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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 46 (1979), S. 123-131 
    ISSN: 1432-0533
    Keywords: Cerebral ischemia ; Mitochondria ; Lysosomes ; Golgi apparatus ; Histochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The ischemic effect on cerebral enzymes and glycogen content was histochemically evaluated in mongolian, gerbils subjected to unilateral common carotid artery occlusion for various periods of time from 1/2 to 9h. In early stages (up to 2h), the only enzyme affected was the phosphorylase which revealed a decreased activity. Thereafter, the observed changes inclusive of glycogen and other enzymes such as the dehydrogenase, nonspecific acid and alkaline phosphatases, leucine aminopeptidase and thiamine pyrophosphatase progressed proportionally to the duration of ischemia. There was an overall inverse appearance of histochemically demonstrated enzymatic disturbances between the severely damaged ischemic regions and its marginal zones; the former revealing a conspicuous decrease and/or loss of enzymatic activities while the latter showing an increase of the same enzymes. Correlating the various ischemic responses of the intracellular organelles it appears that the changes in the lysosomes and Golgi apparatus occurred slower than those of mitochondria.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0533
    Keywords: Cold-lesion injury ; Brain edema ; Blood-brain barrier ; Alkaline phosphatase ; Anionic sites
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Micro-blood vessels (MBVs), located in the area of edema, were studied in cat brain at various time intervals (1 h, 24 h, 7 days) after cold-lesion injury. Both cold-injured and adjacent gyri were examined for blood-brain barrier (BBB) permeability to i. v. injected horseradish peroxidase (HRP) with circulation times of 40 min and 24 h. Evans blue (EB) was used as a tracer for gross evaluation of the extension of brain edema. Localization of alkaline phosphatase (AP) and binding of cationized ferritin (CF), considered as a marker of anionic sites, were also studied ultrastructurally. Twenty-four hours after cold injury, the extravasated edema fluid, outlined by EB tracer, was observed to be spreading through the white matter (WM) into the adjacent gyrus. At this time, numerous, larger than capillary MBVs, presumably arterioles and venules located in the edematous WM, showed accumulations of HRP injected at the time of the operation, in the basement membrane, in abluminal pits, and in numerous pinocytotic vesicles and vacuoles of endothelial cells (ECs). The animals killed after 24 h with 40 min HRP circulation showed extravasation of HRP tracer in a zone underlying the necrotic cold injury lesion. On the other hand, there was no evidence of an abnormal HRP leakage in the further removed areas of edema in the WM, particularly in the adjacent gyrus. These observations suggest that a reverse, vesicular transport of HRP across the ECs of some MBVs represents one of several possible mechanisms responsible for the removal of extravasated proteins and of edematous fluid from brain extracellular space. This reverse transport is accompanied by a disruption of the surface anionic layer and changed polarity of ECs manifested by the relocation of AP activity from luminal to abluminal plasmalemma.
    Type of Medium: Electronic Resource
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