期刊
JOURNAL OF NEUROTRAUMA
卷 27, 期 4, 页码 707-719出版社
MARY ANN LIEBERT, INC
DOI: 10.1089/neu.2009.1071
关键词
animal model; beta-amyloid precursor protein; diffuse axonal injury; injury mechanism; traumatic brain injury
资金
- Shanghai Education Committee [06BZ042]
- Shanghai Municipal Health Bureau [2008115]
- Shanghai Jiao Tong University [YG2009MS14]
Diffuse axonal injury (DAI) is a frequent form of traumatic brain injury, and is usually associated with long-lasting neurological impairments. A new experimental model was developed in the present study to induce DAI in rats by combining low linear and angular accelerations. In most clinical scenarios, DAI is caused by these two forms of acceleration in combination. In the injury-producing facility described here, the rat rotated instantly after it had sustained the impact that produced linear acceleration. Rats rotated rapidly 90 degrees in the coronal plane at a peak angular acceleration of 137 +/- 12 krad/sec(2) with a duration of 33.7 +/- 1.2 msec. The linear acceleration was applied to the rat's head by dropping a 450 g weight from a height of 0.9 m. Rats exposed to the combined accelerations took significantly longer to regain consciousness (11.9 +/- 3.6 min) than control rats (p < 0.01) or rats subjected to purely angular or linear acceleration (p < 0.01). Although macroscopic damage was observed in all brain-injured animals, axonal damage and hemorrhagic tissue tears were only noted in the animals sustaining the combined accelerations. All rats survived the purely linear or angular acceleration, whereas the mortality rate reached 21.7% following the combined accelerations. These results show that this model is capable of reproducing the major histological and neurological changes that are associated with DAI, and that the combination of low linear and angular accelerations can produce non-linear and synergistic effects to induce moderate/severe DAI.
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