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Cyst formation and glial response in the brain lesions of stroke-prone spontaneously hypertensive rats

Fredriksson, K; Kalimo, H; Nordborg, C; Olsson, Y and Johansson, Barbro LU (1988) In Acta Neuropathologica 76(5). p.441-450
Abstract
The brain lesions in spontaneously hypertensive stroke-prone rats (SHRSP) are characterised by multifocal microvascular damage, breakdown of the blood-brain barrier, massive extravasation of plasma constituents and severe brain oedema, with consequent spongy and cystic tissue destruction in the cerebral cortex and basal ganglia as well as loosening of the white matter. In this paper we analyse in greater detail the pathogenetic mechanisms by which the spongy and cystic lesions are formed and the response of astrocytic cells. For this purpose, tracer (Evans blue)-stained brain lesions were examined in 8-month-old SHRSP immunohistochemically and electron microscopically. Sponginess of the neuropil in small lesions and at the periphery of... (More)
The brain lesions in spontaneously hypertensive stroke-prone rats (SHRSP) are characterised by multifocal microvascular damage, breakdown of the blood-brain barrier, massive extravasation of plasma constituents and severe brain oedema, with consequent spongy and cystic tissue destruction in the cerebral cortex and basal ganglia as well as loosening of the white matter. In this paper we analyse in greater detail the pathogenetic mechanisms by which the spongy and cystic lesions are formed and the response of astrocytic cells. For this purpose, tracer (Evans blue)-stained brain lesions were examined in 8-month-old SHRSP immunohistochemically and electron microscopically. Sponginess of the neuropil in small lesions and at the periphery of larger lesions was due to swollen neuronal and astrocytic cell processes, i.e. at this stage the oedema was mainly intracellular. Cystic lesions were formed in the grey matter both by expansion of the extracellular space (ECS) containing protein-rich oedema fluid, and by rupture and subsequent loss of massively swollen cellular elements. In the white matter small slit-formed cysts along the fibre tracts were also formed by the expansion of ECS. In apparently recent lesions astrocytes displayed cyto-plasmic oedema but otherwise were still fairly normal. In more chronic lesions increased numbers of enlarged astrocytes with prominent staining for glial fibrillary acidic protein were present. Their distribution corresponded well to the spread of oedema, i.e. they were prominent around the leaky vessels in the grey matter, in the subpial zone and in the white matter. In the reparative phase the grey matter cysts became lined by astrocytic processes, a new glia limitans. Profuse sheets of glial processes in the neuropil around the cysts reestablished the compactness of the brain parenchyma. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Stroke-prone spontaneously hypertensive rats, Blood-brain barrier, Brain oedema, Astrocytes, Glial fibrillary acidic protein
in
Acta Neuropathologica
volume
76
issue
5
pages
441 - 450
publisher
Springer
external identifiers
  • pmid:3188837
  • scopus:0023686958
ISSN
1432-0533
DOI
10.1007/BF00686382
language
English
LU publication?
yes
id
dacb3ffe-0901-4221-835a-945f0ee73b83 (old id 1104228)
date added to LUP
2008-08-07 12:56:02
date last changed
2017-04-23 04:30:21
@article{dacb3ffe-0901-4221-835a-945f0ee73b83,
  abstract     = {The brain lesions in spontaneously hypertensive stroke-prone rats (SHRSP) are characterised by multifocal microvascular damage, breakdown of the blood-brain barrier, massive extravasation of plasma constituents and severe brain oedema, with consequent spongy and cystic tissue destruction in the cerebral cortex and basal ganglia as well as loosening of the white matter. In this paper we analyse in greater detail the pathogenetic mechanisms by which the spongy and cystic lesions are formed and the response of astrocytic cells. For this purpose, tracer (Evans blue)-stained brain lesions were examined in 8-month-old SHRSP immunohistochemically and electron microscopically. Sponginess of the neuropil in small lesions and at the periphery of larger lesions was due to swollen neuronal and astrocytic cell processes, i.e. at this stage the oedema was mainly intracellular. Cystic lesions were formed in the grey matter both by expansion of the extracellular space (ECS) containing protein-rich oedema fluid, and by rupture and subsequent loss of massively swollen cellular elements. In the white matter small slit-formed cysts along the fibre tracts were also formed by the expansion of ECS. In apparently recent lesions astrocytes displayed cyto-plasmic oedema but otherwise were still fairly normal. In more chronic lesions increased numbers of enlarged astrocytes with prominent staining for glial fibrillary acidic protein were present. Their distribution corresponded well to the spread of oedema, i.e. they were prominent around the leaky vessels in the grey matter, in the subpial zone and in the white matter. In the reparative phase the grey matter cysts became lined by astrocytic processes, a new glia limitans. Profuse sheets of glial processes in the neuropil around the cysts reestablished the compactness of the brain parenchyma.},
  author       = {Fredriksson, K and Kalimo, H and Nordborg, C and Olsson, Y and Johansson, Barbro},
  issn         = {1432-0533},
  keyword      = {Stroke-prone spontaneously hypertensive rats,Blood-brain barrier,Brain oedema,Astrocytes,Glial fibrillary acidic protein},
  language     = {eng},
  number       = {5},
  pages        = {441--450},
  publisher    = {Springer},
  series       = {Acta Neuropathologica},
  title        = {Cyst formation and glial response in the brain lesions of stroke-prone spontaneously hypertensive rats},
  url          = {http://dx.doi.org/10.1007/BF00686382},
  volume       = {76},
  year         = {1988},
}