Library

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    Role of histamine in spinal cord evoked potentials and edema following spinal cord injury: Experimental observations in the rat (1995)
    Springer
    Inflammation research 44 (1995), S. S44 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01674388
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Cytofluorescence localization of adriamycin in the nervous system (1982)
    Springer
    Acta neuropathologica 57 (1982), S. 130-136 
    Details
    ISSN: 1432-0533
    Keywords: Adriamycin ; Doxorubicin ; Bloodnerve barrier ; Peripheral nervous system (PNS)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary By a fluorescence-microscopic technique, the distribution of the antineoplastic glycoside adriamycin (doxorubicin) was studied in the peripheral nervous system (PNS) of normal adult mice after i.v. injection. Doses comparable to those used in patients for treatment of malignant diseases were used. The orange-red fluorescence of the drug was observed in dorsal root ganglia, in the trigeminal ganglia, and in the superior cervical sympathetic ganglia where it was preferentially accumulated in the nuclei of satellite cells. This nuclear labeling was a very quick process which occurred in the superior cervical ganglion within 15 s after the injection. Adriamycin-fluorescent nuclei were also observed in the suprarenal medulla. Fluorescent nuclei were present within the pre- and postganglionic sympathetic nerve trunks close to the superior cervical ganglion but not in the endoneurium of the trigeminal and the sciatic nerves or in the spinal nerve roots. In such structures labeled cells appeared in the connective tissue sheaths covering the nerves and the roots. No adriamycin-induced fluorescence was detected in the myenteric plexus of the intestine. Our study thus shows that i. v. injected adriamycin is distributed preferentially within areas of the PNS where the blood vessels are known to be highly permeable.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00685380
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Uptake of macromolecules into neurons from a focal vasogenic cerebral edema and subsequent axonal spread to other brain regions (1982)
    Springer
    Acta neuropathologica 57 (1982), S. 233-235 
    Details
    ISSN: 1432-0533
    Keywords: Cerebral trauma ; Vasogenic brain edema ; Axonal transport ; Blood-brain barrier ; Nerve cell injury
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Intravenously (i.v.) injected horseradish peroxidase (HRP) which has leaked out of the vessels in a cryogenic cortical injury of adult mice is taken up into a large number of neurons resulting in two different forms of labeling. Diffuse neuronal labeling of, the type previously reported in many conditions with vasogenic brain edema occurred particularly within the primary lesion. The other and more frequent type, here calledgranular neuronal labeling, was present in a wide zone immediately outside the injury. Such neurons contained HRP in numerous cytoplasmic granules and had the same characteristics as normal neurons accumulating HRP after retrograde axonal transport. By using highly sensitive histochemical methods for demonstration of HRP we could also follow bundles of labeled axons out from the primary lesion. Some of them passed the corpus callosum to the fronto-parietal cortex of the contralateral hemisphere. With this report we would like to put emphasize on certain phenomena occurring in neurons which previously have not been particularly recognized in studies on vasogenic brain edema. It can be assumed that in a focal brain lesion components from the edematous fluid and other “wound substances” can be taken up into nerve cell processes and then be intracellularly transported in different directions. In this way, nerve cell populations located in other brain areas and even in the contralateral hemisphere may be influenced by components from the primary injury.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00685395
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 4
    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
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    Cytofluorescence localization of adriamycin in the nervous system (1982)
    Springer
    Acta neuropathologica 58 (1982), S. 193-202 
    Details
    ISSN: 1432-0533
    Keywords: Adriamycin ; Doxorubicin ; Blood-brain barrier ; Circumventricular organs
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary By a fluorescence-microscopic technique the distribution of the antineoplastic anthracyclic compound adriamycin (doxorubicin) was determined in the brain of normal adult mice after intraventricular and arachnoidal injections. These experiments were carried out to circumvent the blood-brain barrier since there are indications that vascular permeability properties determine the extent to which the drug will spread into the brain after systemic administration. In line with this concept we found previously that after i.v. injection the drug leaks into circumventricular organs of the brain. These are special areas which have permeable vessels to a number of substances including adriamycin (Bigotte et al. 1982a). After intraventricular injection the nuclei of ependymal cells throughout the ventricular system contained intensely fluorescent orange-red material characteristic of adriamycin. A thin layer of the brain parenchyma adjacent to the ventricular walls showed fluorescent nuclei. In the corpus callosum, fascia dentata of the hippocampus, and the hypothalamic preoptic nuclei the drug penetrated deeper into the tissue, and the intensity of the drug-induced fluorescence was very high there. In the circumventricular organs two different patterns of intraventricularly injected adriamycin movement were revealed. The organum vasculosum of the lamina terminalis, the subcommissural organ, and the choroid plexus showed a very strong drug-induced nuclear fluorescence both within the parenchyma and in the covering ependyma. The median eminence, the subfornical organ, the postremal area, the neurohypophysis, and the pineal gland did not show any labeling of their parenchyma. The tanycyte ependyma lining the median eminence did not take up any tracer from the ventricular fluid. Adriamycin which passed into the leptomeninges labeled a few cells in the arachnoid as well as neurons and glial cells in the adjacent first and second cortical layers. The drug also penetrated into the optic tracts and nerves. In these areas a marked adriamycin-induced fluorescence was present in the nuclei of oligodendrocytes. Our study thus shows that when the blood-brain barrier is by-passed different types of neurons and glial cells have the capacity to take up and accumulate the drug in their nuclei. Adriamycin can spread into the periventricular parenchyma after intraventricular administration but its movement into the circumventricular organs differs considerably from one area to another. Knowledge about these phenomena is essential for future studies on the neurotoxic action of adriamycin.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00690801
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 6
    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
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 7
    Electronic Resource
    Electronic Resource
    Cytofluorescence localization of adriamycin in the nervous system (1983)
    Springer
    Acta neuropathologica 60 (1983), S. 125-131 
    Details
    ISSN: 1432-0533
    Keywords: Adriamycin (Doxorubicin) ; Blood-nerve barrier ; Perineurium
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Adriamycin (Doxorubicin) is a powerful anthracyclic compound, which is widely used in the treatment of maligant disease. In the rat a single systemic injection of the drug can induce pronounced lesions in peripheral ganglia, whereas in other parts of the peripheral nervous system (PNS) no changes have been reported. Since adriamycin can be directly traced in tissue sections by fluorescence microscopy it is very well suited for experimental studies on the relation between cytotoxic effects and distribution of the drug following various modes of administration. We have previously shown that after an intravenous (i.v.) injection there is an absence of adriamycin-induced nuclear fluorescence in the endoneurium of mouse sciatic nerve (Bigotte et al. 1982b). This could either be due to barrier effects in endoneurial vessels and the perineurium or to a lacking capacity of the endoneurial cell population to take up and retain adriamycin. In the present study the blood-nerve and the perifascicular diffusion barriers were therefore bypassed by endoneurial microinjections of adriamycin. After this mode of administration, Schwann cells, endoneurial mast cells, endothelial cells, and pericytes became labeled. Experimental damage of these barriers induced by ligation of the nerve also resulted in a diffusion of the drug into the endoneurial area and labeling of the same cells. The absence of nuclear binding in the endoneurium of mouse sciatic nerves after i.v. injection of adriamycin is therefore most probably due to a low or absent passage of the drug from the blood into the endoneurium, i.e., a combined barrier action of endoneurial vessels and the perineurium. Other experiments with epineurial application of the drug showed that thin intramuscular (i.m.) nerve branches differ from the sciatic nerve fascicles in allowing small amounts of adriamycin to enter the endoneurium. The present observations are of interest since it can be assumed that patients receiving adriamycin as a cytostatic drug may suffer nerve lesions whenever defects of nerve barriers are present.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00685356
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 8
    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
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 9
    Electronic Resource
    Electronic Resource
    Toxic effects of adriamycin on the central nervous system (1983)
    Springer
    Acta neuropathologica 61 (1983), S. 291-299 
    Details
    ISSN: 1432-0533
    Keywords: Adriamycin ; Doxorubicin ; Neurotoxicity ; Blood-brain barrier ; Circumventricular organs
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Recent experimental studies have shown that the cytotoxic antibiotic adriamycin (doxorubicin) after systemic administration can enter the so-called circumventricular organs (CVO) of the brain of the mouse. The present experiments were performed to find out whether such penetration of the brain is associated with signs of neurotoxic injury. For this purpose, light-and electron-microscopic observations were carried out on three of these organs: the neurohypophysis (NH), median eminence (ME), and postremal area (PA). Pronounced widening of the extracellular space indicating the presence of edema was present in all the regions, particulary in animals examined within 3 days of injection of the drug. Many degenerated axon terminals were observed in the NH and ME. The glial cells within these regions showed rarefaction of the nuclear chromatin, nucleolar segregation, and also cytoplasmic changes. The PA presented marked cellular changes resulting in degeneration of neurons, which was most evident 30 days after the injection. Hence, regions of the CNS outside the blood-brain barrier can be reached by adriamycin after systemic administration, and the drug can induce morphological changes there. The doses of the drug used in the present experiments were comparable to those given to patients for the treatment of malignant tumors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00692000
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 10
    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
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...