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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 88 (1994), S. 287-292 
    ISSN: 1432-0533
    Keywords: Key words Blood-brain-barrier ; Central pontine ; myelinolysis ; Electrolyte-induced demyelination ; Oligodendrocyte ; Pathogenesis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The blood-brain barrier (BBB) was studied in rats with electrolyte-induced demyelination (EID), an experimental model for central pontine myelinolysis. Intravenously injected peroxidase was extravasated at 3 h post hypertonic saline injection (PHS) into regions frequently involved in EID. Increased pinocytotic activity and focal interendothelial gaps were seen at 3 h PHS and less frequently at 48 h PHS. Measurement of total cerebral water content revealed an increase during the hyponatremic phase. This was followed by a marked increase at 3 h PHS with continued increment at 48 h PHS. Intracellular edema with accumulation of fluid within neurites and astrocytic processes was noted during the hyponatremic phase, whereas extracellular edema developed after hypertonic saline injection. The implications of disrupted BBB and its role in the pathogenesis of EID are discussed.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 88 (1994), S. 293-299 
    ISSN: 1432-0533
    Keywords: Key words Blood-brain barrier ; Central pontine ; myelinolysis ; Electrolyte-induced demyelination ; Oligodendrocyte
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract This study presents the electron microscopic evolution of lesions in electrolyte-induced demyelination (EID) in rats, a lesion which bears striking histological and clinical similarity to central pontine myelinolysis. The earliest change was observed during the hyponatremic phase and consisted of minimal intracellular edema present throughout the brain. Following the injection of hypertonic saline, additional changes were observed which were restricted to sites previously reported to be frequently involved in EID. Early dilatation of the inner tongue of oligodendrocyte cytoplasm in myelinated nerve fibers was observed at 3   h post hypertonic saline injection (PHS). This was followed, at 48   h PHS, by the appearance of degenerative changes consistent with dying oligodendrocytes. Well-de- lineated, vacuolar and spongy lesions, seen by light microscopy, were present by 48   h PHS at the same sites as above. Electron microscopically, this appearance was found to be due to striking intramyelinic edema. By 96   h PHS, macrophages containing myelin and other cellular debris were frequently present at these sites. Concomitantly, myelin sheaths underwent vesicular disruption and disintegration. This sequence of events suggests a lesion of the oligodendrocyte-myelin complex, secondary to initial blood-brain barrier damage and edema.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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