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  • 1
    Electronic Resource
    Electronic Resource
    The brain in extreme respiratory acidosis (1982)
    Springer
    Acta neuropathologica 58 (1982), S. 87-94 
    Details
    ISSN: 1432-0533
    Keywords: Hypercapnia ; Rat brain ; Ultrastructure ; Cerebral edema
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary It is presently debated how much cellular acidosis contributes to brain cell damage during ischemia and hypoxia. To study the influence of acidosis occurring in the absence of energy failure, extreme hypercapnia was produced in anesthetized, artificially ventilated, and well oxygenated rats by increasing the inspired CO2 concentration until arterialPCO2 reached 150 or 300 mm Hg. At these CO2 tensions intracellular pH falls from a control value of about 7.05 to about 6.85 and 6.65, respectively. After 45 min the brains were fixed in perfusion and processed for light and electron microscopy. AtPaCO2 150 mm Hg no clear neuronal abnormality was detected, but atPaCO2 300 mm Hg some neuronal changes were observed. Notably, the nuclei showed slightly coarser chromatin than normally. In a few nerve cells mild swelling of mitochondria and dispersion of polysomes as well as detachment of ribosomes from the endoplasmic reticulum appeared. In both groups, slight to moderate astrocytic edema developed. Thus, even extreme hypercapnia, with its acompanying marked tissue acidosis, alters ultrastructure in the brain only to such a moderate extent that irreversible cell damage is unlikely. We conclude, therefore, that acidosis occurring during ischemia or hypoxia is detrimental only if pH is further lowered and/or if it occurs in conjunction with cerebral energy failure.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00691646
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  • 2
    Electronic Resource
    Electronic Resource
    The dentate gyrus in hypoglycemia: Pathology implicating excititoxin-mediated neuronal necrosis (1985)
    Springer
    Acta neuropathologica 67 (1985), S. 279-288 
    Details
    ISSN: 1432-0533
    Keywords: Dentate ; Hypoglycemia ; Excitotoxin ; Dendrites ; Neuronal necrosis ; Membrane breaks ; Cerebrospinal fluid (CSF)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A detailed light- and electron-microscopic study of the damage to the rat dentate gyrus in hypoglycemia was undertaken, in view of the previously advanced hypothesis that hypoglycemic nerve cell injury is mediated by a released neurotoxin. The distribution of neuronal necrosis showed a relationship to the subarachnoid cisterns. Electron microscopy of the dentate granule cells and their apical dendrites revealed dendrosomal, axon-sparing neuronal pathology. Dentate granule cells were affected first in the dendrites in the outer layer of the stratum moleculare, sparing axons of passage and terminal boutons. Subsequently, the neuronal perikarya were affected, and Wallerian degeneration of axons followed. Cell membrane abnormalities preceded the appearance of mitochondrial flocculent densities and degradation of the cytoskeleton, and are suggested to be early lethal changes. The observed early dendrotoxic changes, and the dendrosomal, axon-sparing nature of the lesion implicate an excitotoxin-mediated neuronal necrosis in hypoglycemia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00687813
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  • 3
    Electronic Resource
    Electronic Resource
    Influence of systemic factors on experimental epileptic brain injury (1983)
    Springer
    Acta neuropathologica 60 (1983), S. 81-91 
    Details
    ISSN: 1432-0533
    Keywords: Brain injury ; Status epilepticus ; Hyperoxia ; Hypoxia ; Hypotension ; Vitamin E
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A previous study from the laboratory showed that status epilepticus induced by bicuculline administration to ventilated rats produced astrocytic swelling and nerve cell changes (“type 1 and 2 injury”) particularly in layers 3 and 5 of the neocortex (Söderfeldt et al. 1981). The type 1 injured neurons were characterized by condensation of cyto-and karyoplasm and the less common type 2 cells were characterized by swelling of endoplasmic reticulum including the nuclear envelope. In the present study we explored whether changes in cerebral oxygen availability altered the extent or character of the cellular alterations. Animals with 2 h of status epilepticus were made either hyperoxic (administration of 100% O2), hypoxic (arterialpO2 50 mm Hg) or hypotensive (arterial blood pressure of either 70–75 or 50 mm Hg). Furthermore, we explored whether “oxidative” damage occurred by manipulating tissue levels of α-tocopherol, a known free radical scavenger. Non-epileptic control animals exposed to comparable degrees of hypoxia or hypotension showed no or minimal structural alterations. In the epileptic animals the results were as follows.Hyperoxia did not change the quality or extent of the structural alterations previously observed in normoxic epileptic animals. Neither administration nor deficiency ofvitamin E did modify this pattern of alterations. Inhypoxia the extent of cell damage was the same or somewhat larger than in normoxic, epileptic animals. In addition, neurons often showed cytoplasmic microvacuoles due to swelling of mitochondria. The hypoxic animals also showed swelling of astrocytic nuclei with clumped chromatin. Changes similar to those observed in hypoxic animals also appeared in moderatehypotension (mean arterial blood pressure 50 mm Hg), whereas mild hypotension (70–75 mm Hg) did not change the character of the tissue injury from that seen in hyperoxic or normoxic epileptic rats. The present results demonstrate that the neuronal cell damage that can be observed when the brain is fixed by perfusion after status epilepticus of 2 h duration is not exaggerated by hyperoxia or vitamin E deficiency nor is it ameliorated by a moderate restriction in cerebral oxygen supply or by vitamin E administration. If anything, hypoxia (or moderate hypotension) appears to increase the extent of damage and it clearly alters its ultrastructural characteristics. However, although the results fail to support the notion that epileptic cell damage is “oxidative”, definite conclusions must await information on the cell damage that remains upon arrest of the epileptic activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00685351
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  • 4
    Electronic Resource
    Electronic Resource
    Protective effect of lesion to the glutamatergic cortico-striatal projections on the hypoglycemic nerve cell injury in rat striatum (1987)
    Springer
    Acta neuropathologica 74 (1987), S. 335-344 
    Details
    ISSN: 1432-0533
    Keywords: Hypoglycemia ; Rat striatum ; Glutamate ; Excitotoxic nerve cell injury ; Electron microscopy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In rat striatum severe hypoglycemia causes an irreversible nerve cell injury, which does not become manifest until during the post-insult recovery period. This injury can be ameliorated by lesions of the glutamatergic cortico-striatal pathway, which suggests that an “excitotoxic” effect mediated by the glutamatergic input is the likely cause of the posthypoglycemic nerve cell destruction. In this paper we further characterize the protective effect of abolishing the glutamatergic innervation to striatum at the ultrastructural level. Two weeks after a unilateral cortical ablation rats were subjected to 30 min of severe hypoglycemia with isoelectric EEG and killed either immediately after the insult or following 60 min of recovery induced by restoring the blood glucose levels. Immediately after the hypoglycemic insult the structure of striatum was similar on both sides (except for the changes attributable to the ablation); i.e., the neurons and their dendrites had pale cytoplasm with condensed mitochondria, sparse RER and pinpoint ribosomes. After 60 min restitution numerous striatal neurons on the non-protected, non-ablated side had turned variably dark and condensed, whereas under-neath the ablation they remained similar as immediately after hypoglycemia. This sequence indicates that the most likely cause of nerve cell destruction on the non-protected side is the “excitotoxic” effect mediated by the glutamatergic innervation, which is superimposed on the action of the hypoglycemic insultper se. Furthermore, the primary condensation of neurons and their dendrites indicate existence of another type of acute “excitotoxic” nerve cell injury which differs from the previously described injury characterized by neuronal swelling.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00687210
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  • 5
    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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  • 6
    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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  • 7
    Electronic Resource
    Electronic Resource
    Pathogenesis of brain lesions caused by experimental epilepsy (1981)
    Springer
    Acta neuropathologica 54 (1981), S. 219-231 
    Details
    ISSN: 1432-0533
    Keywords: Status epilepticus ; Nerve cell injury ; Brain edema ; Rat cerebral cortex
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Status epilepticus was induced in rats by the GABA receptor blocking agent, bicuculline, during artificial ventilation and with closely monitored physiologic parameters. After 1 or 2 h of status epilepticus the brains were fixed by perfusion with glutaraldehyde and processed for light and electron microscopy. In the cerebral cortex two different types of changes were present, i.e., nerve cell injuries and status spongiosus. Type 1 injured neurons, mainly in the areas of most marked sponginess (layer 3), displayed progressive condensation of both karyo-and cytoplasm. In the most advanced stages the nucleus could no longer be distinguished from the cytoplasm in the light microscope, and vacuoles of apparent Golgi cisterna origin appeared in the darkly stained cytoplasm. This type of injured neurons comprised 41 and 56% of the cortical neurons after 1 or 2 h of status epilepticus, respectively. Seven to 9% of the neurons showed another type of injury (type 2). They were mainly located in the deeper cortical layers, and showed slit-formed cytoplasmic vacuoles chiefly due to swelling of the endoplasmic reticulum including the nuclear envelope. Marked sponginess of the cortex developed principally in layer 3 and it spread into deeper layers with longer duration of status epilepticus, but the outermost layers retained a compact structure. As judged by electron microscopy, the sponginess resulted mainly from swelling of astrocytes and their processes causing both perivascular and perineuronal vacuolation. The structural changes observed are considered to be caused by astrocytic and to a lesser extent intraneuronal edema related to the seizure activity. Although the exact pathogenetic mechanisms are not known, our findings indicate that hypoxia-ischemia is not a major determinant of the tissue damage observed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00687745
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  • 8
    Electronic Resource
    Electronic Resource
    Reply to the remarks by J. B. Brierley and A. W. Brown (1981)
    Springer
    Acta neuropathologica 55 (1981), S. 323-325 
    Details
    ISSN: 1432-0533
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00690997
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  • 9
    Electronic Resource
    Electronic Resource
    Pathogenesis of brain lesions caused by experimental epilepsy (1983)
    Springer
    Acta neuropathologica 59 (1983), S. 11-24 
    Details
    ISSN: 1432-0533
    Keywords: Status epilepticus ; Nerve cell injury ; Brain edema ; Rat hippocampal formation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Status epilepticus with a duration of 1 or 2 h was induced in rats by i. v. injection of the GABA receptor blocking agent, bicuculline. Immediately there-after, or following a 2 h recovery period, the brains were fixed by vascular perfusion and processed for light and electron microscopy to characterize the type and distribution of morphological changes in the hippocampal formation. In a previous study (Söderfeldt et al. 1981) astrocytic edema and wide-spread neuronal changes of two different kinds occurred in the fronto-parietal cortex of the same animals. Type 1 injured neurons were characterized by condensation of karyoplasm and cytoplasm (type 1a), which in some neurons became so intense that the nucleus could no longer be clearly discerned (type 1b). The type 2 injured neurons had slitformed cytoplasmic vacuoles chiefly caused by dilatation of the rough endoplasmic reticulum. In the hippocampus the most conspicuous alteration was astrocytic edema which was most marked around the perikarya of pyramidal neurons in CA1-CA4 and subiculum. In the dentate gyrus the edema was less pronounced and, when present, affected particularly the hilar zone of the stratum granulosum. The nerve cell changes were less pronounced than in the cerebral cortex. The vast majority of the hippocampal pyramidal neurons in CA1-CA4 showed minor configurational and tinctorial abnormalities (incipient type 1a change). Severe nerve cell alterations (type 1b) were present but very rarely affected the pyramidal neurons of CA1-CA4 and subiculum, whereas in the dentate gyrus pyramidal basket neurons of stratum granulosum and pyramidal nerve cells in stratum polymorhe showed the severe type 1b changes. As compared with the frontoparietal cortex (Söderfeldt et al. 1981) the type 2 changes were extremely rare. In the early recovery period after 1 h of status epilepticus the astrocytic edema and the incipient type 1a changes had almost entirely disappeared, whereas a few condensed and dark-staining type 1b injured neurons remained. Thus, in this model of status epilepticus the most marked response in the hippocampal formation is astrocytic edema in the layers where pyramidal perikarya are located. Incipient, mild nerve cell changes which appear to be reversible were frequent and widespread in the entire hippocampal formation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00690312
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  • 10
    Electronic Resource
    Electronic Resource
    Cerebrovascular lesions in stroke-prone spontaneously hypertensive rats (1985)
    Springer
    Acta neuropathologica 68 (1985), S. 284-294 
    Details
    ISSN: 1432-0533
    Keywords: Stroke-prone spontaneously hypertensive rats ; Blood-brain barrier ; Fibrinoid degeneration ; Brain edema
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The cerebrovascular lesions of severe chronic hypertension were studied by light microscopy in perfusion-fixed, subserially sectioned brains from stroke-prone spontaneously hyptertensive rats (SHRSP). The leakage and spread of plasma proteins were visualized by immunohistochemical detection of extravasated fibrinogen and by using an exogenous marker (Evans blue injected i.v.) for blood-brain barrier (BBB) dysfunction. In most SHRSP the hypertension did not lead to major BBB lesions in spite of a mean arterial pressure around 200 mm Hg at 6–9 months of age. Multifocal BBB damage occurred in a minor group of SHRSP, particularly within the cortex and the deep gray matter. A close spatial correlation was found between the leakage-spread of plasma constituents and the neuropathologic alterations. Fibrinoid degeneration of penetrating arterioles was found within the leakage sites. The surrounding gray matter showed petechial hemorrhages and abundant proteinaceous exudates rich in antifibrinogen-positive material. The current leakage of Evans blue and wide spread of fibrinoid substances suggested long-lasting damage to the BBB. Most neurons within the edematous gray matter had well preserved nuclei surrounded by a rim of cytoplasm with ill-defined outline as if vacuolation or lysis of the peripheral cytoplasm had occurred. The sponginess of the tissue progressed in severe cases to formation of necrotic cysts. Condensed acidophilic neurons were seen in the border zone between the edematous and more compact gray matter. The appearance and distribution of the gray matter lesions deviated in many respects from those commonly seen in regional ischemic infarcts. The fibrin thrombi found close to the cysts might be regarded as secondary events. The extensive spread of antifibrinogen-positive material within the white matter seemed to originate mainly from the chronic leakage sites in the gray matter. Increased number of large astrocytes were seen within the leakage sites and along the spreading pathways for the edema constituents. The white matter showed a rarefied texture with widely dispersed nerve fiber tracts, volume expansion, and occasional cyst formation. The results indicate a crucial pathophysiologic role for the egress, spread, and accumulation of vasogenic edema in the development of the cerebrovascular lesions in SHRSP.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00690831
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