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  • 1
    Electronic Resource
    Electronic Resource
    Structural changes in the rat brain after carotid infusions of hyperosmolar solutions (1988)
    Springer
    Acta neuropathologica 77 (1988), S. 5-13 
    Details
    ISSN: 1432-0533
    Keywords: Blood-brain barrier ; Hyperosmolar solutions ; Electron microscopy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Infusion of hypertonic solutions into the carotid artery is one method by which the blood-brain barrier (BBB) can be opened transiently in experimental animals. This technique has also been tried in clinical situations in which an enhanced uptake of intravenously injected chemotherapeutic drugs into the brain is desired. We have previously found that infusion of hypertonic mannitol or urea into the carotid artery of the rat, leading to a BBB opening, is associated with light microscopic signs of cellular damage in the brain parenchyma. An electron microscopic study has now been made to obtain more detailed information about the events taking place in the rat brain 1 to 72 h after an intracarotid infusion of hyperosmolar solution of mannitol. Toluidine blue-stained semithin epon sections were also available for high-resolution light microscopy of brain samples from urea-infused animals. Intravenously injected Evan's blue dye was used to confirm that BBB opening had occurred as a consequence of the carotid infusions. The infused hemispheres had numerous structural changes. The dominating light microscopic alteration was the presence of multifocal lesions in the gray or the white matter with closely packed microvacuoles causing status spongiosus. Ultrastructurally the microvacuoles corresponded to very pronounced watery swelling of astrocytic processes and to a minor degree to expansion of dendrites and axons. There was also a light or moderate perivascular astrocytic swelling. In the “spongy” lesions as well as occasionally in non-vacuolated parts of the cerebral cortex, there were collapsed electron-dense neurons with pronounced mitochondrial alterations such as severe swelling associated with rupture of christae. Rats with a survival period of 24 h or 72 h showed several disintegrating neurons and accumulation of macrophages. This study shows that carotid infusion of hypertonic mannitol in the rat may cause pronounced neuronal changes as well as multifocal astrocytic swelling. The severity of the nerve cell changes and the presence of macrophages indicate that some of the alterations are irreversible and thus, such a procedure may not be as safe as previously suggested.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00688236
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Nerve cell injury in the brain of stroke-prone spontaneously hypertensive rats (1988)
    Springer
    Acta neuropathologica 76 (1988), S. 227-237 
    Details
    ISSN: 1432-0533
    Keywords: Stroke-prone spontaneously hypertensive rats ; Blood-brain barrier ; Brain edema ; Nerve cell injury ; Electron microscopy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The brain lesions in stroke-prone spontaneously hypertensive rats (SHRSP) are characterized by multifocal microvascular and spongy-cystic parenchymal alterations particularly in the gray matter. An essential feature of the lesions is the presence of edema with massive extravasation of plasma constituents as evidenced by specific gravity measurements, Evans blue technique and immunohistochemistry. The nerve cell injury occurring in the brain lesions in SHRSP is further characterized by light and electron microscopy in the present study. Two types of neuronal changes were seen within the blood-brain barrier (BBB) leakage sites. A small number of neurons with dark condensed nucleus and cytoplasm were found most often at the periphery of recent lesions. The majority of injured neurons were pale and showed intracellular edema confined to the dendrites and perikarya sparing axons and synapses. Their nuclei were weli preserved with finely dispersed chromatin. The swollen and watery cell processes of neurons and astrocytes gave a spongy appearance to the neuropil. The intracellular edema seemed to result in cytolysis. The results suggest that primary anoxiaischemia is not the major pathogenetic mechanism behind the nerve cell injury in severely hypertensive SHRSP, rather it is the massive BBB leakage and consequent brain edema that causes cytolytic destruction of neurons. Secondary focal ischemia as a consequence of occlusion in microvessels may, however, contribute to the nerve cell destruction.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00687769
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  • 3
    Electronic Resource
    Electronic Resource
    Substantia nigra damage induced by ischemia in hyperglycemic rats (1987)
    Springer
    Acta neuropathologica 75 (1987), S. 131-139 
    Details
    ISSN: 1432-0533
    Keywords: Cerebral ischemia ; Hyperglycemia ; Substantia nigra ; Electron microscopy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Preischemic hyperglycemia induced by feeding or glucose infusion worsens the brain damage and the clinical outcome following ischemia of a given duration and density, and characteristically causes postischemic seizure activity. Light microscopy has previously showed that, in the rat, transient hyperglycemic ischemia induced by bilateral carotid occlusion in combination with arterial hypotension causes a uni- or bilateral lesion in the pars reticulata of the substantia nigra. Since this region has a central role in preventing seizure discharges the present study was carried out to determine the ultrastructural characteristics of this lesion. In rats with 10 min of transient hyperglycemic ischemia followed by recirculation for 1 to 18 h, the pars reticulata of the substantia nigra showed signs of status spongiosus, as well as extensive nerve cell alterations. These changes were observed after all recovery periods studied. The spongiotic appearance was mainly caused by swelling of dendrites and, to a lesser degree, by astrocytic swelling. The dendrites were expanded at all recovery times but the severity increased during the later periods of recirculation. These swollen dendrites contained severely expanded mitochondrias and endoplasmic reticulum. The cytoskeletal elements showed disordered lining of microtubules. Two major types of nerve cell alterations were present: a “pale” and a “dark” variety. The pale type was the most frequent cell alteration. It occurred in all experimental groups and at all time points. Redistribution of the nuclear chromatin and of cytoplasmic organelles as well as swelling of the same type as in the dendrites were the essential changes. The dark neurons were much fewer in number and occupied a peripheral position in the pars reticulata. Astrocytic foot processes appeared to be dilated around the dark neurons. Swelling of astrocyte processes was most pronounced in the 1 h recovery animals. Both types of neurons showed severe mitochondrial alterations of the type observed in dendrites. Occasionally, mitochondrial alterations were found in astrocytic processes as well. Blood vessel alterations were lacking. Previous studies have shown that in this model of ischemia the substantia nigra has a relatively well-preserved blood perfusion. In view of this the extensive histopathological lesions are surprising. We speculate that the lesions primarily involve excitotoxic damage to dendrites, with pronounced lactic acidosis playing a contributory role in causing axonal and glial pathology as well.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00687073
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Hypoglycemic brain injury (1980)
    Springer
    Acta neuropathologica 50 (1980), S. 43-52 
    Details
    ISSN: 1432-0533
    Keywords: Hypoglycemia ; Nerve cell injury ; Electron microscopy ; Rat cerebral cortex
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Severe hypoglycemia was induced in rats by insulin. The brain was fixed in situ by perfusion after the spontaneous EEG had disappeared for 30 or 60 min or after recovery had been induced for 30 or 180 min by glucose injection. Samples from the cerebral cortex from the area corresponding to the previous metabolic studies were processed for electron microscopy. The light-microscopic finding of two different types of nerve cell injury, reported in a preceding communication (Agardh et al. 1980), was also verified at the ultrastructural level. The type I injury was characterized by cellular shrinkage, condensation of the cell sap and nuclei, and perineuronal astrocytic swelling. No swelling of mitochondria occurred. The slightly swollen type II injured neurons showed contraction of mitochondria, disintegration of ribosomes, loss of RER, and appearance of membrane whorls, while their nuclear chromatin remained evenly distributed. No transition from one type to the other was observed. Neither type of nerve cell injury in hypoglycemia was like that commonly seen in anoxic-ischemic insults indicating a different pathogenesis in these states despite the common final pathway of energy failure. The loss of endoplasmic membranes and disintegration of ribosomes suggests that these structures might be sacrificed for energy production in the absence of normal substrates. During recovery, though, the number of type I injured neurons decreased while some of the remaining ones appeared even more severely affected, suggesting irreversible damage. Type II injured neurons were no longer seen indicating reversibility of these changes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00688533
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