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  • 1
    Electronic Resource
    Electronic Resource
    The temporal evolution of hypoglycemic brain damage (1985)
    Springer
    Acta neuropathologica 67 (1985), S. 25-36 
    Details
    ISSN: 1432-0533
    Keywords: Hypoglycemia ; Hippocampus ; Neuronal necrosis ; Mitochondria ; Astrocyte ; Endothelial microvilli
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Part I of this paper has documented the evolution of dark neurons into acidophilic neurons in the superficial laminae as well as the reversion of dark neurons to normal neurons in the deep laminae of the cerebral cortex in hypoglycemic brain damage. The present study describes the temporal evolution of hypoglycemic brain damage in the hippocampus. The evolution of dark neurons to acidophilic neurons was confirmed in this brain region. Four additional problems were addressed: Firstly, delayed neuronal death was looked for, and was found to occur in areas of CA1 undergoing mild damage. However, it was not preceded by a morphological free interval, had ultrastructural characteristics distinct from delayed neuronal death in ischemia, and hence should be considered a distinct phenomenon. Secondly, the gradient in the density of neuronal necrosis in the rat hippocampal pyramidal cell band was exploited to test the hypothesis that a more severe insult causes a more rapid evolution of neuronal changes. This was found to be the case, with a temporal spectrum in the timing of neuronal death: Necrosis occurred already after 2 h medially in the sobiculum, and was delayed by up to several weeks laterally in CA1. Thirdly, the almost universal sparing of CA3 pyramidal neurons after 30 min hypoglycemic isoclectricity was exploited to address the question of whether reactive changes, which could with certainty be deemed reversible, occur in CA3. Mitochondrial injury was seen in these cells, and was found to be recoverable. No reactive changes of the type previously described following ischemic insults were observed. Fourthly, the astrocytic and vascular response of the tissue was studied. A sequence of astrocytic changes representing structural and probably metabolic activation of astrocytes was seen, consisting of morphological indices of increased turnover of cellular components. Capillaries demonstrated endothelial pits, vesicles, and prominent microvilli hours to days after recovery. The results demonstrate that, in the hippocampal gyrus as in other brain regions, hypoglycemic brain damage is distinct from ischemic brain damage and likely has a different pathogenesis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00688121
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    The temporal evolution of hypoglycemic brain damage (1985)
    Springer
    Acta neuropathologica 67 (1985), S. 13-24 
    Details
    ISSN: 1432-0533
    Keywords: Hypoglycemia ; Cerebral cortex ; Nerve cell injury ; Dark neurons ; Acidophilic neurons ; Mitochondria ; Golgi apparatus ; Cell necrosis ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In the course of a study on the pathogenesis of neuronal necrosis in severe hypoglycemia, the morphological characteristics reflecting reversible and irreversible neuronal lesions were examined as a function of time following normalization of blood glucose. To that end, closely spaced time intervals were studied in the rat cerebral cortex before, during, and up to 1 year after standardized pure hypoglycemic insults of 30 and 60 min of cerebral isoelectricity. Both the superficial and deep layers of the cerebral cortex showed dark and light neurons during and several hours after the insult. By electron microscopy (EM) the dark neurons were characterized by marked condensation of both karyoplasma and cytoplasm, with discernible, tightly packed cytoplasmic organelles. The light neurons displayed clustering of normal organelles around the nucleus with clearing of the peripheral cytoplasm. Some cells, both dark neurons and neurons of normal electron density, contained swollen mitochondrial with fractured cristae. Light neurons disappeared from the cerebral cortex by 4 h of recovery. Some dark neurons in the superficial cortex and almost all in the deep cortex evolved through transitional forms into normal neurons by 6 h recovery. Another portion of the dark neurons in the superficial cortex became acidophilic between 4 and 12 h, and by EM they demonstrated karyorrhexis with stippled electron-dense chromatin. The plasma membrane was disrupted, the cytoplasm was composed of amorphous granular debris, and the mitochondria contained flocculent densities. These definitive indices of irreversible neuronal damage were seen as early as 4–8 h recovery. Subsequently, the acidophilic neurons were removed from the tissue, and gliosis ensued. Thus, even markedly hyperchromatic “dark” neurons are compatible with survival of the cell, as are neurons with conspicuous mitochondrial swelling. Definite nerve cell death is verified as the appearance of acidophilic neurons at which stage extensive damage to mitochondria is already seen in the form of flocculent densities, and cell membranes are ruptured. Our previous results have shown that hypoglycemic neocortical damage affects the superficial laminae, chiefly layer 2. The present results demonstrate that, following the primary insult, this damage evolves relatively rapidly within the first 4–12 h. We have obtained no evidence that additional necrotic neurons are recruited after longer recovery periods.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00688120
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    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Current concepts on reperfusion injury following focal cerebral ischemia (1999)
    Springer
    Intensivmedizin und Notfallmedizin 36 (1999), S. 260-269 
    Details
    ISSN: 1435-1420
    Keywords: Schlüsselwörter Zerebralischämie ; Reperfusionsschädigung ; Mitochondria ; Key words Cerebral ischemia ; Reperfusion injury ; Mitochondria
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary Reperfusion injury has become a scientific problem of increasing importance, in part because of recent developments of thrombolytic therapy. The mechanisms of reperfusion injury following focal cerebral ischemia, however, are not known in detail. Recent studies strongly suggest that reactive oxygen species (ROS) and calcium overload play an important role in reperfusion injury and that pharmacological interventions against calcium- or free radical-mediated damage could extend the therapeutic window in cerebral ischemia/reperfusion. The mediators involved are known to induce a mitochondrial permeability transition (PT) during the reperfusion period, which is associated with uncoupling of mitochondrial respiration, loss of mitochondrial membrane potential, and a burst production of ROS, leading to cellular death. The mitochondrial PT is considered to be a key process in reperfusion injury following cerebral ischemia, as also observed in other organs such as heart and liver. Pharmacological modulation of mitochondrial permeability changes have the potential to reduce tissue damage due to reperfusion.
    Notes: Zusammenfassung Die Reperfusionsschädigung ist ein an Wichtigkeit zunehmendes wissenschaftliches Problem, z. T. wegen der neueren Entwicklungen in der thrombolytischen Therapie. Die Mechanismen der Reperfusionsschädigung nach fokaler Zerebralischämie sind jedoch in Detail unbekannt. Neuere Studien deuten stark darauf hin, daß reaktive Sauerstoffspezien (ROS) und Kalziumüberladung eine wichtige Rolle bei der Reperfusionsschädigung spielen, und daß pharmakologische Interventionen gegen eine von Kalzium- oder freien Radikalen vermittelte Schädigung die therapeutische Breite bei der Zerebralischämie/ Reperfusion erweitern könnte. Es ist von den entsprechenden Vermittlern bekannt, daß sie eine mitochondriale Permeabilitätstransition (PT) während der Reperfusionszeit induzieren, und eine explosionsartige Produktion von ROS, welche zum Zelltod führt. Der mitochondrialen PT wird eine Schlüsselrolle bei der Reperfusionsschädigung nach Zerebralischämie zugeschrieben, wie auch in anderen Organen z. B. Herz und Leber beobachtet. Eine pharmakologische Modulation der Veränderung der mitochondrialen Permeabilität hat das Potential, reperfusionsbedingte Gewebeschädigung zu reduzieren.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s003900050237
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    Paper (German National Licenses)
    Fulltext
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