• MeSH
• Child MeSH
• Hyponatremia * diagnosis   etiology   therapy   MeSH
• Water Intoxication pathology   MeSH
• Clinical Laboratory Techniques methods   MeSH
• Humans MeSH
• Sodium analysis   blood   urine   therapeutic use   MeSH
• Water-Electrolyte Balance physiology   MeSH
• Check Tag
• Child MeSH
• Humans MeSH
• Publication type
• Review 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.

• MeSH
• Behavior, Animal * MeSH
• Brain Edema etiology   metabolism   pathology   physiopathology   MeSH
• Evans Blue MeSH
• Blood-Brain Barrier metabolism   MeSH
• Water Intoxication complications   metabolism   pathology   physiopathology   MeSH
• Intracranial Hypertension etiology   metabolism   pathology   physiopathology   MeSH
• Rats * MeSH
• Locomotion * MeSH
• Disease Models, Animal * MeSH
• Brain diagnostic imaging   metabolism   pathology   MeSH
• Myelin Sheath pathology   MeSH
• Permeability MeSH
• Tomography, X-Ray Computed MeSH
• Rats, Wistar MeSH
• Animals MeSH
• Check Tag
• Rats * MeSH
• Male MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH

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. Excitability of cortical neurons was tested by cortical stimulation with the intensity required to induce cortical afterdischarge (AD). Animals were divided into three experimental groups (B, C, D) and three control groups (AB, AC, AD). Experimental groups differed in age of water intoxication (12 or 25 days) and age of excitability testing (25 or 35 days). Changes in the duration of AD (seconds) were statistically evaluated. RESULTS: Duration of cortical afterdischarges (AD) in the control groups was at the level literature data. In all experimental groups (B, C, D), excitability of cortical neurons was markedly inhibited. AD was possible to induce only in some of the animals and its average duration was significantly shorter than in control groups. CONCLUSION: This inhibitory effect can be explained by persistent impairment of astrocyte-to-neuron communication, which plays a key role in the process of formation of structural and functional changes during cellular edema. Some of the functional manifestations of the developing edema are influenced by the age of experimental animals. At least some events of this process are not influenced by the age of experimental animals.

• MeSH
• Edema MeSH
• Electric Stimulation MeSH
• Electroencephalography MeSH
• Water Intoxication pathology   MeSH
• Rats MeSH
• Cerebral Cortex cytology   drug effects   MeSH
• Neurons pathology   ultrastructure   MeSH
• Rats, Wistar MeSH
• Aging MeSH
• Animals MeSH
• Check Tag
• Rats MeSH
• Male MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH

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. Animals received distilled water in amount corresponding to 15% of the animal's body weight. The volume was divided into three parts and administered intraperitoneally in 8 hours interval. Axonal changes were recognized as signs of myelin disintegration (oedematous distensions, axonal swelling, vesicles, varicosities) at histological sections stained with Black Gold and classified into four grades of myelin degradation. Hippocampal CA1 and CA3 areas and the dentate gyrus were selected for the study. Methylprednisolone was administered either intraperitoneally or intracarotically. Its effect was studied in two different time intervals: in the acute group (30 minutes after hyperhydration and MP application) and in chronic one (1 week after hyperhydration and MP application). Results: In both the acute and chronic groups, cellular oedema induced by water intoxication brought about apparent damage of myelin (compared to control animals p<0.0001). Intracarotic injection of MP was not able to influence myelin integrity changes either in the acute or in chronic group. However, intraperitoneal administration of MP increased the level of myelin deterioration in the acute group (p 0.05), but improved myelin changes in the chronic group (p<0.005). Conclusion: The effect of MP on axonal impairment during cellular brain oedema induced by water intoxication differs from that during the extracellular osmotic oedema. In the extracellular oedema, cellular metabolism is not significantly affected and myelin changes can be influenced by the neuroprotective effect of MP. The primary cause of cellular oedema is a disorder of cellular metabolism and myelin impairment is one of the structural consequences of such disorder. That is why the myelin changes are not affected by MP administration in a consistent and specific manner.

• MeSH
• Axons drug effects   metabolism   pathology   MeSH
• Brain Edema drug therapy   metabolism   pathology   MeSH
• Glucocorticoids pharmacology   MeSH
• Blood-Brain Barrier drug effects   metabolism   pathology   MeSH
• Water Intoxication drug therapy   metabolism   pathology   MeSH
• Rats MeSH
• Methylprednisolone pharmacology   MeSH
• Myelin Sheath drug effects   metabolism   pathology   MeSH
• Nerve Fibers, Myelinated drug effects   metabolism   pathology   MeSH
• Neuroprotective Agents pharmacology   MeSH
• Osmotic Pressure drug effects   MeSH
• Rats, Wistar MeSH
• Animals MeSH
• Check Tag
• Rats MeSH
• Male MeSH
• Female MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH