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  • 1
    Electronic Resource
    Electronic Resource
    Effects of the noradrenaline neurotoxinN-2-chloroethyl-N-ethyl-2-bromo-benzylamine hydrochloride (DSP4) on the blood-brain barrier (1989)
    Springer
    Acta neuropathologica 78 (1989), S. 28-34 
    Details
    ISSN: 1432-0533
    Keywords: DSP4 ; Noradrenaline ; Blood-brain barrier ; Brain edema ; Brain density
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Cerebral microvessels receive a noradrenergic innervation originating from the locus coeruleus. Previously, many studies have tried to elucidate the role of the central noradrenergic innervation on the blood-brain barrier (BBB). Many of them are based on chemical destruction of the innervation by local injection of 6-hydroxydopamine (6-OHDA) or physical injury to the locus coeruleus. Such methods are not selective and the results reported are contradictory. We have treated mice with a single i. p. injection of the compound,N-2-chloroethyl-N-ethyl-2-bromobenzylamine hydrochloride (DSP4). This substance induces a selective noradrenaline depletion and, unlike 6-OHDA, it can pass into the brain afer an i. p. injection. The animals were allowed to survive for 6 h to 60 days and the BBB was investigated with i.v.-injected horseradish peroxidase (HRP). Brain density values were also determined to find out if edema developed. The light microscopic distribution of HRP in the brain of DSP4-treated animals did not differ from that in control mice, i.e., there were no signs of increased BBB permeability to this protein tracer caused by DSP4. Density determinations revealed statistically significant reduced values in cerebrum (P〈0.005) and rhombencephalon (cerebellum) (P〈0.0005) of animals given 100 mg/kg body wt. of DSP4 indicating development of edema. A minor drop in density of the rhombencephalon (cerebellum) (P〈0.05 at 48 h) and of the cerebrum (statistically not significant) appeared when 50 mg/kg body wt. of DSP4 was injected. Our findings indicate that the BBB to proteins maintains its function but that edema, likely composed of an ultrafiltrate from the blood, will develop after an injection of DSP4. In view of its selective degenerative action on the noradrenergic central neurons, this kind of brain edema is probably a direct consequence of abnormal noradrenergic innervation of the cerebral blood vessels. Our observations are thus in line with the assumption that the noradrenergic innervation influences endothelial permeability in the central nervous system. Alternative pathogenetic mechanisms are discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00687399
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  • 2
    Electronic Resource
    Electronic Resource
    Distribution of exudated FITC-dextrans in experimental vasogenic brain edema produced by a focal cryogenic injury (1984)
    Springer
    Acta neuropathologica 63 (1984), S. 13-17 
    Details
    ISSN: 1432-0533
    Keywords: Vasogenic brain edema ; Brain trauma ; Blood-brain barrier ; FITC-dextrans
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Mice were subjected to cortical cryogenic brain injury, and FITC-dextrans (mol. wt. 20,000 or 150,000) were injected intravenously (i.v.). After a survival period of 4 h the distribution of the FITC-dextrans was determined by a histotechnical procedure described recently (Hultström et al. 1982a). This technique is based on freeze-drying and vapor fixation to immobilize the tracer and to provide tissue fixation. In and around the cryogenic injury both tracers leaked out of the cortical and the leptomeningeal vessels and spread into the brain parenchyma. They were seen as multiple, closely apposed droplets of fluorescent material best recognized by fluorescence microscopy under high magnification. The tracers were also taken up by neuronal perikarya and in glial cell nuclei of, presumably, astrocytic origin. Our study shows that the FITC-dextran technique can be used for experimental studies on the vasogenic form of brain edema. The patterns formed by the extravasated tracers have qualitative similarities to those produced by other more commonly used tracers, such as fluorochrome-labeled serum proteins and peroxidase.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00688465
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  • 3
    Electronic Resource
    Electronic Resource
    Extensive intraneuronal spread of horseradish peroxidase from a focus of vasogenic edema into remote areas of central nervous system (1986)
    Springer
    Acta neuropathologica 71 (1986), S. 177-189 
    Details
    ISSN: 1432-0533
    Keywords: Blood-brain barrier ; Vasogenic cerebral edema ; Brain injury ; Axonal transport ; Brain density
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A study was made of the uptake of horseradish peroxidase (HRP) into neurons from a cryogenic cortical lesion in the mouse brain associated with vasogenic edema, following intravenous administration of the tracer. Particular emphasis was placed on the axonal spread of HRP from the primary lesion to other areas of the central nervous system. The distribution of HRP was studied by light microscopy, using highly sensitive histochemical methods, 3–144 h after the onset of the injury. Extravasated HRP was taken up into nerve cell bodies in and around the primary lesion, forming different patterns of labelling: (1) granular, (2) diffuse, and (3) a combination of granular and diffuse staining. Granularity is considered to be the result of HRP accumulation in lysosomes occurring in undamaged or slightly damaged nerve cells, whereas the diffuse, non-granular pattern presumably occurs in severely damaged neurons. Nerve cell bodies containing HRP reaction product were also found in the contralateral cortex, ipsilateral thalamus, substantia nigra, amygdala and ventral tegmental area, presumably a consequence of retrograde axonal transport of the tracer from the primary mjury. HRP-containing axons were present in the corpus callosum and in the pyramidal tract of the injured hemisphere all the way down to the cervical spinal cord. Labelling of axonal terminals and preterminal axons in the ipsilateral thalamus, entopeduncular nucleus, subthalamic nucleus, substantia nigra and pons indicated anterograde transport of HRP to these regions. Thus very extensive intraneuronal spread of a macromolecular edema component takes place from a primary focal brain lesion to areas located far away from but neuroanatomically connected to this injured region. The brain thus seems to be affected by focal vasogenic edema in many more ways than are recognized at present.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00688038
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  • 4
    Electronic Resource
    Electronic Resource
    An improved Percoll density gradient for measurements of experimental brain edema (1983)
    Springer
    Acta neuropathologica 61 (1983), S. 201-206 
    Details
    ISSN: 1432-0533
    Keywords: Percoll ; Cerebral edema ; Density gradients
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Microgravimetric methods are very useful for quantitative studies on brain edema. One of the techniques available is based on a gradient made up by NaCl and polyvinyl pyrrolidone-coated silica particles (Percoll). The present study was performed to find a way of minimizing fluid shifts between the gradient and the samples. For this purpose, five Percoll density gradients containing various concentrations of sucrose in isotonic saline were prepared. Equivalent samples of normal mouse brain were then added and their second slow movement (drift) indicating interactions between the tissue and the gradient was followed. A concentration of 0.125 M sucrose eliminated the drift of the samples almost entirely. The capacity of this sucrose-containing gradient to reveal brain edema was then evaluated by comparing the density values obtained with those measured in the traditional bromobenzene-kerosene gradient as described by Nelson et al. (1971). For this purpose, we produced in the mouse an acute cytotoxic edema by triethyltin intoxication and a vasogenic edema by a cortical cryogenic injury. The two gradients showed almost identical results. We conclude, therefore, that the 0.125 M sucrose-containing Percoll gradient is a very good alternative to bromobenzene-kerosene gradients used for brain density determinations. Furthermore, Percoll gradients are very stable and contain only non-toxic ingredients.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00691986
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  • 5
    Electronic Resource
    Electronic Resource
    Formation of oedema in transected rat sciatic nerve (1986)
    Springer
    Acta neuropathologica 70 (1986), S. 177-184 
    Details
    ISSN: 1432-0533
    Keywords: Rat sciatic nerve ; Peripheral nerve oedema ; Density measurements ; Wallerian degeneration
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The formation of oedema in peripheral nerves was studied in rats at intervals varying from 6 h to 14 days after transection of the right sciatic nerve. Samples were removed proximal and distal to the injury, and the degree of oedema was determined by a microgravimetric method and by measurements of the water content and of the fascicular area. Distal to the lesion, decreased density values indicating the presence of oedema were observed in samples examined after a survival period of 6 h-14 days. The water content and fascicular area were both increased in samples taken 24 h after the injury. Fourteen days postinjury the water content had increased further. Proximal to the lesion, the water content and the fascicular area were increased in samples examined after a survival period of 24 h. Fourteen days after the injury, the increase in water content was even more pronounced. No changes were detected with the microgravimetric technique 6 and 24 h after the injury. Unexpectedly, animals surviving 14 days showed increased density values. The microgravimetric technique used is a valuable adjunctive method for quantitation of peripheral nerve oedema in the acute phase after a traumatic nerve injury. Later on, loss of axons and of myelin components, together with regenerative phenomena, influence the density values obtained. Quantitative methods for studying chronic peripheral nerve oedema should therefore, be supplemented with other techniques.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00686069
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