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  • 1
    Electronic Resource
    Electronic Resource
    Blood-brain barrier disruption and exacerbation of ischemic brain edema after restoration of blood flow in experimental focal cerebral ischemia (1988)
    Springer
    Acta neuropathologica 76 (1988), S. 62-70 
    Details
    ISSN: 1432-0533
    Keywords: Focal cerebral ischemia ; Blood-brain barrier ; Ischemic brain edema ; Regional cerebral blood flow ; Cerebral reperfusion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The mechanism of exacerbation of ischemic brain edema after blood flow restoration was studied in 20 cats under ketamine and alpha-chloralose anesthesia. Regional cerebral blood flow was measured by the hydrogen clearance method, and the left middle cerebral artery (MCA) was occluded for 6 h in group A, and for 3 h with subsequent 3 h recirculation in group B. Severity of brain edema was assessed by specific gravity measurement of tissue samples taken from coronal brain sections at the MCA area, while severity of blood-brain barrier (BBB) disruption was determined by measuring the amount of extravasated serum albumin by using [125I]albumin and tissue-uptake method in the same samples as those used for gravimetry. Structural and ultrastructural change was correlated with the severity of ischemic brain edema and BBB disruption. The results obtained showed that: (i) ischemic brain edema observed in group A was not associated with BBB opening to serum proteins; (ii) ischemic edema in group B was exacerbated significantly after recirculation in correlation with serum protein extravasation in most of the postischemic area; (iii) in the severely edematous area, serum protein extravasation reached a plateau and morphological examination at this type of area revealed cell membrane disruption especially of astrocytes, with leakage of intracellular substances. Our study indicated that the increase of extracellular osmotic pressure due to leakage of serum proteins via the disrupted BBB and of intracellular substances via the ischemically injured cell membrane into the extracellular space is the mechanism responsible for edema fluid accumulation in exacerbated ischemic brain edema.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00687681
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Experimental study on subacute neurotoxicity of methotrexate in cats (1989)
    Springer
    Acta neuropathologica 78 (1989), S. 291-300 
    Details
    ISSN: 1432-0533
    Keywords: Methotrexate (MTX) ; Experimental neurotoxicity ; Disseminated necrotizing leukoencephalopathy (DNL) ; Axonal degeneration
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary An experimental study on the pathogenesis of methotrexate (MTX)-related neurotoxicity including disseminated necrotizing leukoencephalopathy (DNL) was conducted in cats. MTX was administered to the cerebrospinal fluid (CSF) of adult cats using either an intracisternal intermittent instillation (ICI) model or an intraventricular continuous instillation (IVC) model. Furthermore, the synergistic effects of CSF-flow disturbance with kaolin-induced hydrocephalus, and60Co irradiation were morphologically examined in these models. None of the animals from either the ICI and IVC groups showed DNL, but all animals showed segmental axonal degeneration. suggesting that MTX had a direct toxic effect on the axon. In the ICI groups, no apparent synergistic effect of CSF-flow disturbance and radiation was noted on this axonal change. In the IVC groups, CSF-flow disturbance augmented the degree of the axonal injury. Axonal degeneration and fibrin exudation in the walls of small blood vessels occurred in one animal of the IVC groups with CSF-flow disturbance, suggesting that a toxic effect of MTX on blood vessels is another mechanism of MTX-induced neurotoxicity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00687759
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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