Journal of neurotrauma
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Journal of neurotrauma · Jun 1995
Posttraumatic brain hypothermia provides protection from sensorimotor and cognitive behavioral deficits.
The purpose of this study was to determine the degree of sensorimotor and cognitive protection conferred by posttraumatic brain hypothermia. Baseline measurements were taken on sensorimotor tasks involving forelimb placing and beam-walking, as well as on a spatial navigational task utilizing the water maze. Twenty-four hours after the last baseline measurements, normothermic (37 degrees C) animals were subjected to a fluid percussion pulse (1.9-2.4 atm) over the right parietal sensorimotor cortex. ⋯ In the water maze, there was a distinction between groups in the ability to navigate 48 h after TBI. TBI-N animals performed significantly worse than sham and TBI-H animals (both p < 0.01), whereas there was no significant difference between the scores of sham and TBI-H animals. The present data demonstrate that moderate postinjury brain hypothermia can provide protection from sensorimotor and cognitive behavioral deficits as well as neuropathology in a model of traumatic brain injury associated with early neuronal and microvascular 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.
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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 · Feb 1995
Astrocytic reaction after graded spinal cord compression in rats: immunohistochemical studies on glial fibrillary acidic protein and vimentin.
The relation between the degree of spinal cord compression and the extent of early posttraumatic reaction of astrocytes was investigated in rats using the blocking-weight technique to induce a spinal cord compression at the level of the Th8-9. Immunohistochemistry was used to detect changes in the expression of glial fibrillary acidic protein (GFAP) and vimentin up to 24 h after injury. A mild compression, which did not cause any measurable neurological deterioration, induced a mild increase of GFAP immunoreactivity at 4 h and a more marked and widespread immunoreactivity at 24 h. ⋯ Even a mild compression that does not produce any signs of motor dysfunction can induce widespread astrocyte alterations in the spinal cord. This astrocyte response is more marked in rats with more severe compression leading to more pronounced neurological deterioration. The increase in vimentin immunoreactivity of blood vessels is more localized and occurs in moderate and severe compression of the cord.
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Journal of neurotrauma · Feb 1995
The effect of acute cocaine or lidocaine on behavioral function following fluid percussion brain injury in rats.
One of the goals of our laboratory is to examine how the presence of drugs of abuse will influence traumatic brain injury. Previous studies in our laboratory have shown that cocaine or lidocaine treatment before experimental fluid percussion brain injury in rats reduces the cortical hypoperfusion normally found in the early posttraumatic period. The purpose of the current study was to determine if pretreatment with cocaine or lidocaine is also associated with changes in trauma-induced suppression of reflexes and motor and cognitive dysfunction that occurs following traumatic brain injury (TBI). ⋯ Lidocaine and cocaine did not affect cognitive function on days 11-15 postinjury. The mechanism by which lidocaine improves acute neurological and motor function following brain injury is unknown, but may involve improved posttraumatic cortical blood flow, as seen in our previous study. Our results, along with other studies showing lidocaine to be neuroprotective in animal models of ischemia, suggest that studies of the effect of posttraumatic administration of lidocaine are warranted.