Methylprednisolone Modulates Intracranial Pressure in the Brain Cellular Edema Induced by Water Intoxication
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11110%2F17%3A10369383" target="_blank" >RIV/00216208:11110/17:10369383 - isvavai.cz</a>
Výsledek na webu
<a href="http://www.biomed.cas.cz/physiolres/pdf/66/66_S511.pdf" target="_blank" >http://www.biomed.cas.cz/physiolres/pdf/66/66_S511.pdf</a>
DOI - Digital Object Identifier
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Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
Methylprednisolone Modulates Intracranial Pressure in the Brain Cellular Edema Induced by Water Intoxication
Popis výsledku v původním jazyce
Continuous monitoring of the intracranial pressure (ICP) detects impending intracranial hypertension resulting from the impaired intracranial volume homeostasis, when expanding volume generates pressure increase. In this study, cellular brain edema (CE) was induced in rats by water intoxication (WI). Methylprednisolone (MP) was administered intraperitoneally (i.p.) before the start of CE induction, during the induction and after the induction. ICP was monitored for 60 min within 20 h after the completion of the CE induction by fibreoptic pressure transmitter. In rats with induced CE, ICP was increased (Mean +/- SEM: 14.25 +/- 2.12) as well as in rats with MP administration before the start of CE induction (10.55 +/- 1.27). In control rats without CE induction (4.62 +/- 0.24) as well as in rats with MP applied during CE induction (5.52 +/- 1.32) and in rats with MP applied after the end of CE induction (6.23 +/- 0.73) ICP was normal. In the last two groups of rats, though the CE was induced, intracranial volume homeostasis was not impaired, intracranial volume as well as ICP were not increased. It is possible to conclude that methylprednisolone significantly influenced intracranial homeostasis and thus also the ICP values in the model of cellular brain edema.
Název v anglickém jazyce
Methylprednisolone Modulates Intracranial Pressure in the Brain Cellular Edema Induced by Water Intoxication
Popis výsledku anglicky
Continuous monitoring of the intracranial pressure (ICP) detects impending intracranial hypertension resulting from the impaired intracranial volume homeostasis, when expanding volume generates pressure increase. In this study, cellular brain edema (CE) was induced in rats by water intoxication (WI). Methylprednisolone (MP) was administered intraperitoneally (i.p.) before the start of CE induction, during the induction and after the induction. ICP was monitored for 60 min within 20 h after the completion of the CE induction by fibreoptic pressure transmitter. In rats with induced CE, ICP was increased (Mean +/- SEM: 14.25 +/- 2.12) as well as in rats with MP administration before the start of CE induction (10.55 +/- 1.27). In control rats without CE induction (4.62 +/- 0.24) as well as in rats with MP applied during CE induction (5.52 +/- 1.32) and in rats with MP applied after the end of CE induction (6.23 +/- 0.73) ICP was normal. In the last two groups of rats, though the CE was induced, intracranial volume homeostasis was not impaired, intracranial volume as well as ICP were not increased. It is possible to conclude that methylprednisolone significantly influenced intracranial homeostasis and thus also the ICP values in the model of cellular brain edema.
Klasifikace
Druh
J<sub>imp</sub> - Článek v periodiku v databázi Web of Science
CEP obor
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OECD FORD obor
30105 - Physiology (including cytology)
Návaznosti výsledku
Projekt
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Návaznosti
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Ostatní
Rok uplatnění
2017
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
Physiological Research
ISSN
0862-8408
e-ISSN
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Svazek periodika
66
Číslo periodika v rámci svazku
Supplement 4
Stát vydavatele periodika
CZ - Česká republika
Počet stran výsledku
6
Strana od-do
"S511"-"S516"
Kód UT WoS článku
000422901400008
EID výsledku v databázi Scopus
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