Journal of neurotrauma
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Journal of neurotrauma · Apr 1995
Superoxide dismutase improves posttraumatic cortical blood flow in rats.
Oxygen free radicals, such as the superoxide anion, are known to mediate damage to the cerebral microcirculation following traumatic brain injury. The purpose of this study was to determine if superoxide dismutase (SOD), a scavenger of superoxide anion, could alter posttraumatic cortical blood flow. Following barbiturate anesthesia, rats were surgically prepared for moderate fluid percussion brain injury. ⋯ SOD caused not only greater blood velocity but also less reduction in cortical blood volume after injury. There were no significant differences between the groups with respect to blood pressure or heart rate. This study further supports the role of oxygen radical-mediated cerebrovascular dysfunction following traumatic brain injury and is the first to show the beneficial effect of SOD on cortical blood flow following fluid percussion brain injury.
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Journal of neurotrauma · Apr 1995
A model of parasagittal controlled cortical impact in the mouse: cognitive and histopathologic effects.
Controlled cortical impact (CCI), using a pneumatically driven impactor to produce traumatic brain injury, has been characterized previously in both the ferret and in the rat. In the present study, we applied this technique to establish and characterize the CCI model of brain injury in another species, the mouse, evaluating cognitive and histopathologic outcome. In anesthetized (sodium pentobarbital, 65 mg/kg) male C57BL mice, we performed sham treatment (no injury, n = 12) or CCI injury (n = 12) at a velocity of 5.7-6.2 m/sec and depth of 1 mm, using a 3-mm diameter rounded-tip impounder, positioned over the left parietotemporal cortex (parasagittal). ⋯ Breakdown of the blood-brain barrier was demonstrated with antimouse IgG immunohistochemistry, revealing extravasation of endogenous IgG throughout the ipsilateral cortex, hippocampus, and thalamus. These results suggest that this new model of parasagittal CCI in the mouse mimics a number of well-established sequelae observed in previously characterized brain injury models using other rodent species. This mouse model may be a particularly useful experimental tool for comparing behavioral and histopathologic characteristics of traumatic brain injury in wild-type and genetically altered mice.