Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Brain Edema”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 307 records · Page 17Linked to original sources
PubMed1995

Effects of continual intravenous posttreatment with D-CPP-ene, a potent competitive N-methyl-D-aspartate receptor antagonist, on rat brain edema induced by injection of triethyltin into the cerebral hemisphere.

Brain edema was produced by injecting triethyltin (TET) into the right cerebral hemisphere via the internal carotid artery in rats. TET induced a dose-related increase in mortality rate and brain water content. Immediately after TET-injection (2 mg/head), saline, glycerol (125 mg/ml) or the N-methyl-D-aspartate receptor antagonist (R)-4-(3-Phosphono-2-propenyl)-2-piperazine carboxylic acid (D-CPP-ene; 0.083 and 0.25 mg/ml) was continually infused via the right internal jugular vein at 20 microliters/min for 6 h. The mortality rate and brain water content were significantly decreased after infusion of 0.25 mg/ml D-CPP-ene, but only somewhat reduced after glycerol infusion when compared with the saline group. The results suggest that continual intravenous posttreatment with D-CPP-ene is useful for treatment of brain edema.

Animals↗
PubMedDate not supplied

Electron microscopic evaluation of brain edema in rabbits with galactosamine-induced fulminant hepatic failure: ultrastructure and integrity of the blood-brain barrier.

Brain edema is a major complication of fulminant hepatic failure and is responsible for death in a large percentage of patients. We previously demonstrated the progressive accumulation of water in grey matter areas of the brain in the rabbit with galactosamine-induced fulminant hepatic failure. We now report the electron microscopic morphology of the brain in the same model of acute hepatic failure following the intravenous injection of horseradish peroxidase, an intravascular tracer which forms an electron-dense reaction product. Rabbits with both mild and severe encephalopathy had normal blood pressures and blood gases at the time of study. Fixation of brain tissue was obtained by whole-body perfusion. Marked swelling of the cytoplasm, perineuronal and perivascular processes of astrocytes were noted in cortical gray, but not white, matter areas; the other cellular components of the brain had normal morphology. Capillary endothelial cells were normal, and there was no evidence of horseradish peroxidase in endothelial cell vesicles, basement membranes or the brain parenchyma, suggesting that the blood-brain barrier was impermeable to large molecules. Histologic evidence of brain edema is seen in this model, with swelling of astrocytes as the primary manifestation of the accumulation of water. Damage to astrocytes or inhibition of their function may contribute to the pathogenesis of hepatic encephalopathy in this model.

Animals↗
PubMed2001

Predictors of fatal brain edema in massive hemispheric ischemic stroke.

BACKGROUND AND PURPOSE: Early identification of stroke patients at risk for fatal brain edema may be useful in selecting patients for aggressive interventions. Prior studies suggested that early nausea/vomiting and major hypodensity on baseline computed tomography (CT) were predictive of herniation. METHODS: This study was a retrospective multicenter case-control study of patients with large middle cerebral artery (MCA) strokes admitted within 48 hours of symptom onset. Medical records, laboratory data, and CT scans were analyzed. Cases, defined as patients who died of massive brain swelling, were compared with all remaining patients as controls. RESULTS: Two hundred one patients with large MCA strokes were identified: 94 (47%) died of brain swelling, 12 (6%) died of non-neurological causes, and 95 (47%) survived at day 30. Multivariable analysis, adjusted for age and clustered by center, identified the following predictors of fatal brain edema: history of hypertension (OR 3.0, 95% CI 1.2 to 7.6, P=0.02), history of heart failure (OR 2.1, 95% CI 1.5 to 3.0, P<0.001), elevated white blood cell count (OR 1.08 per 1000 white blood cells/microL, 95% CI 1.01 to 1.14, P=0.02), >50% MCA hypodensity (OR 6.3, 95% CI 3.5 to 11.6, P<0.001), and involvement of additional vascular territories (anterior cerebral artery, posterior cerebral artery, or anterior choroidal artery; OR 3.3, 95% CI 1.2 to 9.4, P=0.02). Initial level of consciousness, National Institutes of Health Stroke Scale score, early nausea/vomiting, and serum glucose were associated with neurological death in bivariable but not multivariable analyses. CONCLUSIONS: Among patients with large MCA infarctions, an increased risk of fatal brain edema is associated with history of hypertension or heart failure, increased baseline white blood cell count, major early CT hypodensity involving >50% of the MCA territory, and involvement of additional vascular territories. These data confirm and expand on prior research with a broad-based patient population. The presence of these risk factors identifies those stroke patients who may require aggressive therapeutic approaches.

Acute Disease↗
PubMed2000

Fluid therapy of acute brain edema in children.

The clinical experience with a new fluid therapy in children with acute brain edema complicated by infectious disease is reported. The clinical data of a retrospective group of 192 patients and a prospective study of 1,302 and 2,279 patients is summarized. One method of fluid therapy for children with acute brain edema is traditional; fluid intake is restricted to less than 1,200 mL/m(2) daily (60 mL/kg daily). Another method is the new fluid therapy regimen used in our prospective study, in which dehydration and fluid replenishment are individualized. On the first day the fluid intake of patients who survived varied from 40 to 208 mL/kg daily. The mortality rate in the two prospective groups was 19.66% in 1,302 patients and 17.2% in 2,279 patients, significantly lower than the 63.5% in the retrospective group (192 patients) (P <0.001). This result indicates that a wide range of fluid intake for children with acute brain edema is allowable during the first days of treatment. The appropriate dehydration and fluid replenishment should be individualized based on close observation of the patient's condition.

Acute Disease↗
PubMed2003

Energy metabolism and cerebral blood flow during cytotoxic brain edema induced by 6-aminonicotinamide.

We investigated the progression of cytotoxic brain edema induced by 6-aminonicotinamide (6-ANA), a potent antimetabolite of nicotinamide, by measuring the time courses of changes in brain tissue water state (with MRI), histology (with H&E staining), energy metabolism (with 31P-NMR), brain hemoglobin concentration (with near-infrared spectroscopy; NIRS), cerebral blood flow and volume (CBF. CBV), mean arterial blood pressure (MABP), and brain activity (with EEG) up to 10 hours (h). Change in cerebrovascular autoregulation was also investigated. 6-ANA (120 mg/kg) was administered intraperitoneally to 30 male Wistar rats (250-350 g). After 10 h, the T2-weighted signal intensity was increased (p < 0.05), and H&E staining showed severe vacuolation of glial cells. ATP production/consumption and intracellular pH were well maintained up to 10 h, while the intensity of the phosphomonoesters (PME) signal was significantly increased (p < 0.05). Oxygen consumption gradually decreased from 4 to 10 h. CBF and MABP were all significantly increased (by 2.5-fold for CBF) (p < 0.05). Theta and delta wave amplitudes were reduced at 10 h. In summary, 6-ANA (120 mg/kg) induced cytotoxic brain edema from 4 to 10 h. Energy balance and brain activity were well maintained up to 10 h, though cerebrovascular autoregulation was impaired.

6-Aminonicotinamide↗
PubMed2001

Systemic complement depletion diminishes perihematomal brain edema in rats.

BACKGROUND AND PURPOSE: The complement cascade is activated after experimental intracerebral hemorrhage (ICH). It remains unclear, however, whether depleting the complement system will improve injury resulting from ICH. This study investigated the effects of systemic complement depletion on brain edema formation after ICH. METHODS: Fifty-six pentobarbital-anesthetized Sprague-Dawley rats were used. Treatment animals were complement-depleted with cobra venom factor (CVF) (intraperitoneally). Control rats received an equal volume of saline injection (intraperitoneally). In both treatment and control rats, autologous blood (100 microL) was infused stereotaxically into the right basal ganglia. Rats were killed 2, 24, or 72 hours later for brain water, ion, and tumor necrosis factor-alpha (TNF-alpha) measurements, for Western blot analysis, and for immunohistochemical studies. Brain edema was quantitated by wet/dry weight. TNF-alpha levels were measured by enzyme-linked immunosorbent assay. Western blot analysis was applied for C9 semiquantification. Immunohistochemistry was used to detect complement C3d, C5a, C9, and myeloperoxidase. RESULTS: Perihematomal brain edema was reduced by systemic complement depletion at 24 hours (78.8+/-0.6% versus 81.5+/-0.8% in control, P:<0.01) and 72 hours (81.5+/-1.5% versus 83.6+/-0.9% in control, P:<0.05), while cerebellar water content was unaffected (78.2+/-0.3% versus 78.0+/-0. 1%). Complement depletion reduced TNF-alpha production 2 hours after ICH. Immunocytochemistry showed that complement depletion significantly reduced perihematomal C9 deposition, C3d production, and the number of C5a- and myeloperoxidase-positive cells. CONCLUSIONS: Complement depletion by CVF attenuates brain edema in ICH, indicating that complement activation plays an important role in ICH-induced brain edema. Preventing complement activation may be effective in the treatment of ICH.

Animals↗
PubMedDate not supplied

Report of Joint Committee for Stroke Resources. IV. Brain edema in stroke.

A classification of brain edema is provided as well as an extensive review of the animal models from which we have derived most of the basic information we have about the formation and resolution of edema. The clinical aspects of cerebral edema in stroke are discussed and also modern methods for identifying cerebral edema in the human. Attention is given to computed tomography and enhanced CT and advances in their application to this condition. Treatment of cerebral edema in the stroke patient using glycerol, dextran 40, mannitol, steroids, and other drugs is discussed and the need pointed out for controlled clinical trials of the therapeutic effectiveness of these agents.

Adrenal Cortex Hormones↗
PubMed2006

Protective effect of the V1a receptor antagonist SR49059 on brain edema formation following middle cerebral artery occlusion in the rat.

There exists no pharmacological treatment for fulminating brain edema. Since evidence indicates that brain aquaporin-4 (AQP4) water channels are modulated by vasopressin V1a receptors, we examined the edema-reducing properties of the selective V1a receptor antagonist, SR49059, following middle cerebral artery occlusion (MCAO). Male Sprague-Dawley rats were randomly assigned to sham procedure, vehicle, or SR49059 infusion at different dosages (each n = 6,480 microL/hr, 640 microL/hr, 720 microL/hr) and starting 60 minutes before or after MCAO. After a 2-hour period of ischemia and 2 hours of reperfusion, the animals were sacrificed for assessment of brain water content, sodium, and potassium concentration. Statistics were performed using an ANOVA followed by a Tukey post hoc analysis. SR049059 treatment reduced brain water content in the infarcted area given at 640 microL/hr (p = 0.036), 720 microL/hr 60 minutes before (p = 0.002) or 60 minutes after (p = 0.005) MCAO. The consecutive sodium shift into the brain was prevented (p = 0.001), while the potassium loss was inhibited only by pre-treatment (p = 0.003). These findings imply that in ischemia-induced brain edema, the selective V1a receptor-antagonist SR49059 inhibits brain edema and the subsequent sodium shift into brain. This substance offers a new avenue in brain edema treatment and prompts further study into AQP4 modulation.

Animals↗
PubMed1985

NMR imaging and spectroscopy of experimental brain edema.

A canine model of experimental brain edema utilizing the classic cold lesion technique was used to identify the optimal nuclear magnetic resonance (NMR) spin-echo imaging parameters needed to detect cerebral edema with maximum sensitivity. Each animal was studied with four separate spin-echo sequences, utilizing pulse intervals ranging from 0.5 to 2.0 seconds. The echo delays following each pulse interval were 28 and 56 msec. Cerebral edema was best identified with the longest pulse interval (2.0 seconds), and the second echo delay (56 msec). T1 and T2 relaxation values were obtained from in vitro spectroscopy. The relaxation times were prolonged in the edematous white matter; however, absolute T1 and T2 values proved of little use in comparing different animals.

Animals↗
PubMed2000

Increased cerebrospinal fluid glutamate and taurine concentrations are associated with traumatic brain edema formation in rats.

Glutamate-mediated excitotoxicity results in cell swelling and contributes to brain edema formation. Since increased extracellular taurine reflects glutamate-induced cell swelling in vitro, elevated CSF taurine could therefore unmask glutamate-mediated cytotoxic edema formation under in vivo conditions. For this, the temporal profile of brain edema and changes in cisternal CSF glutamate and taurine levels were determined in 28 rats following focal traumatic brain injury. Compared to six non-traumatized rats, CSF glutamate (4. 8+/-0.3 vs. 10+/-0.9 microM) and taurine levels (12+/-1.3 vs. 41+/-3 microM) were significantly increased at 8 h after trauma (P<0.001). Over time, CSF glutamate and taurine were significantly increased by 24 (glutamate: 38+/-4.4 microM) and 48 h (taurine: 51+/-4 microM), respectively. While CSF glutamate closely reflected changes in hemispheric water content, alterations in CSF taurine occurred diametrically to those seen for glutamate. Under the present study design, increased CSF taurine could reflect glutamate-induced cell swelling. In addition, neuronal release of taurine with its inhibitory and antiexcitotoxic functions could explain the observed diametric changes in CSF glutamate, CSF taurine, and hemispheric water content. Therefore, increasing taurine could be a therapeutic approach in attenuating post-traumatic glutamate-mediated cell damage.

Amino Acids↗
PubMed1979

Influence of hypoxia on the composition of isolated edema fluid in cold-induced brain edema.

The isolation of edema fluid from cats with cold-induced cerebral edema allowed the study of changes of Na+ and K+ content, lactate dehydrogenase and creatine phosphokinase activity, colloid osmotic pressure and the level of intravenously administered 99mTc-albumin in the edema fluid during a period of hypoxia. The changes consisted of an increase of all mentioned parameters, except Na+; and could be interpreted as a concentration of solutes (but for Na+) in the extracellular edema fluid, concomitant to a reduction of the extracellular space, as the oxygen deficiency caused improper functioning of the cellular Na+-K+ pump, with a resulting shift of fluid (including Na+) into the cellular elements.

Albumins↗
PubMed1986

Inhibition of excitatory neurotransmission with kynurenate reduces brain edema in neonatal anoxia.

Excitatory amino acid neurotransmitters have been implicated in fostering brain edema and neuronal death in ischemia. As both of these processes are involved in nervous system damage during neonatal anoxia, the effect of blockade of cell excitation with kynurenate upon brain water was studied following anoxic-ischemic brain injury in neonatal rats. Such treatment attenuated brain edema immediately after, and 24 h following anoxia-ischemia.

Animals↗
PubMed2000

Bradykinin 2 receptor antagonist LF 16-0687Ms reduces posttraumatic brain edema.

Activation of the kallikrein-kinin system contributes to traumatic brain edema formation. Inhibition of bradykinin 2 (B2) receptors has been shown to successfully reduce brain edema formation. The purpose of this study was to investigate the protective effect of the novel nonpeptide B2 receptor antagonist LF 16-0687Ms in brain-injured rats. Contusion was produced in forty rats by controlled cortical impact injury. Five minutes after trauma rats received a single dose of 0, 3, or 30 mg/kg of LF 16-0687Ms. After 24 hours brain swelling and hemispheric water content were determined. Brain swelling was significantly decreased by 25% in the low and 27% in the high dose group compared to controls (p < 0.03). Water content of the traumatized hemisphere tended to be decreased (80.2 +/- 0.1 vs. 80.4 +/- 0.1%) while water content of the non-traumatized hemispheres tended to be increased after administering LF 16.0687Ms (79.3 +/- 0.1 vs. 79.0 +/- 0.1%). Single administration of the novel nonpeptide B2 receptor antagonist LF 16-0687Ms significantly reduces brain swelling. The missing significant reduction in water content of the traumatized hemisphere, however, could be related to an unspecific increase in water content due to LF 16.0687Ms as suggested by increased water content in the non-traumatized hemisphere.

Animals↗
PubMed2003

Brain edema from intracerebral hemorrhage.

Sequential changes in brain parenchyma surrounding an intracerebral hemorrhage are described here. Re-bleeding occurs within the first several hours after the initial hemorrhage in about 30%, of cases. The coagulation cascade is activated as soon as blood encounters tissue. Perihematomal brain edema develops in response to clot retraction, thrombin formation, erythrocyte lysis, hemoglobin toxicity, complement activation, mass effect, and blood-brain barrier disruption. Early hematoma evacuation interrupts edema formation. The toxicity ofextravasated blood in brain parenchyma has not been studied well in traumatic injury or in hemorrhagic tumor models yet, but similar mechanisms of edema formation are likely to occur in these conditions.

Animals↗
PubMed2006

Bifrontal decompressive craniotomy for malignant brain edema.

OBJECTIVE: To review the outcome of bifrontal decompressive craniotomy used for the treatment of malignant brain edema due to different etiologies. METHODS: The study was carried out at King Khalid University Hospital, Riyadh, Kingdom of Saudi Arabia during the period from January 2000 to June 2005, and included all patients who had malignant brain edema due to different etiology and were treated with bifrontal decompressive craniotomy after failure of aggressive medical treatment. RESULTS: Ten patients were included in the study, 6 males and 4 females; the mean age was 24 years. Seven patients had severe head injury, 2 had aneurysmal subarachnoid hemorrhage, and one had large calcified olfactory groove meningioma. Clinically, all patients, except one, had Glasgow coma scores more than 3 before surgery, and operation was performed in all patients once clinical deterioration was observed and diagnosis confirmed by CT brain scan. The outcome of surgery was good in 70%, poor in 20%, and mortality was 10%. The mean hospital stay was 85 days. CONCLUSION: Bifrontal decompressive craniotomy offers immediate reduction of intracranial pressure to its normal levels, and improves the outcome of malignant brain edema whatever its cause, it should be performed once clinical deterioration is observed.

Adolescent↗
PubMed2003

[Relationship between aquaporin-4 expression in astrocytes and brain edema caused by glioma].

OBJECTIVE: To investigate the relationship between aquaporin-4 (AQP4) water channel expression in astrocytes and brain edema caused by glioma. METHODS: The changes of water transport in in vitro blood-brain barrier models were examined using high-performance liquid chromatography (HPLC), and the expression level of AQP4 was assayed by semiquantitative RT-PCR. RESULTS: The water transport of the in vitro blood-brain barrier model from the luminal side to basolateral side was increased after coculture with glioma cells, which induced significantly decreased expression level of AQP4 in the astrocytes. CONCLUSIONS: Glioma cells can promote water transport in in vitro blood-brain barrier model from the luminal side to abluminal side, and the brain edema induced by the glioma cells may not necessarily be the result of hyperpermeability of the blood-brain barrier to macromolecules in the plasma. The decreased expression level of AQP4 induced by glioma cells may be a molecular mechanism for neoplastic brain edema in patients with glioma.

Animals↗
PubMed2005

Vascular endothelial growth factor antagonist reduces brain edema formation and venous infarction.

BACKGROUND AND PURPOSE: Cerebral venous ischemia often induces severe brain edema. Vascular endothelial growth factor (VEGF), which induces angiogenesis, is also known as vascular permeability (VP) factor. The present study was undertaken to investigate whether the inhibition of VEGF could reduce brain edema formation and cerebral venous infarction (CVI) in a rat 2-vein occlusion (2-VO) model. METHODS: We used 2-VO model in which 2 adjacent cortical veins were photochemically occluded. Male Wistar rats (n=25) were divided into 2 groups: one group was treated with a VEGF antagonist (antagonist group, n=10) and the second group was treated with phosphate-buffered solution (PBS) (PBS group, n=15). VEGF antagonist or PBS was injected intraperitoneally immediately after 2-VO. The developing ischemic infarct was evaluated by magnetic resonance imaging (MRI) and histology 24 hours after occlusion. RESULTS: VEGF expression was observed in the cytoplasm of neurons exclusively in the area of vasogenic edema that was shown as a high-intensity area in the apparent diffusion coefficient of water map. Ischemic volumes calculated from each MR images, which are related to infarction and/or vasogenic edema, respectively, were significantly smaller in the antagonist group as compared with the PBS group (P<0.05) CONCLUSIONS: Our study is the first to provide evidence that the inhibition of VEGF attenuates VP and reduces CVI in the acute stage. Although VEGF is a significant angiogenesis factor, we concluded that the inhibition of VEGF might be a new therapy for both brain edema formation and CVI.

Animals↗