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Nerve cell injury in the brain of stroke-prone spontaneously hypertensive rats

Fredriksson, K; Kalimo, H; Nordborg, C; Johansson, Barbro LU and Olsson, Y (1988) In Acta Neuropathologica 76(3). p.227-237
Abstract
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... (More)
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 well 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 anoxia-ischemia 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. (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 edema, Nerve cell injury, Electron microscopy
in
Acta Neuropathologica
volume
76
issue
3
pages
227 - 237
publisher
Springer
external identifiers
  • pmid:3213425
  • scopus:0023689025
ISSN
1432-0533
DOI
10.1007/BF00687769
language
English
LU publication?
yes
id
2c710d3a-b64b-49ec-9125-ccaeda1ad549 (old id 1104223)
date added to LUP
2008-08-07 12:53:47
date last changed
2017-01-01 07:08:20
@article{2c710d3a-b64b-49ec-9125-ccaeda1ad549,
  abstract     = {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 well 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 anoxia-ischemia 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.},
  author       = {Fredriksson, K and Kalimo, H and Nordborg, C and Johansson, Barbro and Olsson, Y},
  issn         = {1432-0533},
  keyword      = {Stroke-prone spontaneously hypertensive rats,Blood-brain barrier,Brain edema,Nerve cell injury,Electron microscopy},
  language     = {eng},
  number       = {3},
  pages        = {227--237},
  publisher    = {Springer},
  series       = {Acta Neuropathologica},
  title        = {Nerve cell injury in the brain of stroke-prone spontaneously hypertensive rats},
  url          = {http://dx.doi.org/10.1007/BF00687769},
  volume       = {76},
  year         = {1988},
}