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  • 1
    ISSN: 1437-2320
    Keywords: Key words Focal cerebral ischemia ; Programmed neuronal death ; Nimodipine ; Mannitol ; Cerebroprotection
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The present study was conducted to evaluate the effects of nimodipine and mannitol on infarct size and on the amount of apoptosis after transient focal cerebral ischemia. Focal cerebral ischemia was induced in male Sprague-Dawley rats (weight 300–380 g) by transient occlusion of the right middle cerebral artery (MCAO) using an intraluminal thread model. All animals underwent ischemia for 2 h, followed by 24 h of reperfusion. Group I (n=16) was untreated. Group II (n=16) received 15% mannitol (1 g/kg as bolus) and group III (n=9) received 15 µg/kg/h nimodipine intravenously beginning 15 min prior to MCAO. Twenty-four hours after reperfusion, the brain was taken and sectioned in coronal slices. The slices were stained with H&E and with the transferase dUTP nick-end labeling (TUNEL) technique. Histopathological analysis revealed a significant (P〈0.05) decrease in infarct size in the striatum with both drugs: mannitol (group II) 25.4±5.9% and nimodipine (group III) 21.5±11.0% versus control (group I) 34.9±7.0% and in the cortex 2.7±2.0% (group II) and 6.3±2.4% (group III) versus control 14.4±9.0% (group I). The number of apoptotic cells was statistically lower in the therapy groups (group III 9.6, group II 25.8) versus control (group I 57.9) (Mann-Whitney-Wilcoxon U-test Z〉1.96, P〈0.05). This study indicates that mannitol and nimodipine provide neuroprotection by preventing both the necrotic and apoptotic components of cell death after transient focal cerebral ischemia and may be effective as neuroprotective drugs for cerebrovascular surgery.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Radiation Physics and Chemistry 18 (1981), S. 1207-1216 
    ISSN: 0146-5724
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Chemistry and Pharmacology , Energy, Environment Protection, Nuclear Power Engineering , Physics
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 0040-4039
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 0942-0940
    Keywords: Cytoskeleton ; delayed neuronal death ; nerve growth factor (NGF) ; neurofilament (NF)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We investigated the protective action of nerve growth factor (NGF) on delayed neuronal death, and we also studied the involvement of the 200 kDa neurofilament (NF 200) cytoskeletal proteins. Wistar rats were divided into three groups: Group I, in which transient forebrain ischaemia was produced; Group II, ischaemic group which received intraventricular administration of artificial cerebrospinal fluid (CSF); and Group III, ischaemic group which received intraventricular administration of 2 Μg of 2.5 S NGF. Forebrain ischaemia in these rats was produced by causing transient bilateral occlusion of the common carotid arteries and lowering the mean blood pressure to 50 mmHg for 8 minutes. On the 1st and 7th day after ischaemia we histologically examined neuronal death in the hippocampal CA1 sector. On the 7th day after ischaemia, mean cell death (degenerative cell number/total cell number) was 87±9% in group I (n=7), 51±36% in group II (n=7), and 14±16% in group III (n=8) (p〈0.05 vs. group II). The concentration of NF 200 in the hippocampal homogenate was measured by the Western blotting method on the 1st and 7th day after ischaemia. On the 1st day it was found to be 67±11% of that in the control group in group I (n=6), 73±21% in group II (n=6), and 84±7% in group III (n=6) (p〈0.05 vs. group II). The concentration of NF 200 in all groups remained at the same level until the 7th day after ischaemia (each group, n=6). These results suggest that 1) intraventricular NGF has a protective effect on delayed neuronal death, 2) these protective actions occur within one day after ischaemia, and 3) these effects may be mediated by the suppressed degradation and/or promoted restoration of neuronal cytoskeletal proteins.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Acta neurochirurgica 142 (2000), S. 1031-1036 
    ISSN: 0942-0940
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Acta neurochirurgica 138 (1996), S. 580-583 
    ISSN: 0942-0940
    Keywords: Ciliary neurotrophic factor (CNTF) ; cerebral ischaemia ; delayed neuronal cell death ; rat hippocampus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The neuroprotective effect of neurotrophic factors has been demonstrated in experimental cerebral ischaemia recently. These include nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), insulin-like growth factor-1 (IGF-1), and basic fibroblast growth factor (basic FGF). The neuroprotective effect of ciliary neurotrophic factor (CNTF), however, has not been studied so far. We have examined the neuroprotective effect of recombinant rat CNTF in a rat forebrain ischaemia model. A continuous infusion of CNTF was started 1 week before the induction of ischaemia and continued until 1 week after the ischaemia. Reversible forebrain ischaemia was induced by 7 minutes of bilateral carotid occlusion with hypotension. Neuronal cell death in the hippocampal CA1 sector was evaluated 1 week after the ischaemia. For the control group artificial CSF (cerebrospinal fluid) was infused instead of CNTF. Per cent neuronal cell death was 83.4 ± 5.9% (mean ± SEM, n=5) in the control group, and 71.1 ± 10.0% (mean ± SEM, n=5) in the CNTF group. Although percentage of neuronal cell death was lower in the CNTF group, the difference was not statistically significant. This result suggests that the protective effect of CNTF in the rat forebrain ischaemia model may be limited compared with other neurotrophic factors. It is considered that the number of neurons protected by CNTF may be small.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Acta neurochirurgica 142 (2000), S. 1123-1128 
    ISSN: 0942-0940
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 0942-0940
    Keywords: PET ; moyamoya disease ; cerebral blood flow ; cerebral blood volume
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Regional cerebral blood flow (rCBF), oxygen extraction fraction (rOEF), cerebral metabolic rate for oxygen (rCMRO2) and cerebral blood volume (rCBV) in nine cases of moyamoya disease in adults were studied with positron emission CT (PET) scan, using15O steady-state methods. Three cases showed ischaemic symptoms and the other six cases showed haemorrhagic symptoms. PET scan was performed during the chronic stage. Control data were obtained from eight normal volunteers. Regional cerebral blood flow and other physiological parameters in cerebral gray matter, white matter and basal ganglia were compared with normal controls. All nine cases of Moyamoya disease showed decreased rCBF, though not significant, in cerebral gray matter, white matter and basal ganglia. Reduction of rCBF was significant in the cerebral cortex of six haemorrhagic cases. This significant decrease was considered to be due to diaschisis and also brain atrophy caused by the cerebral haemorrhage. There was a significant increase in rCBV in white matter of the both ischaemic and haemorrhagic cases. The calculated value of CBF/CBV is considered to be an index of perfusion pressure. This value was significantly decreased in all three regions, though rOEF was not significantly increased in moyamoya disease. Hence the cerebral circulation in adults with moyamoya disease appears to be characterized by a mild decrease in perfusion pressure and prolonged circulated time.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Acta neurochirurgica 120 (1993), S. 26-32 
    ISSN: 0942-0940
    Keywords: Arteriovenous malformation ; basal ganglia ; cerebral blood flow ; diaschisis ; thalamus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We investigated the haemodynamic dysfunction and secondary thalamic and brainstem atrophy in 24 patients with angiographically proven cerebral arteriovenous malformations (AVM) and no clinical history of cerebral haemorrhage. Cerebral blood flow (CBF) was measured by the method using either stable Xenon or single photon emission computerized tomography (SPECT). Morphological changes in the thalamus and brainstem were evaluated by magnetic resonance imaging (MRI). Two factors are considered to influence hypoperfusion in the ipsilateral cerebral and contralateral cerebellar hemisphere and secondary atrophy of the thalamus and brainstem. One is the size of the nidus and the other is the involvement of the basal ganglia. It is presumed that continuous haemodynamic stress over a long period of time may cause irreversible histological changes in areas remote from the lesion, especially in the AVM which demonstrates involvement of the basal ganglia or a large nidus.
    Type of Medium: Electronic Resource
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