Currently, intracranial pressure (ICP) is the primary clinical monitoring parameter for traumatic brain injury (TBI). However, during the hyperacute phase of TBI, ICP value lags behind changes of brain temperature (BT) and neurometabolic activity. This is due to the compensatory capacity of the intracranial space. Here, we explored BT changes and concentration changes of cytochrome c (∆Ccytc) during the hyper-acute phase of TBI. Nine mice were randomly divided into control group, mild TBI group, and severe TBI group. The mouse TBI model is created by using various levels of striking force. The strike device is designed and improved based on Feeney's free fall model. BT can be measured by a minimally invasive measurement probe, allowing for the observation of changes in both time and spatial distribution. ∆Ccytc was calculated using an intrinsic optical signal imaging system (IOSI). The relationship between BT and ∆Ccytc was analyzed during the development of mice TBI models.
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