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  • 1990-1994  (3)
  • 1960-1964
  • Edema  (2)
  • Alcohol consumption  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Edema formation and cellular alterations following spinal cord injury in the rat and their modification with p-chlorophenylalanine (1990)
    Springer
    Acta neuropathologica 79 (1990), S. 604-610 
    Details
    ISSN: 1432-0533
    Keywords: Trauma ; Spinal cord injury ; Edema ; Serotonin ; p-CPA
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The possibility that serotonin can modify the early pathological sequences occurring in spinal cord trauma was investigated in a rat model. To that end we took advantage of the possibility of influencing serotonin pharmacologically by treating animals with a serotonin synthesis inhibitor, p-chlorophenylalanine (p-CPA) before the production of the injury and compared the results with injured, untreated controls. A unilateral incision was made into the dorsal horn of the lower thoracic cord (about 2.5 mm deep, 4.5 mm long) and the trauma. The injured region from untreated animals showed macroscopically at that time a pronounced swelling and the water content had increased by 3.5% as compared to intact controls. The segments rostral and caudal to the lesion also exhibited a profound increase in water content. Light microscopy revealed a significant expansion of the spinal cord as compared to controls. The swelling was most pronounced in the gray matter on the injured side. Electron microscopy showed distorted neurons, swollen astrocytes and extracellular edema in the gray matter in and around the primary lesion. There was also a sponginess in the surrounding white matter with disruption of myelin, collapsed axons and widened periaxonal spaces. Pretreatment of the rats with p-CPA significantly reduced the swelling of the injured spinal cord and there was no visible expansion. The ipsilateral edema in the central gray matter was considerable less pronounced as compared to that in untreated animals. The increase in water content was less than 1% in these animals. The neuronal and glial cell changes were also markedly reduced in the drugtreated rats. The disruption of myelin and the vacuolation of the gray matter were much less severe. Our results show that p-CPA can markedly modify the edema and the cellular changes occurring in the traumatic spinal injury and indicate that serotonin is somehow involved in the production of the early, and thus important, pathological events.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00294237
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Early perifocal cell changes and edema in traumatic injury of the spinal cord are reduced by indomethacin, an inhibitor of prostaglandin synthesis (1993)
    Springer
    Acta neuropathologica 85 (1993), S. 145-153 
    Details
    ISSN: 1432-0533
    Keywords: Spinal cord trauma ; Edema ; Myelin basic protein ; Indomethacin ; Prostaglandins
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The possibility that prostaglandins participate in the formation of perifocal edema and cell changes following a localized trauma to the spinal cord was investigated in a rat model. A laminectomy was performed in urethane-anesthetized animals at the thoracic T10–11 segment. Using a scalpel blade a unilateral lesion, about 2 mm deep and 5 mm long was made 1 mm to the right of the midline. The deepest part of the injury occupied Rexed's lamina VII of the dorsal horn. Animals were pretreated with the prostaglandin synthesis inhibitor, indomethacin (10 mg/kg, i.p. 30 min prior to trauma). Five hours after the injury the water content was determined and cell changes in and around the primary lesion were examined by light and electron microscopy. Normal and injured rats without indomethacin pretreatment served as controls. Untreated injured rats showed a profound increase of water content in the traumatized T10–11, the rostral (T9) and caudal (T12) segments compared with normal rats. These segments also exhibited marked cell changes in ipsilateral and contralateral dorsal and ventral horns. The gray matter had a spongy appearance and some nerve cells were condensed and distorted. The white matter contained many distorted fibers. Immunostaining for myelin basic protein showed a marked reduction of reaction product in the injured animals compared with normal rats. Ultrastructurally widened extracellular spaces, cytoplasmic vacuolation, swollen and condensed neurons, swollen astrocytes and vesiculation of myelin were frequent findings. Pretreatment of rats with indomethacin significantly reduced the accumulation of water in the traumatized and in the rostral and caudal segments. The structural changes were less pronounced particularly in the cranial and caudal segments. The results indicate that prostaglandins somehow are involved in the pathophysiology of perifocal spinal cord injury and influence both the fluid microenvironment and the early cell changes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00227761
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Initial sensitivity, acute tolerance and alcohol consumption in fischer 344 and long evans rats (1991)
    Springer
    Psychopharmacology 105 (1991), S. 175-180 
    Details
    ISSN: 1432-2072
    Keywords: Initial sensitivity ; Acute tolerance ; Alcohol consumption ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In separate groups of Fischer 344 and Long Evans rats, initial sensitivity and acute tolerance to ethanol were determined in a jumping test. Sensitivity measurements in each strain were carried out in separate subgroups at ethanol doses of 1.5, 2.0, and 2.5 g/kg IP. Similarly, acute tolerance was measured in different subgroups of each strain using the method of two successive doses of ethanol (2 + 0.4 g/kg; 2 + 0.7 g/kg and 2 + 1.0 g/kg, respectively). After completion of sensitivity and acute tolerance measurement, acute tolerance was then tested in all rats. Based on their acute tolerance values, they were divided into three groups: high, medium, and low. Two weeks after the last acute tolerance test, six rats from each group (i.e., the six highest and six lowest from the high and low acute tolerance groups, respectively, and six from the midrange of the medium tolerance group) were tested for voluntary ethanol drinking in the limited access model. Long Evans rats had lower initial CNS sensitivity to ethanol-induced impairment of jumping performance than Fischer 344 rats. Long Evans rats also drank significantly more alcohol than the Fischer 344 but there was no significant difference in acute tolerance development between these two strains. Moreover, within each strain the rats differing in acute tolerance development (i.e., high, medium, and low) showed no difference in alcohol consumption. These results suggest that acute tolerance development is not the main determinant of differences in ethanol drinking.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02244305
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    Paper (German National Licenses)
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