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

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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.