Journal of neurotrauma
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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.
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Journal of neurotrauma · Feb 1995
Plasma and cerebrospinal fluid concentrations of 4-aminopyridine following intravenous injection and metered intrathecal delivery in canines.
Potassium channel blockade by 4-aminopyridine (4-AP) has been shown to initiate modest levels of functional recovery in spinal-injured dogs and people following intravenous administration; however, the relevant central nervous system (CNS) concentration mediating these effects is not known. We have determined the concentrations of 4-aminopyridine in plasma and cerebrospinal fluid following intravenous administration (0.5 mg/kg) in large (> 22 kg) dogs, using liquid column chromatography. Plasma levels are initially high (> 1 microgram/mL) and fall rapidly to levels less than 100 ng/mL by about 2 h postinjection. ⋯ The levels of 4-AP in lumbar samples of CSF near the lumbar delivery site suggest a very steep gradient of the drug, with local concentrations easily reaching 1 microgram/mL or higher (10- to 20-fold higher than can be safely produced by IV administration). The most frequent adverse reaction to intrathecal 4-AP delivery was a mild hindlimb tremor, fully reversible following reduction in the rate of drug delivery or termination of delivery. This route of drug administration relative to clinical spinal cord injury is discussed.