Effect of methylprednisolone on experimental brain edema in rats - own experience reviewed
Jazyk angličtina Země Česko Médium print
Typ dokumentu časopisecké články, přehledy
PubMed
35099248
PubMed Central
PMC8884394
DOI
10.33549/physiolres.934818
PII: 934818
Knihovny.cz E-zdroje
- MeSH
- edém mozku farmakoterapie metabolismus patologie MeSH
- glukokortikoidy farmakologie MeSH
- hematoencefalická bariéra účinky léků metabolismus patologie MeSH
- kapilární permeabilita účinky léků MeSH
- krysa rodu Rattus MeSH
- methylprednisolon farmakologie MeSH
- modely nemocí na zvířatech MeSH
- mozek účinky léků metabolismus patologie MeSH
- neurony účinky léků metabolismus patologie MeSH
- neuroprotektivní látky farmakologie MeSH
- potkani Wistar MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- přehledy MeSH
- Názvy látek
- glukokortikoidy MeSH
- methylprednisolon MeSH
- neuroprotektivní látky MeSH
Brain edema - a frequently fatal pathological state in which brain volume increases resulting in intracranial pressure elevation - can result from almost any insult to the brain, including traumatic brain injury. For many years, the objective of experimental studies was to find a method to prevent the development of brain edema at the onset. From this perspective, the use of methylprednisolone (MP) appears promising. High molecular MP (MW>50 kDa) can be incorporated into the brain - in the conditions of the experimental model - either by osmotic blood-brain barrier disruption (BBBd) or during the induction of cellular edema by water intoxication (WI) - a condition that increases the BBB permeability. The time window for administration of the MP should be at the earliest stages of edema. The neuroprotective effect of MP on the permeability of cytoplasmatic membranes of neuronal populations was proved. MP was administrated in three alternative ways: intraperitoneally during the induction of cytotoxic edema or immediately after finishing cytotoxic edema induction in a dose of 100 mg/kg b.w.; into the internal carotid artery within 2 h after finishing cytotoxic edema induction in a dose of 50 mg/kg b.w.; into internal carotid artery 10 min after edema induction by BBBd in a dose of 50 mg/kg b.w.
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