外伤代谢后遗症和器官死亡的重要介质。为了研究大鼠头部创伤后 TNF α 和 LT 的作用，通过流体冲击损伤装置产生 1000mmHg 的中度脑损伤。撞击后 24 小时，撞击部位、海马和浅表旁矢状皮层区域发生流体冲击性脑水肿，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，在远处撞击部位观察到的微血管损伤可能是由 TNF α 引起的，TNF α 是在撞击后早期由包括神经胶质细胞在内的脑组织直接合成的。撞击后 24 小时经常观察到白细胞浸润到远程撞击部位。除此之外，目前的免疫电子显微镜研究表明，在远程撞击地点的白细胞和神经胶质细胞中检测到了 LT 的反应。该数据表明，TNF α 引起的血管损伤会诱发脑缺血，而缺血性损伤会促进 LT 合成。 LT 对脑组织具有有效的细胞毒活性，我们想提一下，LT 是中度脑损伤后导致液体冲击性脑水肿形成的辅助因子。