Journal of neurotrauma
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Journal of neurotrauma · Jan 1988
Traumatic brain injury in the rat: effects on lipid metabolism, tissue magnesium, and water content.
Tissue levels of free fatty acids (FFA), total phospholipid, cholesterol, thromboxane B2, water, Na+, K+, and Mg2+ were measured in rat brain after lateral fluid-percussion brain injury of moderate severity (2.0-2.2 atm). Brains of injured animals and sham-operated controls were frozen in situ with liquid N2 at 10 min, 4 h, and 24 h postinjury and removed. The left parietal cortex, which has been shown previously histologically to be the site of maximal injury, was dissected for analysis. ⋯ Small decreases in tissue K+ occurred at 4 h; tissue Na+ levels were found to be slightly increased only at 24 h. These results are consistent with the hypothesis that changes in lipid metabolism and Mg2+ content of brain after injury may play a role in the pathophysiology of irreversible, posttraumatic tissue damage. In contrast, significant edema formation does not occur in this model and does not, therefore, appear to be a factor in the injury process.
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Journal of neurotrauma · Jan 1988
Spinal cord contusion in the rat: somatosensory evoked potentials as a function of graded injury.
A weight-drop technique was used to produce mild, moderate, or severe spinal cord contusive injury in rats. At 4 weeks after injury, somatosensory evoked potentials (SEPs) were recorded with silver ball electrodes placed over the somatosensory cortex of anesthetized rats to measure the response to sciatic nerve stimulation. Both SEP area and amplitude were measured and were highly correlated with each other. ⋯ Measures of residual function consisted of a motor score, inclined plane test, and a combined behavioral score based on several neurologic functions. No correlation between latency of the SEP with degrees of contusive injury was observed. The data indicate that the SEP can be used as one criterion in the assessment of the severity of a lesion in a rat model of a graded spinal cord injury.
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Journal of neurotrauma · Jan 1988
Controlled cortical impact: a new experimental brain injury model.
A new experimental model of mechanical brain injury was produced in the laboratory ferret (Mustela putorius furo) using a stroke-constrained pneumatic impactor. Cortical impacts were made on vertex to the intact dura mater overlying the cerebral cortex with contact velocities ranging from 2.0 to 4.0 m/sec and with deformations of 2.0 to 5.0 mm. The dwell time of the impact and the stability of the skull during impact were verified with high speed (1000 to 3000 frames/sec) cineradiography. ⋯ The spectrum of anatomic injury and systemic physiologic responses closely resembled aspects of closed head injury seen clinically. This procedure complements and improves on existing techniques by allowing independent control of contact velocity and level of deformation of the brain to facilitate biomechanical and analytic modeling of brain trauma. Graded cortical contusions and subcortical injury are produced by precisely controlled brain deformations, thereby allowing questions to be addressed regarding the influence of contact velocity and level of deformation on the anatomic and functional severity of brain injury.
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Journal of neurotrauma · Jan 1988
Interaction of contact velocity and cord compression in determining the severity of spinal cord injury.
Rate, depth, and duration of compression are the principal determinants of experimental spinal cord injury (SCI) severity. Since existing models do not allow independent control of these variables, the interaction of these factors has not been fully elucidated. The purpose of this study was to define the interactive relation of velocity (V) and compression (C) in SCI using a constrained stroke pneumatic impactor that allowed independent control of these variables. ⋯ However, as velocity increases, SCI severity becomes a function of the viscous response (VC), demonstrating the rate sensitivity of spinal cord tissue. Tolerance to SC compression decreases as the rate of deformation increases. This helps to explain apparent discrepancies between compression and severity of experimental SCI.
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Journal of neurotrauma · Jan 1988
The effects of scopolamine and traumatic brain injury on central cholinergic neurons.
This study examined the effects of scopolamine and fluid percussion traumatic brain injury (TBI) on the activity of cholinergic neurons in specific areas of the rat brain 12 min, 4 h, and 24 h after injury. Acetylcholine (ACh) turnover, used as an index of cholinergic neuronal activity, was determined using gas chromatography-mass fragmentography. ⋯ The responses of thalamic, hippocampal, and amygdaloid cholinergic neurons to TBI did not differ substantially in scopolamine-pretreated rats from those studied previously in untreated fluid-percussion-injured rats. However, cholinergic neurons in the cingulate-frontal cortex of rats receiving TBI did respond in a different manner to scopolamine than those of rats receiving sham injury, suggesting a disruption of regulation of cortical cholinergic neurons following this model of TBI.