Selective vulnerability of the hippocampus to the cytotoxic edema; magnetic resonance imaging and fluorescence microscopy studies in the rats.

Objectives: Changes in the hippocampus induced by water intoxication were studied using fluorescence microscopy (FM) and magnetic resonance imaging (MRI).

Methods: In three animals (rats), intracellular/extracellular distribution of Evans blue (EB) in cerebral cortex and hippocampus of both hemispheres was revealed by injection of EB into the internal carotid artery (ICA) in hyperhydrated rats (water intoxication, WI). A total of 8 experimental rats were used for the MRI study.

Intracranial pressure and mean arterial pressure monitoring in freely moving rats via telemetry; pilot study.

Objectives: Accurate values of the intracranial pressure (ICP) and mean arterial pressure (MAP) are the prerequisite for calculating cerebral perfusion pressure (CPP). Increased ICP values decrease CPP. The origin of ICP increase in the clinical cases after brain ischemia and diffuse brain injury is the cellular brain edema (CE).

Cytotoxic brain edema induced by water intoxication and vasogenic brain edema induced by osmotic BBB disruption lead to distinct pattern of ICP elevation during telemetric monitoring in freely moving rats.

Objectives: A novel method of long-term telemetric monitoring of mean arterial pressure (MAP) and intracranial pressure (ICP) for the determination of current cerebral perfusion pressure (CPP) and the time course of ICP in freely moving rats under physiological conditions and with increased ICP due to the induced cerebral edema were studied.

Methods: The brain edema, that caused volume enlargement and ICP elevation was achieved in entirely experimental conditions without any parallel pathological process. Vasogenic/extracellular edema was induced by osmotic blood-brain barrier disruption (BBBd) and for induction of cytotoxic/intracellular edema the water intoxication model (WI) was used.

Locomotion in young rats with induced brain cellular edema - effects of recombinant human erythropoietin.

Objectives: Effect of recombinant human erythropoietin (rhEPO) on spontaneous motor activity was tested in young rats after intraperitoneal (i.p.) administration of rhEPO, followed by induction of cellular brain edema (CE).

Cellular brain edema induced by water intoxication in rat experimental model.

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.

Study of locomotion, rearing and grooming activity after single and/or concomitant lesions of central and peripheral nervous system in rats.

Objective: Locomotion, rearing and grooming represent different forms of behaviour and motor activity in rats. In this study, changes in these activities were analysed in relation to impaired function of the nervous system by single and/or concomitant lesions representing an experimental model of the dual diagnosis.

Methods: 32 rats were divided into 4 groups of 8 rats: intact rats, rats with single lesion of peripheral nervous system (PNS) - Marcaine neuropathy, rats with single CNS lesion - cellular brain edema induced by water intoxication, and the concomitant lesions (combination of CNS and PNS lesion in one rat).

An experimental model of the "dual diagnosis": Effect of cytotoxic brain edema plus peripheral neuropathy on the spontaneous locomotor activity of rats.

Objective: The aim of the study was to find how a simultaneous impairment of the CNS (cellular brain edema induced by water intoxication) and PNS (blockade of the right forelimb brachial plexus by local anesthewtic - Marcaine) affects spontaneous locomotor activity of adult rats.

Methods: Rats were divided into groups of animals without water intoxication (without WI) - A,B,C, and those that were water intoxicated (induction of brain edema - after WI) - D,E,F. Both groups were further divided into intact ones (A,D), animals with PNS lesion (Marcaine) (B,E) and sham-operated animals (C,F).

Neuronal excitability changes depend on the time course of cellular edema induced by water intoxication in young rats.

Objectives: The aim of the study was to determine whether the functional state of neurons is affected by the duration of the induced cellular edema and by the age of animals tested. The cellular edema was induced by water intoxication and neuronal functions were tested by the standard method of electrical stimulation of neurons of the cerebral cortex.

Methods: water intoxication was induced by standard method of fractionated hyperhydration.

Biochemical manifestations of the nervous tissue degradation after the blood-brain barrier opening or water intoxication in rats.

Objectives: The aim of the study was to determine changes of biomarkers of nervous tissue degradation in experimental model of osmotic blood-brain barrier opening or water intoxication and to find whether they correspond to changes in well defined clinical entities.

Methods: In the cerebro-spinal fluid taken via the suboccipital puncture, myelin basic protein (MBP ng/ml), neuron-specific enolase (NSE ng/ml) and TAU-protein (Tau pg/ml) were determined by ELISA in 19 controls and 29 experimental rats several hours or one week after the experimental intervention.

Results: Significant difference between the control and experimental groups was revealed only for the concentration of myelin basic protein.

CT density decrease in water intoxication rat model of brain oedema.

Objectives: The aim of this study was to determine whether water intoxication affects the radiodensity of brain tissue in CT scan examination in the rat model of brain oedema.

Methods: A standard CT scan of the brain was obtained in a group of rats, first at control conditions (controls - CG) and then after hyperhydration (oedema model-EG) in the region of interest (ROI) corresponding to the area of coronary sections with pixel size 0.125 mm in position A (bregma +2.

Neuronal excitability after water intoxication in young rats.

Objectives: Our previous experiments with animal models revealed that water intoxication induces brain oedema and opens plasma membranes. Present study is aimed to determine whether the standard method of hyperhydration can influence cerebral microenvironment also in young rats. Neuronal functions were tested by standard electrical cortical stimulation.

Effect of methylprednisolone on the axonal impairment accompanying cellular brain oedema induced by water intoxication in rats.

Objectives: Our previous experiments proved that methylprednisolone (MP) can significantly reduce axonal impairment accompanying extracellular oedema induced by the osmotic challenge (load) on the blood-brain barrier (BBB). The aim of the present work was to identify whether MP can affect myelin impairment accompanying intracellular oedema induced by water intoxication.

Methods: For induction of cellular brain oedema, the standard model of water intoxication was chosen.

Methylprednisolone reduces axonal impairment in the experimental model of brain oedema.

Objectives: In our earlier paper we demonstrated that opening of the blood-brain barrier with an osmotic insult induces brain oedema which represents a factor triggering axonal impairment accompanied with myelin disintegration. The aim of the present study was to find whether methylprednisolone can reduce such axonal impairment in our model of brain oedema.

Methods: Brain oedema was induced by osmotic blood-brain barrier opening with 20% mannitol applied selectively into the internal carotid.

Time-dependent axonal impairment in experimental model of brain oedema.

Objectives: Clinically very serious condition of ischaemia and brain injury which are often associated with brain oedema is frequently accompanied by the impairment of the structural integrity of axons. We wondered whether the brain oedema (without ischemia brain injury) can induce structural axonal impairment.

Methods: Brain oedema was induced by osmotic blood-brain barrier opening with 20% mannitol applied selectively into the internal carotid.

Cytogenetic analyses in 81 patients with brain gliomas: correlation with clinical outcome and morphological data.

Specific gene mutations, loss of heterozygosity, deletions and/or amplifications of entire chromosomal regions and gene silencing have been described in gliomas. 82 samples from 81 patients were investigated to detect the deletion of TP53, RB1, CDKN2A genes, deletion of 1p36 and 19q13.3 region, amplification of EGFR gene, trisomy of chromosome 7 and monosomy of chromosome 10 in glial cells.