Cellular brain edema induced by water intoxication in rat experimental model
Jazyk angličtina Země Švédsko Médium print
Typ dokumentu časopisecké články
PubMed
30431738
PII: NEL390318A02
Knihovny.cz E-zdroje
- MeSH
- chování zvířat * MeSH
- edém mozku etiologie metabolismus patologie patofyziologie MeSH
- Evansova modř MeSH
- hematoencefalická bariéra metabolismus MeSH
- intoxikace vodou komplikace metabolismus patologie patofyziologie MeSH
- intrakraniální hypertenze etiologie metabolismus patologie patofyziologie MeSH
- krysa rodu Rattus * MeSH
- lokomoce * MeSH
- modely nemocí na zvířatech * MeSH
- mozek diagnostické zobrazování metabolismus patologie MeSH
- myelinová pochva patologie MeSH
- permeabilita MeSH
- počítačová rentgenová tomografie MeSH
- potkani Wistar MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus * MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- Evansova modř MeSH
OBJECTIVES: This paper presents our own rat model of the cellular brain edema, induced by water intoxication (WI). The basic principle of the model is an osmotic imbalance in the cell membrane followed by an intracellular flow of sodium and simultaneous accumulation of water leading to the subsequent increase of BBB permeability. METHODS: The usefulness of the model was tested in precisely specified conditions whose results were clearly expressed. The procedure determined both how WI induces cellular edema as well as the disturbances caused by cellular edema. RESULTS: The evidence of existing cellular edema with increased BBB permeability was proved by intracellular accumulation of intravital dye with a large molecular size; increased brain-water content was confirmed by using the dry/wet weight method and by the decrease in CT density; the elevated intracranial pressure (ICP) due to the expanding volume was determined by continuous monitoring the ICP; the structural lesions were proved by identification of the myelin disintegration; and the impaired nervous functions was demonstrated by the of open field test method. CONCLUSION: Our experimental model can help the future studies of pathophysiology of cellular brain edema and is suitable for testing neuroprotective agents.
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