Abstract
To investigate the role of tumor necrosis factor-α (TNFα) after traumatic head injury in rats, moderate brain injury of 1000 mmHg was generated by an original fluid percussion injury device. TNFα levels in cerebrospinal fluid (CSF) gradually increased during the first 1 h, rose to a maximal elevation at 3 h and 6 h and returned to basal values by 24 h. Horseradish peroxidase tracer experiments revealed that primary microvascular damage appeared as early as 15 min after impact, but rapidly recovered and 1 h after impact secondary microvascular damage occurred in the hippocampus and parasagittal cortex. By immunoelectron microscopy, TNFα reactions were detected in the lysosomes of microglia accumulated at the impact site of the cortex 30 min after impact, and 1 h after impact these reactions were mainly detected at the glial cells (such as microglia and astrocytes) in the hippocampus and parasagittal cortex. Therefore the delayed microvascular damage observed in sites remote from the impact may be induced by TNFα which is synthesized mainly by glial cells. The present study suggests that TNFα conveyed from the microglial cells is one cofactor contributing to the fluid percussive brain edema formation after moderate brain injury.
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Received: 13 February 1997 / Received in revised form: 10 July 1997
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Kita, T., Liu, L., Tanaka, N. et al. The expression of tumor necrosis factor-α in the rat brain after fluid percussive injury. Int J Leg Med 110, 305–311 (1997). https://doi.org/10.1007/s004140050093
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DOI: https://doi.org/10.1007/s004140050093