Cerebral perfusion pressure (CPP) is the net pressure gradient that drives oxygen delivery to cerebral tissue. It is the difference between the mean arterial pressure (MAP) and the intracranial pressure (ICP). As CPP is a calculated value, MAP and ICP must be measured simultaneously. In research models, anesthetized and acute monitoring is incapable of providing a realistic picture of the relationship between ICP and MAP under physiological and/or pathophysiological conditions. For long-term monitoring of both pressures, the principle of telemetry can be used. The aim of this study was to map changes in CPP and spontaneous behavior using continuous pressure monitoring and video recording for 7 days under physiological conditions (group C - 8 intact rats) and under altered brain microenvironment induced by brain edema (group WI - 8 rats after water intoxication) and neuroprotection with methylprednisolone - MP (group WI+MP - 8 rats with MP 100 mg/kg b.w. applicated intraperitoneally during WI). The mean CPP values in all three groups were in the range of 40-60 mm Hg. For each group of rats, the percentage of time that the rats spent during the 7 days in movement pattern A (standard movement stereotype) or B (atypical movement) was defined. Even at very low CPP values, the standard movement stereotype (A) clearly dominated over the atypical movement (B) in all rats. There was no significant difference between control and experimental groups. Chronic CPP values with correlated behavioral type may possibly answer the question of whether there is a specific, universal, optimal CPP at all.
Brain edema is a fatal pathological state in which brain volume increases as a result of abnormal accumulation of fluid within the brain parenchyma. A key attribute of experimentally induced brain edema - increased brain water content (BWC) - needs to be verified. Various methods are used for this purpose: specific gravimetric technique, electron microscopic examination, magnetic resonance imaging (MRI) and dry/wet weight measurement. In this study, the cohort of 40 rats was divided into one control group (CG) and four experimental groups with 8 rats in each group. The procedure for determining BWC using dry/wet weight measurement was initiated 24 h after the completion of edema induction by the water intoxication method (WI group); after the intraperitoneal administration of Methylprednisolone (MP) together with distilled water during edema induction (WI+MP group); 30 min after osmotic blood brain barrier disruption (BBBd group); after injection of MP via the internal carotid artery immediately after BBBd (BBBd + MP group). While induction of brain edema (WI, BBBd) resulted in significantly higher BWC, there was no increase in BWC in the MP groups (WI+MP, BBBd+MP), suggesting a neuroprotective effect of MP in the development of brain edema.
- MeSH
- edém mozku * chemicky indukované diagnostické zobrazování patologie MeSH
- edém patologie MeSH
- hematoencefalická bariéra MeSH
- krysa rodu rattus MeSH
- methylprednisolon farmakologie MeSH
- mozek MeSH
- voda MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
Magnetic resonance imaging has been used for evaluating of a brain edema in experimental animals to assess cytotoxic and vasogenic edema by the apparent diffusion coefficient (ADC) and T2 imaging. This paper brings information about the effectiveness of methylprednisolone (MP) on experimental brain edema. A total of 24 rats were divided into three groups of 8 animals each. Rats with cytotoxic/intracellular brain edema induced by water intoxication were assigned to the group WI. These rats also served as the additional control group CG when measured before the induction of edema. A third group (WIMP) was intraperitoneally administered with methylprednisolone 100 mg/kg during water intoxication treatment. The group WI+MP was injected with methylprednisolone 50 mg/kg into the carotid artery within two hours after the water intoxication treatment. We evaluated the results in four groups. Two control groups (CG, WI) and two experimental groups (WIMP, WI+MP). Rats were subjected to MR scanning 24 h after edema induction. We observed significantly increased ADC values in group WI in both evaluated areas - cortex and hippocampus, which proved the occurrence of experimental vasogenic edema, while ADC values in groups WIMP and WI+MP were not increased, indicating that the experimental edema was not developed and thus confirming the protective effect of MP.
- MeSH
- antiflogistika farmakologie MeSH
- edém mozku diagnostické zobrazování farmakoterapie patologie MeSH
- hipokampus diagnostické zobrazování účinky léků MeSH
- krysa rodu rattus MeSH
- magnetická rezonanční tomografie metody MeSH
- methylprednisolon farmakologie MeSH
- modely nemocí na zvířatech MeSH
- mozek diagnostické zobrazování účinky léků MeSH
- mozková kůra diagnostické zobrazování účinky léků MeSH
- potkani Wistar MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
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. The animals were scanned before WI, then the experimental brain edema was induced by WI and MR scanning was performed at day 1 and day 8 after WI. Besides standard T2-weighted imaging an apparent diffusion coefficient (ADC) and transverse relaxation time (T2) were evaluated. RESULTS: Hyperhydration brought about the largest intracellular deposits of EB in CA3 hippocampal region, followed by the cerebral cortex and CA1 hippocampal region with the lowest amount of intracellular EB in the dentate gyrus. A higher apparent diffusion coefficient (corresponding to a vasogenic edema) was found the first day after hyperhydration in the cortex and in the CA1 and CA3 regions with no changes in dentate gyrus. CONCLUSION: Both FM and MRI confirmed a selectively higher vulnerability to hyperhydration and hyponatremia (achieved by water intoxication) of the hippocampal cells compared to dentate gyrus cells.
- MeSH
- edém mozku * diagnostické zobrazování MeSH
- Evansova modř MeSH
- fluorescenční mikroskopie MeSH
- hipokampus * diagnostické zobrazování MeSH
- intoxikace vodou MeSH
- krysa rodu rattus MeSH
- magnetická rezonanční tomografie MeSH
- mozek MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
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. RESULTS: The results showed significantly elevated values of ICP both in conditions of osmotic blood-brain barrier disruption (BBBd model) and cytotoxic/intracellular edema (WI model) compared to intact rats. The average values of ICP were significantly higher in WI model compared to osmotic BBBd model. Distinct pattern of elevated ICP, related to the selected way of experimental brain edema induction, was found. In the experimental model of osmotic BBB disruption, the elevation of ICP started earlier but was of very short duration. In WI model the elevation of ICP was present during the whole period of monitoring. CONCLUSION: Our results indicate that purely experimental models of brain edema (WI, BBBd) without any parallel pathological process can compromise the basic brain homeostatic activity.
- MeSH
- edém mozku diagnóza etiologie patofyziologie MeSH
- hematoencefalická bariéra patofyziologie MeSH
- intoxikace vodou komplikace diagnóza patofyziologie MeSH
- intrakraniální hypertenze komplikace diagnóza patofyziologie MeSH
- intrakraniální tlak fyziologie MeSH
- krysa rodu rattus MeSH
- monitorování fyziologických funkcí metody MeSH
- mozek patofyziologie MeSH
- mozkový krevní oběh fyziologie MeSH
- potkani Wistar MeSH
- telemetrie MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
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). Short-term monitoring of ICP and MAP is possible only in the unconscious patients, in experiments with rats it used to be possible only in general anesthesia. Long-term monitoring of ICP or MAP in the clinical practice is not possible. We therefore introduce an experimental model with telemetric monitoring. METHODS: ICP (subdurally) and MAP (intracarotically) were monitored in freely moving rats for 72 hours by DSI™ (Data Sciences International) telemetry system. The control group consisted of 8 rats, the experimental group had 8 animals with CE-induced by water intoxication. RESULTS: The mean MAP, ICP and CPP values were significantly higher in the experimental group. Average values of MAP were 19.9 mmHg (18%), ICP 5.3 mmHg (55%), CPP 14.5 mmHg (15% higher). CONCLUSION: The results of the pilot study verified possibilities of long-term telemetric monitoring of the mean arterial and intracranial pressures for the determination of current cerebral perfusion pressure in freely moving rats under physiological conditions and with increased intracranial pressure due to the induced cerebral edema. Detailed analysis of the course of the curves in the experimental group revealed episodes of short-term CPP reduction below the optimum value of 70 mmHg. Interpretation of these episodes requires simultaneous monitoring of rat behavior.
- MeSH
- ambulantní monitorování přístrojové vybavení metody MeSH
- arteriální tlak * MeSH
- edém mozku patofyziologie MeSH
- intrakraniální tlak * MeSH
- krysa rodu rattus MeSH
- mozkový krevní oběh MeSH
- pilotní projekty MeSH
- technologie dálkového snímání přístrojové vybavení metody MeSH
- telemetrie přístrojové vybavení metody MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
Study of motor activity is an important part of the experimental models of neural disorders of rats. It is used to study effects of the CNS impairment, however studies on the peripheral nervous system lesions are much less frequent. The aim of the study was to extend the spectrum of experimental models of anterior limb movement disorders in rats by blockade of the right anterior limb brachial plexus with the local anesthetic Marcaine (Ma), or with aqua for injection administered into the same location (Aq) (with control intact group C). Two other groups with anterior limb movement disorders underwent induction of cellular brain edema by water intoxication (MaWI and AqWI). Results showed a lower spontaneous motor activity of animals in all experimental groups versus controls, and lower spontaneous motor activity of animals in the MaWI group compared to other experimental groups in all categories. There was no difference in spontaneous activity between the groups Ma, Aq and AqWI. Our study indicates that alterations of spontaneous motor activity may result from the impaired forelimb motor activity induced by the anesthetic effect of Marcaine, by the volumetric effect of water, as a result of induced brain edema, or due to combination of these individual effects.
- MeSH
- edém mozku komplikace patofyziologie MeSH
- intoxikace vodou komplikace patofyziologie MeSH
- krysa rodu rattus MeSH
- modely nemocí na zvířatech * MeSH
- pohybová aktivita fyziologie MeSH
- pohybové poruchy etiologie patofyziologie MeSH
- potkani Wistar MeSH
- přední končetina patofyziologie MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
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.
- MeSH
- antidiuretika toxicita MeSH
- desmopresin toxicita MeSH
- edém mozku chemicky indukované metabolismus MeSH
- hmotnostní úbytek fyziologie MeSH
- intoxikace vodou chemicky indukované metabolismus MeSH
- krysa rodu rattus MeSH
- potkani Wistar MeSH
- tělesná hmotnost fyziologie MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
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). Induced changes in the spontaneous horizontal locomotor activity was studied by open field test (OFT). METHODS: CE was induced by water intoxication (WI) using standard method of fractional hyperhydration accompanied with desmopressin administration. Using the accepted method of OFT average time spent in locomotion (s) was determined. 48 young rats at the age of 25, and 35 days were divided into three groups - controls, rats after WI (OFT followed after 44 hours), and rats administered with rhEPO prior to application WI (OFT after 48 hours). RESULTS: In 35-day-old rats rhEPO administration increased the spontaneous locomotor activity, previously decreased by cellular edema. In 25-day-old rats, rhEPO administration prior to the induced CE, decreased spontaneous locomotor activity. CONCLUSION: Presented results demonstrate the neuroprotective capacity of rhEPO, manifested by elimination of the suppressive influence of CE on the locomotion in 35-day-old rats. In 25-day-old rats the neuroprotective effect was not present. These results confirmed that the 10 day interval in the development may represent a different stage of brain maturation in the relation to the neuroprotective effect of rhEPO.
- MeSH
- chování zvířat účinky léků MeSH
- edém mozku patofyziologie MeSH
- erythropoetin farmakologie MeSH
- intoxikace vodou patofyziologie MeSH
- krysa rodu rattus MeSH
- lokomoce účinky léků MeSH
- neuroprotektivní látky farmakologie MeSH
- pohybová aktivita účinky léků MeSH
- potkani Wistar MeSH
- rekombinantní proteiny farmakologie MeSH
- věkové faktory MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články 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
- chování zvířat * MeSH
- edém mozku etiologie metabolismus patologie patofyziologie MeSH
- Evansova modř MeSH
- hematoencefalická bariéra metabolismus MeSH
- intoxikace vodou komplikace metabolismus patologie patofyziologie MeSH
- intrakraniální hypertenze etiologie metabolismus patologie patofyziologie MeSH
- krysa rodu rattus * MeSH
- lokomoce * MeSH
- modely nemocí na zvířatech * MeSH
- mozek diagnostické zobrazování metabolismus patologie MeSH
- myelinová pochva patologie MeSH
- permeabilita MeSH
- počítačová rentgenová tomografie MeSH
- potkani Wistar MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus * MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
