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  • 1
    ISSN: 1437-773X
    Schlagwort(e): Key words X-ray microanalysis ; Mitochondria ; Hippocampal CA1 ; Repeated brief cerebral ischemia ; Calcium ; Aluminum
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract To elucidate the interrelationship between delayed neuronal death and calcium accumulation, an X-ray microanalysis technique was used to detect the elemental composition of deposits in mitochondria and nuclei after three 3-min bilateral common carotid arterial occlusion at 1-h intervals. Morphological changes in the CA1 pyramidal neurons were also observed. After 3 days of ischemia-recirculation, damaged mitochondria, electron-dense deposits in mitochondria, and rupture of nuclear membranes were evident. Calcium and aluminum were detected in those electron deposits in the mitochondria and nuclei. These findings support the hypothesis on delayed calcium-related cell death. Accumulation of aluminum in mitochondria and nuclei may be an additional factor involved in delayed neuronal death.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 2
    Digitale Medien
    Digitale Medien
    Springer
    Medical electron microscopy 32 (1999), S. 175-183 
    ISSN: 1437-773X
    Schlagwort(e): Key words Cerebral blood flow ; Blood–brain barrier ; Repeated brief cerebral ischemia ; Hippocampal CA1 ; Ultrastructure
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract Neuronal damage and changes in cerebral blood flow (CBF) and the permeability of the blood–brain barrier (BBB) following repeated brief periods of ischemia were studied in Mongolian gerbils. The cerebral ischemia was produced by three repeated occlusions of bilateral common carotid arteries for 3 min at 1-h intervals. CBF and permeability of the BBB were examined with tracers (China ink and silver nitrate) at 1, 3, and 7 days post ischemia using light and electron microscopy. Three days after the reperfusion, significant extravasation of tracers, consequential reduction of CBF, extensive neuronal destruction, and intravascular platelet aggregation were observed. Such vascular changes in the CA1 region were more severe than those in the frontal cortex. These findings strongly support the view that microcirculatory disturbance may be a mechanism responsible for delayed neuronal death in the CA1 region of the hippocampus.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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