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  • 1
    Electronic Resource
    Electronic Resource
    Spinal cord evoked potentials and edema in the pathophysiology of rat spinal cord injury (1998)
    Springer
    Amino acids 14 (1998), S. 131-139 
    Details
    ISSN: 1438-2199
    Keywords: Nitric oxide ; Spinal cord evoked potentials ; Edema ; Cell changes ; p-CPA ; Diazepam ; Immunohistochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The possibility that nitric oxide is somehow involved in the early bioelectrical disturbances following spinal cord injury in relation to the later pathophysiology of the spinal cord was examined in a rat model of spinal cord trauma. A focal trauma to the rat spinal cord was produced by an incision of the right dorsal horn of the T 10–11 segments under urethane anaesthesia. The spinal cord evoked potentials (SCEP) were recorded using epidural electrodes placed over the T9 and T12 segments of the cord following supramaximal stimulation of the right tibial and sural nerves in the hind leg. Trauma to the spinal cord significantly attenuated the SCEP amplitude (about 60%) immediately after injury which persisted up to 1h. However, a significant increase in SCEP latency was seen at the end of 5h after trauma. These spinal cord segments exhibited profound upregulation of neuronal nitric oxide synthase (NOS) immunoreactivity, and the development of edema and cell injury. Pretreatment with a serotonin synthesis inhibitor drug p-chlorophenylalanine (p-CPA) or an anxiolytic drug diazepam significantly attenuated the decrease in SCEP amplitude, upregulation of NOS, edema and cell injury. On the other hand, no significant reduction in SCEP amplitude, NOS immunolabelling, edema or cell changes were seen after injury in rats pretreated with L-NAME. These observations suggest that nitric oxide is somehow involved in the early disturbances of SCEP and contribute to the later pathophysiology of spinal cord injury.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01345253
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Brain derived neurotrophic factor and insulin like growth factor-1 attenuate upregulation of nitric oxide synthase and cell injury following trauma to the spinal cord (1998)
    Springer
    Amino acids 14 (1998), S. 121-129 
    Details
    ISSN: 1438-2199
    Keywords: Brain derived neurotrophic factor ; Insulin like growth factor-1 ; Nitric oxide ; Spinal cord injury ; Edema ; Cell injury ; Blood-spinal cord barrier ; Immunohistochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The possibility that brain derived neurotrophic factor (BDNF) and insulin like growth factor-1 (IGF) induced neuroprotectivn is influenced by mechanisms involving nitric oxide was examined in a rat model of focal spinal cord injury. BDNF or IGF-I (0.1 μg/10 [1 in phosphate buffer saline) was applied topically 30 min before injury on the exposed spinal cord followed by repeated doses of growth factors immediately before and 30 min after injury. Thereafter application of BDNF or IGF was carried out at every 1 h interval until sacrifice. Five hours after injury, the tissue pieces from the T9 segment were processed for nNOS immunostaining, edema and cell injury. Untreated injured rats showed a profound upregulation of nNOS which was most pronounced in the nerve cells of the ipsilateral side. A marked increase in the blood-spinal cord barrier (BSCB) permeability to125I-albumin, water content and cell injury in these perifocal segments was also found. Pretreatment with BDNF and IGF significantly reduced the upregulation of nNOS in the spinal cord. This effect of the growth factors was most pronounced in the contralateral side. Rats treated with these neurotrophic factors showed much less signs of BSCB damage, edema and cell injury. These results suggest that BDNF and IGF pretreatment is neuroprotective in spinal cord injury and that these neurotrophic factors have the capacity to down regulate nNOS expression following trauma to the spinal cord. Our data provide new experimental evidences which suggest that BDNF and IGF may exert their potential neuroprotective effects probably via regulation of NOS activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01345252
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    The tissue distribution in BALB/c mice of C-14-labeled JM216, an orally active platinum antitumour compound (1996)
    Springer
    Cancer chemotherapy and pharmacology 39 (1996), S. 170-175 
    Details
    ISSN: 1432-0843
    Keywords: Key words JM216 ; Platinum tissue distribution ; BALB/c mice ; Carbon 14
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The ammine/amine platinum(IV) dicarboxylates have been developed as orally active platinum antitumor agents, and one of these, [PtCl2(NH3)(C6H11NH2) (OCOCH3)2] (JM216), is undergoing clinical trials at present. A synthesis method was developed to radiolabel JM216 with carbon 14 at the carboxylate carbon. The labeling efficiency was 92%, and the purity as shown by high-performance liquid chromathography (HPLC) was 96% after recrystallisation. The radiolabeled JM216 was given orally to BALB/c mice and detailed tissue-distribution data were obtained (blood plasma, kidney, liver, spleen, brain, lung, muscle and skin) for time points of 2 h and 2, 6 and 10 days. Comparison of these data with previously reported data for distribution of platinum obtained by atomic absorption spectroscopy has shown distinct differences, especially for the liver and the kidney. This clearly indicates a difference in behaviour between the labeled ligand and the platinum centre, suggesting detachment of the ligand in vivo.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002800050555
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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