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  • Keywords: Amino acids  (5)
  • Spinal cord trauma  (3)
  • 1
    ISSN: 1438-2199
    Keywords: Keywords: Amino acids ; Nerve lesion ; Neuropathic pain ; Heme oxygenase ; Carbon monoxide ; Cell injury ; Immunohistochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary. The influence of carbon monoxide (CO) on chronic spinal nerve lesion induced spinal cord neurodegeneration was examined using immunohistochemical expression of the constitutive isoform of its synthesising enzyme, hemeoxygenase-2 (HO-2) in a rat model. Spinal nerve lesion at L-5 and L-6 level was produced according to the Chung model of neuropathic pain and rats were allowed to survive for 8 weeks. Sham operated rats, in which the spinal nerves were exposed but not ligated, served as controls. Ligation of spinal nerves in rats resulted in an upregulation of HO-2 expression which was most pronounced in the ipsilateral gray matter of the spinal cord compared to the contralateral side. In these rats, morphological investigations showed distorted neurons, membrane disruption, synaptic damage and myelin vesiculation. Sham operated rats did not show an upregulation of HO-2 expression and the structural changes in the spinal cord were absent. These observations strongly suggest that spinal nerve lesion is associated with an increased production of CO which is somehow contributing to the neurodegenerative changes in the spinal cord, not reported earlier.
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  • 2
    ISSN: 1438-2199
    Keywords: Keywords: Amino acids ; Hyperthermia ; Heat stress ; Brain edema ; Nitric oxide synthase ; Heme oxygenase ; Oxidative stress ; H-290/51 ; Cell injury
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary. Influence of a new anti-oxidant compound H-290/51 on expression of nitric oxide synthase (NOS) and heme oxygenase (HO) enzymes responsible for nitric oxide (NO) and carbon monoxide (CO) production, respectively was examined in the CNS following heat stress in relation to cell injury. Exposure of rats to 4 h heat stress at 38°C in a biological oxygen demand (BOD) incubator (relative humidity 50–55%, wind velocity 20–25 cm/sec) resulted in profound edema and cell injury in many parts of the cerebral cortex, hippocampus, cerebellum, thalamus, hypothalamus and brain stem. Immunostaining of constitutive isoforms of neuronal NOS (nNOS) and HO-2 revealed marked upregulation in damaged and distorted neurons located within the edematous brain regions. Pretreatment with H-290/51 (50 mg/kg, p.o., 30 min before heat stress) significantly reduced the edematous swelling and cell injury and resulted in a marked attenuation of nNOS and HO-2 expression. These observations suggest that upregulation of NOS and HO is associated with cell injury, and the antioxidant compound H-290/51 is neuroprotective in heat stress.
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  • 3
    ISSN: 1438-2199
    Keywords: Keywords: Amino acids ; Hyperthermia ; Heat stress ; Heat shock protein (HSP 72 kD) ; Edema ; Cell injury ; Antioxidants ; EGB-761-BN 52021
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary. Influence of the extract of Gingko biloba (EGB-761) and one of its constituent Gingkolide B (BN-52021) on hyperthermia induced cellular damage and heat shock protein (HSP 72 kD) response was examined in a rat model. Rats subjected to 4 h heat stress at 38°C in a biological oxygen demand (BOD) incubator (relative humidity 50–55%, wind velocity 20–25 cm/sec) resulted in profound edema and cell injury in many parts of the cerebral cortex, hippocampus, cerebellum, thalamus, hypothalamus and brain stem. Immunostaining of HSP 72 kD showed marked upregulation in the damaged and distorted neurons located within the edematous area. Pretreatment with EGB-761 (50 mg/kg/day, p.o.) and BN-520 21 (2 mg/kg, p.o.) per day for 5 days significantly reduced HSP expression and attenuated cell damage. Our results show that EGB-761 and its component Gingkolide B (BN-52021) has the capacity to reduce edema and cell injury following hyperthermia and this effect of the compound is somehow associated with a reduction in cellular stress response as evidenced with a reduction in HSP expression.
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  • 4
    ISSN: 1438-2199
    Keywords: Keywords: Amino acids ; Spinal cord injury ; Heme oxygenase ; Heat shock protein ; Carbon monoxide ; Growth factors ; BDNF ; IGF-1 ; Immunohistochemistry ; Cell injury ; Spinal cord edema
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary. The influence of brain derived neurotrophic factor (BDNF) or insulin like growth factor-1 (IGF-1) on spinal cord trauma induced carbon monoxide (CO) production and cellular stress response was examined using immunostaining of the constitutive isoform of the hemeoxygenase (HO-2) enzyme and the heat shock protein (HSP 72 kD) expression in a rat model. Subjection of rats to a 5 h spinal trauma inflicted by an incision into the right dorsal horn at T10–11 segment markedly upregulated the HO-2 and HSP expression in the adjacent spinal cord segments (T9 and T12). Pretreatment with BDNF or IGF-1 significantly attenuated the trauma induced HSP expression. The upregulation of HO-2 was also considerably reduced. These results show that BDNF and IGF-1 attenuate cellular stress response and production of CO following spinal cord injury which seems to be the key factors in neurotrophins induced neuroprotection.
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  • 5
    ISSN: 1438-2199
    Keywords: Keywords: Amino acids ; Growth hormone ; Spinal cord injury ; Edema formation ; Spinal cord evoked potentials ; Spinal cord edema ; Cell injury
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary. The influence of exogenous rat growth hormone on spinal cord injury induced alterations in spinal cord evoked potentials (SCEP) and edema formation was examined in a rat model. Repeated topical application of rat growth hormone (20 μl of 1 μg/ml solution) applied 30 min before injuryand at 0 min (at the time of injury), 10 min, 30 min, 60 min, 120 min, 180 min, and 240 min, resulted in a marked preservation of SCEP amplitude after injury. In addition, the treated traumatised cord showed significantly less edema and cell changes. These observations suggest that growth hormone has the capacity to improve spinal cord conduction and attenuate edema formation and cell injury in the cord indicating a potential therapeutic implication of this peptide in spinal cord injuries.
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  • 6
    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.
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  • 7
    ISSN: 1432-0533
    Keywords: Spinal cord trauma ; Glial fibrillary acidic protein ; Serotonin ; p-Chlorophenylalanine ; Immunohistochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The possibility that serotonin may influence the early response of astrocytes around a spinal cord trauma was investigated in a rat model by making a unilateral incision into the right dorsal horn of the T10-11 segments. One group of rats received a serotonin synthesis inhibitor, p-chlorophenylalanine (p-CPA) before injury in doses which cause a depletion of serotonin in the cord. Another group of traumatised rats did not receive p-CPA. All animals were allowed to survive for 5 h. Samples for immunohistochemistry were taken from the T9, T10-11 and T12 segments of the cord. Paraffin sections were immunostained for glial fibrillary acidic protein (GFAP) using monoclonal antibodies and avidin-biotin complex technique. Trauma to the cord resulted in a marked increase of GFAP immunoreactivity in all the investigated segments, particularly in the ipsilateral side. Pretreatment with p-CPA markedly reduced the GFAP response. This drug did not by itself influence the GFAP immunoreactivity of the cord of untraumatised rats. Our results show that trauma to the spinal cord induces a rapid enhancement of GFAP immunoreactivity in the cord which is present even far away from the primary lesion. This response can be prevented by pretreatment with the serotonin synthesis inhibitor, p-CPA. The results indicate that serotonin influences the increase of GFAP immunoreactivity following spinal cord injury either directly or indirectly, for instance by its microvascular reactions.
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  • 8
    ISSN: 1432-0533
    Keywords: Serotonin (5-hydroxytryptamine, 5-HT) ; Spinal cord trauma ; Ventral horn ; p-Chlorophenyl alanine ; Immunohistochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The possibility that serotonin (5-hydroxytryptamine, 5-HT) is involved in the early tissue reactions occurring in spinal cord trauma was examined in a rat model using an immunocytochemical technique. The injury was made in the form of a 5-mm long and 2.5-mm wide lesion of the right dorsal horn at the level of T10–11. Injured rats, pretreated with the 5-HT synthesis blocking agent, p-chlorophenyl alanine (p-CPA) were compared with untreated injured controls and the animals were allowed to survive for 5 h. The distribution of 5-HT was examined in proximal and distal cross-sections of the cord, located 2 and 5 mm away from the injury. Normal rats showed immunoreactive material in nerve cell processes and in a few nerve cell bodies of the ventral horns. The trauma to the spinal cord caused a marked increase in 5-HT immunoreactivity in the segments located 2 mm proximal and distal to the injury, particularly in the ipsilateral ventral horn. The segment located 5 mm distal to the lesion showed a similar increase in immunoreactivity but it was apparently less pronounced in the corresponding proximal segment. Treatment with p-CPA markedly reduced the trauma-induced increase in 5-HT immunoreactivity in all the segments. These immunohistochemical findings were in line with the changes in the contents of 5-HT measured biochemically in corresponding spinal cord segments. At the onset of the trauma to the spinal cord 5-HT is thus present in the tissue, mainly in the form of 5-HT-containing nerve cell processes. Biochemical determinations also revealed that there is an increased amount of 5-HT in the traumatized spinal cord. The present study indicates that this is at least partly due to an increased amount of 5-HT in neurons and nerve cell processes of the perifocal region. The pathophysiollogical significance of the observed 5-HT-reaction in spinal cord injury is not known in all its details. However, 5-HT might be implicated in such tissue reaction, such as increased microvascular permea bility and edema formation occurring in the early period after trauma.
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