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PubMed1994

Cerebral blood flow of rats with water-intoxicated brain edema.

Water intoxication brain edema was produced in rats by intraperitoneal loading of excessive amounts of distilled water (DW). In 10% and 20% groups, DW in amounts of 10 or 20% of body weight was injected, respectively. Water content of brain tissue increased proportionally to the amount of injected water, as follows: 79.8% of wet weight in control, 80.5 and 82.4 in 10% and 20% DW groups, respectively. Since cerebral blood flow (CBF) values measured by laser Doppler (LD) flowmetry were found to give a good correlation with those by hydrogen clearance method in a preliminary experiment, CBF measurement were carried out using LD flowmetry thereafter. Before the injection, CBF values were around 50 ml/min/100 g. Two hours after the water loading, CBF values in 10% and 20% DW groups were 25.6 and 20.3 ml/100 g/min, respectively. CBF values under these edematous condition decreased significantly (p < 0.001 by paired t-test) in proportion to the severity of the brain edema.

Animals↗
PubMed1979

[Effect of nootropil and contvykal on the structural changes in the central nervous system in hypoxic brain edema].

The brain cortex of rabbits exposed to 15-minute ishemia in the presence of monitored hypotonia was studied in 27 experiments in order to verify the efficacy of nootropil and contrykal as agents intended for the treatment of posthypoxic edema of the brain. The therapeutic efficacy was assessed on the basis of the evidence obtained with the aid of light and electron microscopy. It was found that nootropil exerts a favourable action on the ultrastructure of intracellular organella of the neuron: mitochondria, lysosomes, ribosomal apparatus, nuclear envelope, etc. Under the effect of nootropil and contrykal the posthypoxic microcirculatory changes showed signs of compensation and proved reversible. Manifestations of posthypoxic edema of the brain were less pronounced. It is suggested that the efficacy of the treatment regimen offered is related to the normalizing effect of nootropil on metabolic and repair processes in neurons and cellular elements pertaining to the microcirculatory system as well as with a direct action of contrykal on the local factors of capillary permeability.

Animals↗
PubMed2002

Experimental intracerebral hemorrhage: effect of lysed erythrocytes on brain edema and blood-brain barrier permeability.

Understanding the mechanism of edema formation following intracerebral hemorrhage (ICH) is important for developing treatment protocols for this condition. This study examines the role of red blood cell (RBC) lysis and hemoglobin in edema formation following ICH. Significant brain edema developed after 24 hours in rats infused with lysed RBCs and this was associated with a 3-fold increase blood brain barrier (BBB) permeability to alpha-aminoisobutyric acid. We have previously shown that intracerebral injection of packed RBCs does not cause edema formation at one day but does at three days. In this study, we found that packed RBCs did not cause significant BBB disruption at one day but produced a 4-fold increase in BBB permeability at three days. These studies show that following ICH the leakage of substances inside the RBC, facilitated by cellular lysis, results in delayed edema. This was confirmed by both experimentally induced lysis and naturally occurring in-vivo lysis.

Animals↗
PubMed2004

Continuous measurements of cerebral tissue oxygen pressure during hyperbaric oxygenation--HBO effects on brain edema and necrosis after severe brain trauma in rabbits.

INTRODUCTION: Severe brain injury is one of the most frequent causes of severe disability in the young. In acute management of brain trauma, new approaches based on experimental animal investigations should be sought. METHODS: Twenty male, juvenile Chinchilla-Bastard rabbits received standardized cold-injury-induced-brain-trauma (CIBT). A metal probe (temperature -196 degrees C) was applied epidurally over 10 s. The hyperbaric oxygenation (HBO) group (n=10) underwent 90-min HBO sessions with 100% oxygen at 2.5 atmospheres absolute (1 h, 24+/-2 h, 48+/-2 h after CIBT). Cerebral tissue pO2-measurements were performed 60 min after CIBT, during the three HBO sessions and on day 4. The control group (n=10) underwent no treatment. Animals were sacrificed on day 4, and brains were analyzed histologically. RESULTS: In the HBO group, pO2 measurements showed a significant increase in pO2 between day 1 and day 4, whereas no significant changes were observed in the control group. During the first HBO session, mean pO2 was 169 mm Hg, during the second 305 mm Hg and during the third 420 mm Hg. The mean area of necrosis was 16.2 mm2 in the HBO group, in the control group 19.9 mm2. The areas of brain edema were significantly smaller in the HBO group. Mortality in the HBO group was 0%, in the control group 20%. CONCLUSION: HBO appears to be beneficial as an adjunct treatment of severe head trauma. To find optimal treatment protocols, further clinical studies must be developed.

Animals↗
PubMed2005

Correlation of cell apoptosis with brain edema and elevated intracranial pressure in traumatic brain injury.

OBJECTIVE: To study the correlation between brain edema, elevated intracranial pressure (ICP) and cell apoptosis in traumatic brain injury (TBI). METHODS: In this study, totally 42 rabbits in 7 groups were studied. Six of the animals were identified as a control group, and the remaining 36 animals were equally divided into 6 TBI groups. TBI models were produced by the modified method of Feeney. After the impact, ICP of each subject was recorded continuously by an ICP monitor until the animal was sacrificed at scheduled time. The apoptotic brain cells were detected by an terminal deoxynucleotide-transferase-mediated dUTP-digoxigenin nick end labeling (TUNEL) assay. Cerebral water content (CWC) was measured with a drying method and calculated according to the Elliott formula. Then, an analysis was conducted to determine the correlation between the count of apoptotic cells and the clinical pathological changes of the brain. RESULTS: Apoptotic cell count began to increase 2 h after the impact, and reached its maximum about 3 days after the impact. The peak value of CWC and ICP appeared 1 day and 3 days after the impact, respectively. Apoptotic cell count had a positive correlation with CWC and ICP. CONCLUSIONS: In TBI, occurrence of brain edema and ICP increase might lead to apoptosis of brain cells. Any therapy which can relieve brain edema and/or decrease ICP would be able to reduce neuron apoptosis, thereby to attenuate the secondary brain damage.

Animals↗
PubMed1987

Effects of intracarotid hyperosmolar mannitol in triethyl tin (TET)-induced rat brain edema--preservation of blood-brain barrier (BBB) in TET edema.

The effect of intracarotid hyperosmolar mannitol on the blood-brain barrier (BBB) in triethyl tin (TET)-induced rat brain edema was examined by using intravenous Evans blue (EB, MW 68,000) and Adriamycin (ADM, MW 580) as tracers. Three ml of 1.4 M mannitol solution were administered through the right carotid artery during 45 s for BBB opening. The barrier was opened for 60-120 minutes and then re-established. The reversibility was preserved in TET-treated rats and controls. In fact, the intravenous injection of EB stained both TET-treated and non-treated cerebral hemispheres with mannitol-induced transient BBB disruption, but not without BBB disruption. BBB was resistant to both high and low molecular weight substances in TET-induced edema. The importance of this hyperosmotic studies provides the evidence for normal BBB function in TET-induced brain edema.

Animals↗
PubMed1989

Effect of MCI-186 on brain edema in rats.

We induced brain edema in 72 rats by injecting 5 microliters of 3.0% wt:vol polyvinyl acetate into the left internal carotid artery, producing permanent embolization in the left cerebral hemisphere, which developed ipsilateral brain edema reproducibly. Edema was assessed 24 hours after embolization by determining the brain water content and the sodium and potassium concentrations. In this model, the free radical scavenger MCI-186 at 1.0 and 3.0 mg/kg i.v. prevented brain edema in a dose-dependent manner. At 3.0 mg/kg i.v., MCI-186 significantly reduced water content by 1.5% and improved the sodium-potassium balance to within the normal range in the embolized left hemisphere. Dexamethasone at 1.0 mg/kg i.v. did but at 3.0 mg/kg i.v. did not significantly inhibit the development of brain edema. Indomethacin at 4.0 mg/kg i.p. had no effect on brain edema. We suggest that the cyclooxygenase metabolites of arachidonic acid liberated from neuronal cell membrane phospholipids are not likely to be involved in the pathogenesis of permanent brain edema induced by polyvinyl acetate. Our results suggest that MCI-186 attenuates brain edema by suppressing the production of lipoxygenase metabolites, including free radicals or lipid peroxides, and that it may prove valuable for the treatment of brain edema associated with cerebral ischemia.

Animals↗
PubMed1991

[Mediator substances of brain edema in cerebral ischemia].

Brain edema in focal or global cerebral ischemia is associated with formation and release of pathophysiologically active mediator compounds. Therapeutical methods which interfere with mediator compounds under these circumstances might improve specificity of treatment of ischemic brain edema and thereby effectivity. Ischemic brain edema has a vasogenic and cytotoxic component. Extravasation of edema fluid under these conditions can be attributed to ischemic damage of the elements of the blood-brain barrier, the cerebrovascular endothelium. The development of ischemic cell swelling involving nerve- and glial cell processes can not be viewed only as manifestation of cell damage resulting from e.g. energy failure but also as an attempt to maintain or reestablish homeostasis important for cell survival and nerve cell function. The acidosis-induced cell swelling is a case in point. Accumulation of H(+)-ions in the cell causes activation of ion exchange mechanisms to protect or normalize the intracellular pH, respectively. Consequently, Na(+)- and Cl-ions together with water accumulate in the cell as the final process underlying cell swelling. Further, the increased concentrations of glutamate and K(+)-ions found in ischemic brain tissue cause glial cell swelling secondary to an active accumulation of this material together with water in the intracellular compartment in an attempt to normalize the extracellular milieu. A therapeutical inhibition of those mechanisms underlying ischemic cell swelling would prevent reestablishment of the homeostasis and, thereby, enhance secondary tissue damage. A focal brain tissue necrosis, such as an ischemic infarct or traumatic contusion can be utilized to illustrate the pathophysiological significance of the formation and release of mediator compounds of secondary brain damage.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2000

Role of nitric oxide in blood-brain barrier permeability, brain edema and cell damage following hyperthermic brain injury. An experimental study using EGB-761 and Gingkolide B pretreatment in the rat.

The role of oxidative stress in hyperthermia induced upregulation of constitutive and inducible isoforms of nitric oxide synthase (NOS) in the central nervous system (CNS) was investigated using immunohistochemistry in a rat model. Exposure of rats to heat stress at 38 degrees C for 4 h resulted in marked upregulation of constitutive NOS (cNOS) and a mild but significant expression of inducible NOS (iNOS) in several brain regions exhibiting leakage of the blood-brain barrier (BBB), brain edema formation and cell injury. Pretreatment with the potent antioxidative compound EGB-761 or its constituent, Ginkgolide B significantly attenuated upregulation of cNOS and iNOS in the brain and also reduced the BBB permeability disturbances, brain edema and cell injury. These neuroprotective effects were most marked in the EGB-761 pretreated rats. Our observations strongly suggest that (i) EGB-761 and Ginkgolide B pretreatment offer significant neuroprotection in hyperthermic brain injury, (ii) upregulation of cNOS and iNOS are injurious to the cell and, (iii) oxidative stress plays an important role in NOS expression and cell injury.

Animals↗
PubMed1979

Effects of dexamethasone on tumor-induced brain edema and its distribution in the brain of monkeys.

A human choriocarcinoma was successfully adapted to grow in the brain of monkeys (Macaca mulatta), thus providing a model of tumor-induced brain edema. Four animals were given dexamethasone (3 mg/kg/day) during 3 to 5 days after the onset of clinical signs, and the other five received no treatment for the same period. Tissue water and electrolyte content of treated and untreated animals were compared in cortex and white matter at various distances from the edge of the tumor. In untreated animals, 67.9% and 23.6% swelling was detected in adjacent and remote white matter, respectively, but only 11.8% swelling was noted in adjacent cortex. In animals treated with dexamethasone these percentages of swelling were improved to 32.4% and 11.9% in the corresponding white matter, and to 4.9% in adjacent cortex. The electrolyte changes shown in edematous brain of control animals also demonstrated significant improvement in the dexamethasone-treated group. Tissue radioactivity of 3H-dexamethasone at 60 minutes after intravenous injection was high in the periphery of tumor, adjacent cortex, and white matter, but low in the center of tumor, remote cortex, and white matter. The sites with high concentrations of dexamethasone also showed significant improvement of brain edema after dexamethasone treatment, suggesting that dexamethasone may act directly at these loci.

Animals↗
PubMed2003

Temporal profiles of cerebrospinal fluid leukotrienes, brain edema and inflammatory response following experimental brain injury.

The post-traumatic changes of leukotrienes LTC4, LTD4, LTE4, and LTB4 in cerebrospinal fluid of rats from 10 min to 7 days were investigated after controlled cortical impact in relation to brain edema and cellular inflammatory response. LTC4 increased five-fold at 4 h, normalized at 24 h, and showed another four-fold increase at 7 days. The same pattern was observed for LTD4 and LTE4. LTB4 however, behaved differently: concentrations were lower and levels peaked two-fold at 24 h. Edema in the injured hemisphere increased continuously up to 24 h without change contralaterally. Leukocyte infiltration, macrophage presence and microglia activation were most prominent at 24 h, 7 days and 24 h respectively. Leukotriene changes in CSF seem to reflect those in the affected tissue, with a time delay and in lower concentrations, and were not linearly correlated to brain edema. The initially high leukotriene levels are rather likely to contribute to the cytotoxic edema than to enhance a vasogenic edema component. The profile of LTB4 was parallel to the time course of leukocyte infiltration, indicating initiation of infiltration as well as prolonged production by leukocytes themselves. The second leukotriene peak at 7 days is likely to follow a different pathway and might be related to a production in macrophages or activated glia.

Animals↗
PubMed1990

Role of leukotrienes as mediator compounds in brain edema.

Leukotrienes accumulate in brain tissue after cerebral ischemia and in brain tumors. Thus, their release might contribute to the blood-brain barrier damage observed under these conditions and, hence, brain edema. The effect of these substances on the permeability of pial vessels and whether inhibition of LT synthesis reduces cold injury brain edema were studied. The pial vasculature of cats was studied by fluorescence microscopy. The cortex was superfused with LTC4, LTD4, or LTE4 via a cranial window. Na(+)-fluorescein was intravenously administered as blood-brain barrier indicator. LT concentrations up to 2 microM did not induce any leakage of the blood-brain barrier indicator into the parenchyma. However, all LTs tested constricted pial arteries and veins. Brain edema formation was studied in rabbits with cold injury. BW755C, an inhibitor of cyclooxygenase and lipoxygenase preventing formation of LTs, was given before and after trauma. Control animals received saline only. BW755C was ineffective in attenuating cold injury edema. Hemispheric swelling in control animals was 7.8 +/- 1.1%, and 7.7 +/- 0.4% in animals with treatment. LTs, even when administered to the brain in concentrations exceeding levels occurring under pathological conditions, did not induce barrier damage, nor did inhibition of LT synthesis attenuate formation of vasogenic edema. The results provide further evidence against LTs as mediator compounds of this process.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
PubMed1988

Ultrastructural alterations of human cortical capillary basement membrane in perifocal brain edema.

The fine structural alterations of cortical capillary basement membrane have been studied in 16 patients with perifocal edema associated to brain tumors, traumatic injuries complicated with subdural or epidural hematoma or hygroma and congenital malformations, such as hydrocephalus, Arnold-Chiari and Alport's syndromes and vascular anomalies. The basement membrane displayed homogeneous and nodular thickening, vacuolization, rarefaction and reduplication. Its average thickness varied according to the etiology and severity of brain edema. In nine patients with moderate brain edema the thickness ranged from 71.97 to 191.90 nm and in the remaining seven patients with severe brain edema it varied from 206.66 to 404.22 nm. The basement membrane complex appeared apparently intact in moderate edema and showed glio-basal dissociation in severe edema. In areas of highly increased cerebro-vascular permeability, the basement membrane showed matrix disorganization and bifurcations acting as abluminal transcapillary channels. In regions of total brain necrosis, its structural stability was lost showing loosening, dissolution and rupture. Proliferation of collagen fibers was also found in three cases. Basement membrane swelling was interpreted as an overhydration of its matrix. The thickening, rarefaction and vacuolization seem to be induced by the increased vacuolar and vesicular transendothelial transport. The degenerated areas feature a finely granular precipitate interpreted as a protein or glycoprotein degraded matrix.

Adolescent↗
PubMed2003

3-[2-[4-(3-chloro-2-methylphenyl)-1-piperazinyl]ethyl]-5,6-dimethoxy-1-(4-imidazolylmethyl)-1H-indazole dihydrochloride 3.5 hydrate (DY-9760e), a novel calmodulin antagonist, reduces brain edema through the inhibition of enhanced blood-brain barrier permeability after transient focal ischemia.

An alteration of the blood-brain barrier (BBB) permeability contributes to the development of brain edema after stroke. In this study, we evaluated the effects of 3-[2-[4-(3-chloro-2-methylphenyl)-1-piperazinyl]ethyl]-5,6-dimethoxy-1-(4-imidazolylmethyl)-1H-indazole dihydrochloride 3.5 hydrate (DY-9760e), a novel calmodulin antagonist, on brain edema formation and BBB integrity in rats subjected to transient focal ischemia. DY-9760e (1 mg/kg/h) was intravenously infused for 6 h, starting immediately after reperfusion of a 1-h middle cerebral artery occlusion. Treatment with DY-9760e significantly suppressed the increase in water content and the extravasation of Evans blue dye after transient focal ischemia. Analysis of a magnetic resonance imaging method revealed that DY-9760e significantly prevented the development of brain edema in the cortical region of the ipsilateral hemisphere. Trifluoperazine, a calmodulin antagonist that is structurally different from DY-9760e, also attenuated brain edema elicited by transient focal ischemia. Furthermore, DY-9760e and trifluoperazine reduced tumor necrosis factor-alpha-induced hyperpermeability of inulin through a cultured brain microvascular endothelial cell monolayer, suggesting an involvement of calmodulin in the regulation of brain microvascular barrier function. The present results demonstrate that DY-9760e ameliorates brain edema formation and suggest that this effect may be mediated in part by the inhibition of enhanced BBB permeability after ischemic insults. Thus, DY-9760e is expected to be a therapeutic drug for treatment of acute stroke patients.

Animals↗
PubMed2003

Antioxidant compounds EGB-761 and BN-52021 attenuate brain edema formation and hemeoxygenase expression following hyperthermic brain injury in the rat.

Role of carbon monoxide (CO) in hyperthermic brain injury induced brain pathology was examined in a rat model using immunohistochemistry of the hemeoxygenase-2 (HO-2) enzyme. Exposure of rats to 4 h heat stress at 38 degrees C resulted in profound hyperthermia, breakdown of the blood-brain barrier (BBB), brain edema formation, cell damage and expression of HO-2 in several brain regions. Pretreatment with potent antioxidant compounds EGB-761 and BN-52021 markedly reduced the HO-2 expression, BBB breakdown, brain edema formation and cell damage without attenuating the hyperthermic response. This effect was most marked in animals treated with EGB-761. These observations suggest that upregulation of HO-2 representing generation of CO plays important roles in hyperthermic brain injury, and oxidative stress seems to be one of the most important signals in inducing HO-2 expression in hyperthermia, not reported earlier.

Animals↗
PubMed2003

Brain edema in acute liver failure.

Brain edema and consequent increase in intracranial pressure is a major complication of acute liver failure (ALF) and is a major cause of death in this condition. Rapid accumulation of ammonia in brain has been implicated in the pathogenesis of brain edema in ALF. Increased brain ammonia may cause brain swelling via the osmotic effects of an increase in astrocytic glutamine concentration or by inhibition of glutamate removal from brain extracellular space. Acute liver failure results in altered expression of several genes in the brain, some of which code for proteins involved in central nervous system function such as the glutamate transporter GLT-1, the astrocytic structural protein, glial fibrillary acidic protein, and the water channel protein, aquaporin IV. Loss of expression of GLT-1 results in increased extracellular brain glutamate. Therapeutic measures currently used to prevent and treat brain edema in acute liver failure include mannitol; strategies aimed at lowering of gut ammonia production are generally ineffective. Studies in experimental animals suggest that mild hypothermia or the use of L-ornithine-L-aspartate may be useful in the prevention of brain edema in these patients.

Ammonia↗
PubMed1993

Blockade of AMPA receptors reduces brain edema following opening of the blood-brain barrier.

The aim of our study was to evaluate whether blockade of alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptors could reduce brain edema in two experimental models of edema following opening of the blood-brain barrier (BBB). The brain specific gravity was determined 2 h after opening the BBB by a 30-s infusion of protamine sulfate (10 mg in 200 microliters 0.9% NaCl) or arabinose (1.5 or 1.8 mol/L, 0.06 ml.s-1) into the right internal carotid artery. Cisternal CSF was withdrawn for albumin determination before the carotid infusion and before killing 2 h later. After infusion of protamine sulfate or arabinose, CSF albumin increased in all groups. The brain specific gravity was significantly lower in the right than in the left (control) frontal, parietal, and occipital cortex and striatum. NBQX (2,3-dihydroxy-6-nitro-7-sulfamoylbenxo(F)quinoxaline), an AMPA receptor antagonist, given intravenously 10 min after opening the BBB (5 mg/kg), significantly increased the specific gravity in the treated rats (p < 0.01 for the difference from control rats) without reducing CSF albumin or albumin extravasation in the brain as evaluated with Evans blue. We hypothesize that intracerebral (glial?) AMPA receptors may play a role in brain edema following opening of the BBB.

Animals↗