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At least 127 records · Page 7Linked to original sources

PubMed1994

Peritumoral brain edema and cortical damage by meningioma.

Forty supratentorial meningiomas were analyzed to identify factors causing peritumoral brain edema. Parasagittal, sphenoid ridge, and olfactory groove meningiomas induced edema more frequently than those in other locations. Meningothelial meningiomas were more invasive than other types and were associated with more peritumoral edema. Brain edema correlated significantly with tumor size and histological evidence of leptomeningeal and cortical damage from the tumor. Larger tumors destroy the leptomeninges and cerebral cortex, allowing direct transmission of edema fluid into the white matter, resulting in vasogenic edema.

Adult↗

PubMed1977

Osmotic opening of the blood-brain barrier in the rhesus monkey without measurable brain edema.

The blood-brain barrier in the rhesus monkey was opened to intravascular Evans blue-albumin, without causing brain edema or altering brain electrolytes, by perfusing 2.5 molal recrystallized D,L-lactamide into the internal carotid artery for 20--30 sec. Gross neurological and behavioral sequelae were absent in 7 of 8 animals with barrier opening, and 2 days after perfusion no statistically significant changes were observed in sodium, potassium or water contents of perfused as compared to unperfused gray and white matters of brains of the 7 normal animals. Brain endema may not have developed because parenchymal albumin was excreted or metabolized by 2 days. It is suggested also that closure of the barrier after several hours prevents salt from accompanying plasma fluid into the brain. Entry of fluid without salt would reduce, before measurable edema developed, any transcapillary osmotic gradient established by prior entry of plasma albumin.

Animals↗

PubMed1991

Increased capillary permeability in rat brain induced by factors secreted by cultured C6 glioma cells: role in peritumoral brain edema.

To investigate whether brain tumors secrete a factor(s) responsible for peritumoral brain edema, we studied the effect of conditioned medium from cultured C6 glioma cells on rat brain capillary permeability. Three different fractions of conditioned medium were obtained. SUP-N was a culture supernatant incubated 4 hours in serum-free medium. SUP-C was the 60-100 fold concentrated fraction obtained by dialysis-concentration of SUP-N; it contained 950 micrograms/ml of protein greater than 10 k-daltons from 3 x 10(8) cells. SUP-L was a water-dispersible lipid fraction from SUP-N; the major components of SUP-L were neutral lipids and free fatty acids. The supernatant fractions and their corresponding control solutions were infused into normal rat brain, and capillary permeability was determined using quantitative autoradiography by measuring the unidirectional entry constant, K (micrograms l/g.min), of 14C-alpha-aminoisobutyric acid (14C-AIB) into brain tissue. SUP-C and SUP-L significantly increased capillary permeability of normal brain; the effect of SUP-C was more intense and extensive than that of SUP-L. The highest mean K value (Kmax) of SUP-C was 10.83 +/- 0.99 and that of the control was 2.53 +/- 0.22 (p less than 0.001). The Kmax of SUP-L was 5.61 +/- 0.23 and that of the control was 2.67 +/- 0.36 (p less than 0.01). A time-course study after infusion of SUP-C demonstrated that more than 1.5 hours is required for the supernatant fraction to open the barrier and that the effect of SUP-C was reversible. The increase of capillary permeability induced by SUP-C was significantly inhibited by pretreatment of rats with dexamethasone (10 mg/kg, ip) 1 hour before intracerebral infusion of SUP-C (Kmax (untreated): 8.30 +/- 0.82, Kmax (treated): 1.33 +/- 0.64, p less than 0.001). These results indicate that experimental brain tumors secrete at least two different diffusible factors responsible for capillary endothelial leakage in normal brain. One is a protein of molecular weight greater than 10 k-daltons, whose effect is inhibited by glucocorticoids, and the other is a waterdispersible lipid.

Animals↗

PubMed2003

Neuropeptide release influences brain edema formation after diffuse traumatic brain injury.

The mechanisms associated with edema formation after traumatic brain injury (TBI) have not been fully elucidated. In peripheral tissue injury, the neurogenic component of inflammation plays a significant role in increased vascular permeability and edema formation. However, few studies have examined the role of neuropeptide induced neurogenic inflammation following TBI. Adult male Sprague-Dawley rats were either left untreated, or pre-treated with capsaicin (125 mg/kg s.c.) or equal volume vehicle, and injured 14 days later using the 2-meter impact-acceleration model. Subgroups of animals were assessed for blood brain barrier (BBB) permeability (Evans Blue), brain edema (wet weight/dry weight) and functional outcome (Barnes maze and Rotarod) for up to 2 weeks post-trauma. Increased BBB permeability was present in untreated animals between 3 and 6 h after injury but not at later time-points. Edema was maximal at 5 h after trauma, declined and then significantly increased over the 5 days post-trauma. In contrast, capsaicin pre-treated, neuropeptide-depleted animals exhibited no significant increase in BBB permeability or edema compared to vehicle treated animals after injury. Notably, motor and cognitive impairments were significantly reduced in the capsaicin-pretreated animals. We conclude that neurogenic inflammation contributes to the development of edema and posttraumatic deficits after diffuse TBI.

Animals↗

PubMed1998

Nitric oxide synthase immunoreactivity related to cold-induced brain edema.

To determine the relationship between brain edema and the expression of nitric oxide synthase (NOS), we immunohistochemically studied the distribution and level of NOS in rat brain cold injury model. Vasogenic brain edema was produced by cortical freezing lesion. NOS immunohistochemical studies were performed 4 and 8 h, 1, 3, 5, 7, 14 and 21 days after injury. In control normotensive rats, immunoreactivity for NOS was observed in scattered neuronal cells as reported previously, but there was no reactivity in glial cells. In the present study in the cold injury model, however, fibrinogen staining showed extravasated plasma fluid extending to the white matter contralateral to the site of cold injury. NOS immunoreactivity was observed in most reactive astrocytes and a proportion of the microglial cells and macrophages in the white matter not only just beneath the area of cold injury but also in the contralateral side. The nerve cells in the edematous region scarcely showed additional immunoreactivity for NOS. The distribution of increased NOS relatively corresponded with the sites of extravasated plasma fluid demonstrated by fibrinogen staining. Electron microscopically, NOS was observed in astrocytes along the rough endoplasmic reticulum suggesting that NOS was produced in the cells and not taken up from the surroundings. Based on these findings, we postulate that brain edema and the simultaneously generated free radicals or some extravasated plasma components may induce expression of NOS in the reactive cells, and that the NO thus generated may be involved in the development of diffuse degeneration of the white matter which accompanies brain edema.

Animals↗

PubMed2004

[Effect of focal hypothermia on traumatic brain edema and the content of lactic acid in the brain tissue in rats].

UNLABELLED: Objective To investigate the effect of focal hypothermia (LH) on traumatic brain edema and the content of lactic acid in rat brain tissue. METHODS: One hundred and sixty-eight adult SD rats were randomly divided into 6 groups: Group A, sham injury group; Group B, traumatic brain injury controlled group; Group C, treated by LH with water at 0 degree C; Group D, treated by LH with water at 10 degrees C; Group E, treated by LH with water at 20 degrees C; Group F, treated by LH with water at 25 degrees C. All rats except those in Group A were subjected to traumatic brain injury (TBI) with Feeney's method. LH began for animals in Group C - F 30 minutes after the TBI. Regional brain temperature reached the target temperature of 31 degrees C within 20-30 minutes and maintained for 3 hours. Each group was divided into 4 sub-groups by investigating the duration after the TBI: 1, 3, 5 or 7 day sub-group. At the end of investigation, the rats were killed and water content (WC) and concentration of lactic acid (LA) in the brain tissues were measured. RESULTS: Compared with Group A, WC and LA of Group B increased significantly at each investigation duration (P < 0.05). Compared with Group B, WC and LA of Group C did not change (P > 0.05), but those of Group D, E, and F decreased significantly (P < 0.05). WC and LA of group C were the highest among Group C - F. CONCLUSION: Focal hypothermia with water of 10 degrees C, 20 degrees C, and 25 degrees C but not 0 degrees C has some effect on traumatic brain edema and the temperature at 20 degrees C and 25 degrees C are the better. The mechanism of focal hypothermia may be associated with inhibiting acidosis of lactic acid.

Animals↗

PubMed1999

Mild hypothermia modifies ammonia-induced brain edema in rats after portacaval anastomosis.

BACKGROUND & AIMS: The pathogenesis of brain edema in fulminant hepatic failure is still unresolved. Mild hypothermia (33 degrees-35 degreesC) can ameliorate brain edema after traumatic brain injury. We evaluated mild hypothermia in a model of ammonia-induced brain edema in which accumulation of brain glutamine has been proposed as a key pathogenic factor. METHODS: After portacaval anastomosis, anesthetized rats were infused with ammonium acetate at 33 degrees, 35 degrees, and 37 degreesC or vehicle at 37 degreesC. Water and glutamine levels in the brain, cardiac output, and regional and cerebral hemodynamics were measured when intracranial pressure increased 3-4-fold (ammonia infusion at 37 degrees) and matched times (other groups). RESULTS: Mild hypothermia reduced ammonia-induced brain swelling and increased intracranial pressure. Brain glutamine level was not decreased by hypothermia. Brain edema was accompanied by a specific increase in cerebral blood flow and oxygen consumption, which were normal in both hypothermic groups. When the ammonia infusion was continued in hypothermic rats, plasma ammonia levels continued to increase and brain swelling eventually developed. CONCLUSIONS: Mild hypothermia delays ammonia-induced brain edema. In this model, an increase in cerebral perfusion is required for brain edema to become manifest. Mild hypothermia could be tested for treatment of intracranial hypertension in fulminant hepatic failure.

Acetates↗

PubMed1992

Effect of clonidine on experimental brain edema in the rat.

Several experimental brain edema models are currently available for drug evaluation. Brain edemas are essentially vasogenic and/or cytotoxic, and eicosanoids are involved in the development of these edemas. Thus, a new model developed in our laboratory, which was obtained by phospholipase A2 intracerebral injection was used to study the antiinflammatory effect of clonidine. The copper wire edema model was chosen as reference. Edemas were evaluated by determining the swelling and Na+ and K+ tissue concentrations of each hemisphere. Drugs were administered intraperitoneally. Dexamethasone was the only drug to inhibit copper wire-induced edema, whereas indomethacin and clonidine as well as dexamethasone exhibited marked antiedematous activity in our model. The effect of clonidine, which could be inhibited by prior administration of yohimbine, suggests that central alpha 2-adrenergic stimulation is involved in reducing experimental brain edema.

Animals↗

PubMed2005

Free radicals as triggers of brain edema formation after stroke.

Brain edema is a leading cause of death after stroke. Cytotoxic edema, which is most severe in astrocytes, begins within a few minutes of adenosine triphosphate depletion and reflects the ultimate infarct size. Vasogenic edema is caused by uncontrolled fluid leakage from the blood to the brain parenchyma through a weakened blood-brain barrier (BBB) and contributes to an actual net volume increase of the brain, which often leads to death. Recent research on ischemia-induced injury mechanisms of the microvasculature has led to the disclosure of the mechanisms and cellular pathways leading to BBB breakdown. In addition, the introduction of magnetic resonance imaging to clinical practice has enabled the evaluation of edema severity in stroke patients and differentiation between cytotoxic and vasogenic edema. Free radicals exert their deleterious actions during both cytotoxic and vasogenic edema. They can contribute to BBB disruption directly and can also trigger molecular pathways related to the dysfunction of ion transporters in the cell membrane and those related to increased vascular permeability. The development of effective therapeutic strategies aimed at reducing brain edema based on targeting specific molecular pathways involved may reduce death and disability from stroke.

Blood-Brain Barrier↗

PubMed2004

Effect of ifenprodil, a polyamine site NMDA receptor antagonist, on brain edema formation following asphyxial cardiac arrest in rats.

OBJECTIVE: Brain edema occurs in experimental and clinical cardiac arrest (CA) and is predictive of a poor neurological outcome. N-Methyl--aspartate (NMDA) receptors contribute to brain edema elicited by focal cerebral ischemia/reperfusion (I/R). Ifenprodil, a NMDA receptor antagonist, attenuates brain edema and injury size in rats after focal cerebral I/R. We assessed the hypothesis that ifenprodil reduces CA-elicited brain edema. METHODS: Eighteen male Sprague-Dawley rats were assigned to group 1 (normal control, n=6), group 2 (placebo-treated CA, n=6), or group 3 (ifenprodil-treated CA, n=6). CA was induced by 8 min of asphyxiation and the animals were resuscitated with cardiopulmonary resuscitation (CPR), ventilation, epinephrine (adrenaline), and sodium bicarbonate (NaHCO3). Ifenprodil of 10 mg/kg or a placebo vehicle was given intraperitoneally 5 min before CA. Brain edema was determined by brain wet-to-dry weight ratio at 1 h after resuscitation. RESULTS: There were no differences between groups 2 and 3 in all physiological variables at baseline. Time from asphyxiation to CA was 201.5 +/- 7.5 s in group 2 and 160.7 +/- 10.4 s in group 3 (P<0.001). Resuscitation time was 68.2 +/- 13.3 s in group 2 and 92.8 +/- 18.2 s in group 3 (P<0.05). Ifenprodil decreased mean arterial pressure (MAP) before asphyxiation, from 128 +/- 7 in group 2 to 82 +/- 15 mmHg in group 3 (P<0.001), and negated immediate post-resuscitation hypertension. Brain wet-to-dry weight ratio was 5.64 +/- 0.44 in group 1, 7.34 +/- 0.95 in group 2 (P<0.01 versus group 1), and 5.93 +/- 0.40 in group 3 (P<0.05 versus group 2). CONCLUSIONS: Ifenprodil reduces CA-elicited brain edema. In addition, we observed significant hemodynamic changes caused by ifenprodil.

Animals↗

PubMed1994

Ammonia-induced brain edema and intracranial hypertension in rats after portacaval anastomosis.

Brain edema, leading to intracranial hypertension and brain herniation, is a major cause of death in fulminant liver failure. Astrocyte swelling is a prominent neuropathological feature in experimental fulminant liver failure. It has been postulated that the osmotic effects of glutamine, generated in astrocytes from ammonia and glutamate in a reaction catalyzed by glutamine synthetase, could mediate brain swelling. Normal rats and rats that received a portacaval anastomosis were infused with ammonium acetate or a sodium acetate control; brain water in cerebral cortex was measured with the gravimetry method, intracranial pressure by means of a cisterna magna catheter and cortical amino acids using high-performance liquid chromatography. Although brain edema was detected in both groups receiving ammonia, it was of a greater magnitude in portacaval anastomosis rats (80.94% + 0.17% vs. 80.24% + 0.09%, p < 0.01), resulting in the development of intracranial hypertension. When portacaval anastomosis rats were infused with ammonium acetate and pretreated with 150 mg/kg methionine-sulfoximine, an inhibitor of glutamine synthetase activity, brain edema was ameliorated and intracranial pressure did not rise. A dose-dependent reduction in brain glutamine levels was seen with increasing doses of methionine-sulfoximine; however, brain edema did not decrease beyond the 150 mg/kg dose, suggesting that the increase in brain water was not solely a result of glutamine accumulation. We conclude that brain edema of a magnitude that results in intracranial hypertension is more likely to develop in rats after portacaval anastomosis receiving a continuous ammonia infusion. The osmotic effects of glutamine appear to mediate, but only in part, the increase in brain water seen in this preparation.(ABSTRACT TRUNCATED AT 250 WORDS)

Ammonia↗

PubMed1992

Effect of torasemide on intracranial pressure, mean systemic arterial pressure and cerebral perfusion pressure in experimental brain edema of the rat.

The study was performed to establish whether a lipophilic loop diuretic, torasemide could modify intracranial pressure and cytotoxic brain edema. Brain edema was induced by water intoxication in nephrectomized rats. Following intravenous injection of 100 mg torasemide/kg body weight at 50, 60, 70, 90 and 120 min, a significant decrease of intracranial pressure was observed.

Animals↗

PubMed2003

Effects of ganglioside GM1 on reduction of brain edema and amelioration of cerebral metabolism after traumatic brain injury.

OBJECTIVE: To observe the effects of ganglioside GM1 on reduction of brain edema and amelioration of cerebral metabolism after traumatic brain injury (TBI). METHODS: An acute experimental closed TBI model in rats was induced by a fluid-percussion brain injury model. At five and sixty minutes after TBI, the animals were intraperitoneally injected by ganglioside GM1 (30 mg/kg) or the same volume of saline. At the 6th hour after TBI, effects of ganglioside GM1 or saline on changes of mean arterial pressure (MAP), contents of water, lactic acid (LA) and lipid peroxidation (LPO) in the injured cerebral tissues were observed. RESULTS: After TBI, MAP decreased and contents of water, LA and LPO increased in brain injury group; however, MAP was back to normal levels and contents of water, LA and LPO decreased in ganglioside GM1 treated group, compared with those in brain injury group (P < 0.05). No significant difference between the saline treated group and the brain injury group (P > 0.05) was observed. CONCLUSIONS: Ganglioside GM1 does have obvious neuroprotective effect on early TBI.

Animals↗

PubMed1990

Ischemic brain edema as a complication of decompensated hypovolemic shock.

Four-hour arterial hypotension (decompensated phase) in dogs caused by acute blood loss, when the level of arterial pressure of 40 mmHg was maintained beginning from the 2nd and 3rd h by intra-arterial intermittent blood transfusion is an adequate model for reproducing a moderate ischemic edema of the brain. Pronounced hypoperfusion and considerable disturbances in blood fluidity testified to greater severity of hypoxic and hemorheological disturbances in the microvessles of the brain in decompensated animals than in their compensated counterparts. The formation of a brain edema is based on disturbed fluid circulation closely related to the structural pathology of the organelle membranes of the cells of the nervous and vascular tissues. The pathology of the organelle membranes of the cell elements of the vascular tissue leads to direct diffusion of the liquid through the vessel wall into the brain parenchyma thus disturbing intertissue relations. The pathology of the cell element membranes of the nervous tissue (neurocytes, oligodendrogliocytes and astrocytes) leading to intracellular disturbance of fluid circulation makes its contribution to changes in inter-tissue interactions. Brain hyperhydration was revealed only in animals that had sustained decompensated hypovolemic shock.

Animals↗

PubMed2006

Spontaneous intracerebral hemorrhage in humans: hematoma enlargement, clot lysis, and brain edema.

Early hematoma enlargement and delayed clot lysis contribute to brain injury after intracerebral hemorrhage (ICH). We investigated hematoma growth, clot lysis, and brain edema formation in patients with spontaneous ICH. A total of 17 spontaneous ICH patients who received regular medication were chosen for this study. All patients had their first CT scan within 5 hours of onset of symptoms (day 0). The patients then underwent second, third, and fourth CT scans at 1, 3, and 10 days later. Hematoma size and absolute and relative brain edema volumes were measured. Hematoma enlargement was defined as a > 33% increase in volume. Relative brain edema volume = absolute brain edema volume/hematoma size. Hematoma enlargement occurred in 4 of the 17 ICH patients (24%) within the first 24 hours. The hematoma sizes were reduced significantly at day 10 (p < 0.05) because of clot lysis. However, both absolute and relative brain edema increased gradually with time (p < 0.01). These results suggest that delayed brain edema following ICH may result from hematoma lysis. This study also shows that early hematoma enlargement occurs in Chinese patients with ICH. Reducing early hematoma growth and limiting clot lysis-induced brain toxicity could be potential therapies for ICH.

Brain Edema↗

PubMed1985

Alterations of the eicosanoid synthetic capacity of rat brain microvessels following ischemia: relevance to ischemic brain edema.

To know the mechanism underlying ischemic brain edema, a time-course analysis of the eicosanoid synthetic capacity of brain microvessels was carried out using unilateral, middle cerebral artery (MCA)-occluded rats. Concomitant with the development of brain edema the synthetic capacity of all products, including cyclooxygenase and lipoxygenase products, increased significantly. Next the effects of 15-hydroperoxyarachidonic acid (15-HPAA) on the synthetic capacity of microvessels were examined. The drug caused a generalized increase of each product, the profile of which was similar to that obtained with ischemic hemispheres, although the ratios of each product differed somewhat among them. The enhanced synthesis of eicosanoids by 15-HPAA was markedly suppressed by radical scavengers such as alpha-tocopherol, hydroquinone, and 1,2-bis(nicotineamide)-propane. Furthermore, the evolution of brain edema was virtually suppressed by the systemic administration of 1,2-bis(nicotineamide)-propane. The above result suggests that the enzyme activity of the arachidonic acid (AA) cascade of microvessels is stimulated by its own products. Such a mechanism will form a vicious cycle that accelerates the accumulation of free radicals within microvessels and thus may play a role in the progressing disruption of the blood-brain barrier (BBB) following ischemia.

Animals↗

PubMed1985

[Effect of hyperbaric oxygenation on the course of experimental brain edema].

The authors studied experimental brain edema and morphological changes in the cerebral tissue in 2 groups of animals: the test group receiving hyperbaric oxygenation (HBO) and the control group. The test animals showed a more favourable course of brain injury. Microscopic examination revealed a lesser degree of brain edema and intensification of reparative processes in the cerebral tissues of animals receiving HBO.

Animals↗

PubMed1994

Vascular permeability factor in brain metastases: correlation with vasogenic brain edema and tumor angiogenesis.

Metastatic brain tumors are almost always associated with vasogenic brain edema, which in turn plays a pivotal role in the evolution of neurological morbidity associated with these lesions. Attention has recently focused on a group of proteinaceous vascular permeability factors (VPF's) that are capable of inducing angiogenesis and promoting increased capillary permeability. To test the hypothesis that metastatic brain tumors expressing VPF's are associated with peritumoral cerebral edema, a rabbit polyclonal immunoglobulin (Ig) G anti-VPF was used to immunostain pathological specimens of metastatic cerebral tumors obtained from 22 patients who underwent surgery at Yale-New Haven Hospital. Magnetic resonance (MR) imaging was used to correlate VPF staining in tumor tissue with the occurrence of peritumoral brain edema. A histological study of the microvasculature was then conducted by immunostaining the specimens for endothelial cell factor VIII surface antigen, using two gliosis specimens as controls. Results revealed 21 of 22 tumors stained positively for VPF's; the negative-VPF tumor was a melanoma that exhibited no peritumoral edema. Twenty of 22 tumors had MR imaging-evident vasogenic edema. The presence and intensity of VPF immunostaining of microvascular features were noted and compared. Factor VIII staining demonstrated tumor vascularity to be most abundant in VPF-rich regions of tumor. The authors therefore report a high correlation between the presence of VPF's and the occurrence of peritumoral brain edema associated with cerebral metastases.

Brain Edema↗