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Start Over Creator Marešová, D.

2. Loss of body weight is accompanying cellular brain edema induced by water intoxication in the rat

Creator:
Kozler, P. , Marešová, D., and Pokorný, J.
Format:
bez média and svazek
Type:
model:article and TEXT
Subject:
Weight loss, Water intoxication, and Brain edema
Language:
English
Description:
Induction of cellular cerebral edema (CE) was achieved by a standard method of water intoxication which consisted of fractionated intraperitoneal administration of distilled water (DW) together with the injection of desmopressin (DP). Using metabolic cage, fluid and food balance was studied in two groups of eight animals: group C – control; group CE – cellular edema induced by water intoxication. For each rat the intake (food pellets and water) and excretion (solid excrements and urine) were recorded for 48 h together with the initial and final body weight. CE animals consumed significantly less food, drank less water and eliminated the smallest amount of excrements. The induction of cellular cerebral edema was accompanied with a significant loss of body weight (representing on average 13 % of the initial values) mainly due to a reduction of food intake. This phenomenon has not yet been reported.
Rights:
http://creativecommons.org/publicdomain/mark/1.0/ and policy:public

3. Methylprednisolone modulates intracranial pressure in the brain cellular edema induced by water intoxication

Creator:
Kozler, P., Marešová, D., and Pokorný, J.
Type:
article, model:article, and TEXT
Subject:
intracranial pressure monitoring, water intoxication, brain edema, and methylprednisolone
Language:
English
Description:
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.
Rights:
http://creativecommons.org/publicdomain/mark/1.0/ and policy:public

4. The action of pramiracetam on consequences of hypobaric hypoxia is only moderate

Creator:
Marešová, D. and Mareš, P.
Type:
article, model:article, and TEXT
Subject:
pramiracetam, hypoxia, epileptic afterdischarges, and hippocampus
Language:
English
Description:
The possible protective action of pramiracetam, a pyrrolidinone nootropic drug, against hypobaric hypoxia was studied in two age groups of immature rats with implanted electrodes. Epileptic afterdischarges induced by hippocampal stimulation were used as a measure of hypoxic damage. Pramiracetam did not substantially change these afterdischarges in 12- and 18-day-old rat pups which were not exposed to hypoxia. Hypobaric hypoxia (simulated altitude of 7000 m for one hour) led to prolongation of the first afterdischarge in both age groups. Pramiracetam did not influence this prolongation in 12-day-old rats. The first afterdischarge was shortened significantly in 18-day-old animals but not to the level of rats not exposed to hypoxia. The afterdischarges elicited by repeated stimulations (four times at 10 min intervals) did not differ in pramiracetam-treatcd and control rats.
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public