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PubMed2001

Cerebral hyperemia and nitric oxide synthase in rats with ammonia-induced brain edema.

BACKGROUND/AIM: Brain edema is a common fatal complication in acute liver failure. It is related to an acute change in brain osmolarity secondary to the glial accumulation of glutamine. Since high cerebral blood flow (CBF) precedes cerebral herniation in fulminant hepatic failure we first determined if an increase in brain water and glutamine are prerequisite to a rise in CBF in a model of ammonia-induced brain edema. Secondly, we determined if such a cerebral hyperperfusion is mediated by nitric oxide synthase (NOS). METHODS: Male rats received an end-to-side portacaval anastomosis (PCA). At 24 h, they were anesthetized with ketamine and infused with ammonium acetate (55 microM/kg per min). Studies were performed at 60, 90, 120, 150 and 180 min after starting the ammonia infusion and once the intracranial pressure had risen three-fold (mean 210'). Brain water (BW) was measured using the gravimetry method and CBF with the radioactive microsphere technique. Glutamine (GLN) in the CSF was sampled via a cisterna magna catheter. The neuronal NOS was specifically inhibited by 1-2-trifluoromethylphenyl imidazole (TRIM, 50 mg/kg intraperitoneally) and in separate studies nonspecifically by N-omega-nitro-L-arginine (L-NNA, 2 microg/kg per min intravenously) RESULTS: At 90', brain water was significantly increased (P < 0.015) as compared to the 60' group while CBF was significantly different at 150'. A significant correlation was observed between values of CBF and brain water (r = 0.88, n = 36, P < 0.001). Administration of either TRIM or L-NNA did not prevent the development of cerebral hyperperfu. sion and edema. CONCLUSION: We observed that cerebral hyperemia follows an initial rise in brain water content, rather than in the cerebrospinal fluid concentration of glutamine. The rise in CBF further correlated with brain water accumulation and was of critical importance for the development of intracranial hypertension. The unique mechanism for the rise in CBF in hyperammonemia was not prevented by NOS inhibition indicating that NO is not the mediator of high CBF and intracranial hypertension.

Ammonia↗
PubMed1984

Submicroscopic changes of cortical capillary pericytes in human perifocal brain edema.

Human brain capillary pericytes were studied by electron microscopy. Cortical biopsies from 17 patients with brain edema associated to brain trauma, tumors and congenital malformations were analysed. The data obtained in this study showed that pericytes like endothelial cells exhibited remarkable edematous changes, increased vacuolar and vesicular transport, formation of transient transpericytal channels and tubular structures, demonstrating pericyte brain barrier dysfunction. Images of normal and contracted pericytes showing shallow and deep nuclear invaginations, nuclear basal lamina, actin and myosin-like filaments and coupled interaction with endothelial cells through macula occludens were also encountered. Some pericytes displayed hypertrophic and necrotic changes. Phagocytic pericytes exhibited ingested erythrocytes. Hypertrophic pericytes inducing basement membrane splitting and degenerated pericytes with lacunar enlargement of endoplasmic reticulum, deposit of dense osmiophilic bodies and glycogen granules, vacuolization, hydropic changes of Golgi apparatus, and pleomorphic mitochondria were also found. Certain micropinocytotic vesicles seem to be orientated to multivesicular bodies suggesting that pericytes might play some role in edema resolution. Evidence of pericyte transformation into microglial cells or division into phagocytic cells and pericyte migration were not found.

Brain↗
PubMed1981

Role of platelets in vasogenic brain edema. II. Contribution of platelet serotonin in brain edema.

In this study of the function of platelets after CNS injury, platelets were treated with serotonin labeled with radioactive carbon (14C) in animals subjected to a freezing lesion of the cerebrum. The distribution of platelet serotonin was measured by counting the specific activity of 14C-labeled serotonin in tissue and by autoradiography. Some of the animals were treated with RA-233, which inhibits the formation of platelet plugs after endothelial damage and the release of serotonin from platelets. Platelet serotonin accumulated near the surface of the cortex at the site of injury in all animals. More cerebral edema developed in animals treated with the platelet inhibitor than in untreated animals, probably because platelet aggregates were inhibited from forming and were not available to plug leaks in the traumatized vessels. Serotonin did not appear to facilitate the spread of edema.

Animals↗
PubMedDate not supplied

Brain edema and the blood brain barrier in galactosamine-induced fulminant hepatic failure rats. An animal model for evaluation of liver support systems.

Rats with galactosamine-induced fulminant hepatic failure (FHF) have been a popular animal model for the evaluation of liver support systems. Because development of brain edema is a major and frequent complication during FHF, it was studied for this report. The degree of hepatocyte necrosis closely paralleled the severity of coma. Abnormalities in the orientation of hepatocellular organelles were evident as early as grade I hepatic coma, 24 hr after galactosamine-induced liver damage. Galactosamine caused a characteristic pattern of hepatocyte necrosis such that the endoplasmic reticulum completely surrounded the nucleus to cause karyolysis and subsequent cell death. Quantitative measurements of brain water content revealed evidence of brain edema with increasing severity of coma. Brain edema resulted in a greater than 4% swelling of the brain during this period. Light microscopy showed increasing cerebral and cerebellar edema during progressive stages of FHF. Electron microscopy studies revealed evidence of progressive cerebral edema, particularly in the perivascular region of cerebral capillaries. Marked swelling of perivascular astrocytes was evident as early as 24 hr after galactosamine-induced FHF when the animals were in Grade I hepatic coma. Abnormal swelling and distortion of astroglia, including its subcellular organelles, and the presence of cytoplasmic vacuoles, was clearly evident during the deeper stages of hepatic coma (Grades II-IV). Trypan blue dye infusion studies revealed evidence of extensive blood-brain barrier (BBB) breakdown beginning in Grade III coma.

Animals↗
PubMed1988

[Ultrastructure of capillary permeability in human brain tumor--Part 6: Metastatic brain tumor with brain edema].

Metastatic brain tumors very often cause severe brain edema. We examined ultrastructural findings of capillaries of these tumors and discussed the causes of cerebral edema as compared with those of glioblastoma which were previously reported. Four specimens were examined: two adenocarcinomas from the lung, one squamous cell carcinoma from the lung and one adenocarcinoma from the breast. These replicas and ultrathin sections were examined by transmission electron microscope. The following characteristic structures were detected; the capillary endothelium was proliferated, had marked infolding, and an increased number of pinocytotic vesicles and vacuoles. Short and elongate intercellular junctions were present. No open junction was detected. The basal lamina lost its three layered appearance and was irregular in width. Among these, an appearance of capillary fenestration was the most conspicuous features and observed in almost all capillaries. Two different pathogenesis for making vasogenic edema are proposed in metastatic brain tumor and glioblastoma. The frequent fenestration of the former and activated pinocytotic vesicles of the latter are responsible for extravasation of the edema fluid. The differences in distribution patterns of fenestration in metastatic brain tumor cannot be identified with respect to histological types.

Adenocarcinoma↗
PubMed1994

Effect of barrier opening on brain edema in human brain tumors.

Blood-brain barrier (BBB) opening was carried out in 10 patients with cerebral lesions, and the MRI findings were evaluated following the barrier opening. An intra-arterial injection of 10% glycerol (4 ml/kg, 1 approximately 2 ml/s) was given as a hyperosmotic solution. T2-weighted MRI was undertaken using a TOSHIBA 22A at 30 minutes after BBB opening. Barrier-opening MRI was performed 10 times in 10 patients, including 5 cases of glioblastoma multiforme, 2 cases of astrocytoma, 1 case of malignant lymphoma, 1 case of cerebral contusion and 1 case of neurinoma. The high-intensity area (HIA) was compared with that in MRI without barrier opening. Three types of changes of HIA in MRI were observed after BBB opening as follows. Type 1: Expansion of the HIA was noted in 4 of 5 cases of glioblastoma multiforme, the 1 case of malignant lymphoma and the 1 case of cerebral contusion. Type 2: Almost no change was observed in the 1 case of neuronoma. Type 3: A decrease in HIA was noted in the 2 cases of astrocytoma and in 1 case of glioblastoma multiforme. The MRI following BBB opening evidently showed 3 types of changes according to the degree of BBB disruption. Glioblastoma multiforme or contusion with a severely disrupted BBB revealed an increase in HIA following barrier opening. Benign posterior fossa neurinoma showed no change in HIA after barrier opening. Moderate malignant tumors exhibited a decrease in HIA on barrier-opening MRI. It was concluded that malignant tumors have a severely damaged BBB, which is readily disrupted by osmotic barrier opening.

Adult↗
PubMed2003

Brain edema -- a new classification.

Brain edema is a reaction to any brain injury and can be the first stage in the beginning of intracranial hypertension. This paper puts forth a modern classification of brain edema types, based on a etiopathogenic interpretation. The hydroelectrolitic and/or proteinic buildup can occur within cells and/or in the extracellular space and differentiates three types of brain edema: cellular brain edema; extracellular brain edema and combined brain edema. Cellular brain edema (cytotoxic brain edema) occurs through intracellular hyperosmolarity or extracellular hypotonicity. Extracellular brain edema (interstitial) appears as a result of the buildup of edema fluid in the extracellular space of the brain parenchyma and can be: hydrostatic extracellular brain edema (through ultrafiltration), oncotical extracellular brain edema (vasogen brain edema) and hydrocephalic extracellular brain edema. Combined brain edema includes in variable ratios both types of brain edema, cellular and extracellular; they can be present together from the beginning or can appear successively.

Animals↗
PubMed2006

Astrocytes co-express aquaporin-1, -4, and vascular endothelial growth factor in brain edema tissue associated with brain contusion.

INTRODUCTION: Brain edema may be life threatening. The mechanisms underlying the development of traumatic brain edema are still unclear; however, mixed mechanisms including vasogenic, ischemic, and neurotoxic types of edema may be contributors. Recent studies indicate that astrocytes, aquaporins (AQPs; a protein family of water channels), and vascular endothelial growth factor (VEGF) may have important roles in the formation and resolution of brain edema. We studied the expression of AQPs and VEGF in the edematous brain. METHODS: We investigated the expression of AQP1, AQP4, and vascular endothelial growth factor (VEGF) in contusional brain tissue surgically obtained from 6 patients. Glial fibrillary acidic protein (GFAP) was also stained to detect astrocytes and to clarify the location of those proteins. The specimens received immunohistological staining and 3-color immunofluorescent staining, and were observed using confocal laser scanning microscopy. RESULTS: AQP1, AQP4, and VEGF were co-expressed in GFAP-positive astrocytes. AQP1 and AQP4 were expressed strongly in astrocytic end-feet. The astrocytes were located in the edematous tissue, and some cells surrounded cerebral capillaries. CONCLUSION: Our results suggest that AQP1, AQP4, and VEGF are induced in astrocytes located in and surrounding edematous tissue. Those astrocytes may regulate the water in- and out-flow in the injured tissue.

Adolescent↗
PubMedDate not supplied

Brain edema and blood-brain barrier permeability following quantitative cerebral microembolism.

Cerebral microemboli were formed in rats by injecting 4,000 carbonized microspheres, 50 +/- 10 mu in diameter, labelled with 85Sr, into the internal carotid artery. The use of radioactive microspheres as embolic agents enabled the number of microspheres to be determined in each cerebral hemisphere. The microspheres were mainly distributed in the cerebral hemisphere on the side of the injection. In 61 rats this hemisphere contained 582 +/- 20 microspheres against 99 +/- 9 in the contralateral hemisphere. Brain edema was assessed by measuring brain content of water, sodium and potassium. Blood-brain barrier (BBB) permeability was determined by brain accumulation of 125I-albumin. In the ipsilateral hemisphere brain edema and an increase in BBB permeability appeared 6 hours after embolization and progressed up to 48 hours. Twenty-four hours after embolization, significant correlations were observed between the microsphere content of the cerebral hemispheres and 1) the increases in water and sodium levels, 2) the decrease in potassium level, 3) the increase in BBB permeability. The study of these correlations should make it possible to ignore the poor reproducibility of embolizations and to analyze with increased accuracy the results of various experiments.

Animals↗
PubMed2006

Effects of chloride flux modulators in an in vitro model of brain edema formation.

Brain edema is a serious consequence of hemispheric stroke and traumatic brain injury and contributes significantly to patient mortality. In the present study, we measured water contents in hippocampal slices as an in vitro model of edema formation. Excitotoxic conditions induced by N-methyl-D-aspartate (NMDA, 300 microM), as well as ischemia induced by oxygen-glucose deprivation (OGD), caused cellular edema formation as indicated by an increase of slice water contents. In the presence of furosemide, an inhibitor of the Na,K,Cl-cotransporter, NMDA-induced edema were reduced by 64% while OGD-induced edema were unaffected. The same observation, i.e., reduction of excitotoxic edema formation but no effect on ischemia-induced edema, was made with chloride transport inhibitors such as DIDS and niflumic acid. Under ischemic conditions, modulation of GABAA receptors by bicuculline, a GABA antagonist, or by diazepam, a GABAergic agonist, did not significantly affect edema formation. Further experiments demonstrated that low chloride conditions prevented NMDA-induced, but not OGD-induced, water influx. Omission of calcium ions had no effect. Our results show that NMDA-induced edema formation is highly dependent on chloride influx as it was prevented by low-chloride conditions and by various compounds that interfere with chloride influx. In contrast, OGD-induced edema observed in brain slices was not affected by modulators of chloride fluxes. The results are discussed with reference to ionic changes occurring during tissue ischemia.

Animals↗
PubMed1994

Brain edema formation after brain injury, shock, and resuscitation: effects of venous and arterial pressure.

BACKGROUND: Recent work suggests that increased intracranial pressure (ICP) following brain injury and shock is related to increased central venous pressure (CVP) following resuscitation. OBJECTIVE: To analyze the relationship of intravascular pressures to edema formation and ICP in an experimental model. METHODS: In a porcine model of cryogenic brain injury and hemorrhagic shock, we studied CVP, mean arterial pressure (MAP), ICP, and cortical water content (CWC, as cortical specific gravity) at baseline (BL), 45 minutes after shock (H45), and 1, 3, 6, 12, and 24 hours (H) after resuscitation. Group 1 was the control group, group 2 brain injury only, group 3 shock only, and group 4 brain injury and shock. RESULTS: Brain injury significantly increased ICP and CWC. Mean arterial pressure significantly correlated with ICP (r = 0.54, p = 0.02) and with CWC (r = -0.48, p = 0.03) in group 4 at 24H but not in the other groups at any time period. There was no significant correlation between CVP and ICP or CWC in any group at any time interval. CONCLUSIONS: These data suggest that brain edema formation in the injured hemisphere is related to MAP and not CVP, but variability in MAP accounts for only 29% of the variability in CWC and ICP, suggesting the importance of factors other than hydrostatic pressure in determining the amount of edema and the ICP after brain injury. Previous work demonstrating the significant correlation of polymorphonuclear leukocyte infiltration with ICP (r = 0.71, p < 0.001) and with CWC (r = -0.63, p < 0.001) suggests that inflammation may be one of these factors.

Animals↗
PubMed1987

[Distribution and constitutional changes of edema fluid in cytotoxic brain edema analyzed by electron microscopy and differential scanning calorimetry].

To understand the pathogenesis of brain edema, we studied distribution and constitutional changes of brain-tissue water by morphological and thermoanalytical methods in cytotoxic brain edema induced by 6-aminonicotinamide (6-ANA). Ninety-two Wistar rats were divided into three groups; Group I rats receiving physiological salt solution intraperitoneally served as controls. Group II and III animals were intraperitoneally given 120 mg/kg and 36 mg/kg of 6-ANA respectively. All animals were starved after injection of drugs to exclude differences in water intake. Then they were decapitated at 3, 6, 12, 24, 36 or 48 hours to measure specific gravity (SG) of large brain tissue (1.1-1.5 g), and to evaluate water content (WC) and free water ratio (FWR) of small brain-tissue samples (15-35 mg) taken from the frontal cortex; WC was measured by a drying-weighing method, and FWR was analyzed with a differential scanning calorimeter. Moreover morphological changes of the frontal cortex of the brain were studied in Group II (n = 12) at 3, 6, 12, 24 and 48 hours with an electron microscope. Neurological status of animals administered 6-ANA (Group II and III) deteriorated with time. Morphological studies showed that perivascular astrocytes and astrocytic processes in the cerebral cortex were swollen most remarkably at 48 hours. However neuronal and endothelial cells were almost intact. The FWR of Group I decreased significantly about four per cent (p less than 0.001) after being starved for 48 hours. But the SG and WC of the group showed little change.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Aminonicotinamide↗
PubMed1984

Relationship between specific gravity, water content, and serum protein extravasation in various types of vasogenic brain edema.

Vasogenic brain edema was induced in cats by cold injury (six animals), brain tumors (five animals), and brain abscesses (six animals). Water and electrolyte content, specific gravity, blood volume, and the amount of extravasated serum proteins were determined in small tissue samples taken from gray and white matter at various distances from the lesion. Edema was strictly confined to the white matter of the affected hemisphere and declined from the lesion to the more peripheral regions. It was characterized by the extravasation of serum proteins and an increase of water and sodium content with little or unpredictable changes of potassium and blood volume. The calculated sodium content of edema fluid varied between 129 and 135 mueq/ml, and serum protein content between 8.1 and 11.9 mg/ml. In all three types of edema, specific gravity and water content correlated closely with the same slope and intercept of the calculated regression (y = 1.119-0.0011 x, r = -0.91). The results obtained indicate that the main denominator of specific gravity of edematous white matter is water content and that this relationship is not significantly altered by variations of blood volume or serum protein content.

Animals↗
PubMed1979

Dynamics of cerebral edema. The role of an intact vascular bed in the production and propagation of vasogenic brain edema.

Brain edema was produced in cats by a standardized cortical freezing lesion. With a careful microsurgical tehnique, the injured cortex was removed as a single piece, either immediately after induction or at 2, 4, or 8 hours after lesion production. The injured brain was either discarded or replaced in its bed. Brain edema and the defect in the blood-brain barrier were assessed by determining percent dry weight, increase in volume of white matter, and spread of Evans' blue by planimetry. The results indicate that 1) if the lesion is removed immediately after production, formation of the expected vasogenic brain edema is completely abolished; 2) replacement of the frozen brain is unable to induce significant increase in permeability of the surrounding blood-brain barrier or a significant amount of brain edema; and 3) if the lesion is removed at 2, 4, or 8 hours with or without replacement, advancement of the edema front and increase in the amount of edema is stopped. It appears that an intact vascular bed is necessary for the extracellular fluid component of brain edema, and that no edemagenic factors exist within the injured brain in this model that influence either the production or propagation of the increased extracellular fluid volume.

Animals↗
PubMed1986

Stimulation of astrocytes affects cytotoxic brain edema.

Cytotoxic brain edema has been produced in rats by subacute intoxication with triethyltin (TET). Some animals were allowed to recover spontaneously, others were post-treated with an extract of Ginkgo biloba (EGB) for 1 to 4 weeks, beginning 3 days after intoxication was stopped. The time course of the resolution of the edema was studied biochemically and morphologically by light microscopy, histochemistry and electron microscopy (EM). Morphometric evaluation showed that the spontaneous reabsorption of TET-induced edema was very slow: it was evident only 2 weeks after ending TET administration and it required more than 4 weeks to be completed. EGB therapy markedly decreased the vacuolation, as well as the abnormal levels of water and sodium contents, 1 week after beginning the treatment. Less influence of EGB was observed at the later stages. During spontaneous recovery, astroglial cells in the edematous white matter of TET-intoxicated animals showed short and swollen processes containing few organelles, low levels of NADH- and NADPH-tetrazolium reductase activities and glial fibrillary acidic protein (GFAP)-immunofluorescence for about 2 weeks. During EGB therapy the astrocytes regained their cellular processes, containing intense oxidative enzyme activities and GFAP-immunofluorescence as early as after 1 week of treatment. In the EM, astrocytes often appeared hypertrophic, surrounding myelin vacuoles and displaying phagocytosis of myelin debris. We conclude that EGB can accelerate the reabsorption of TET-induced cerebral edema and improve the astroglial reaction.

Animals↗
PubMed1982

[Nuclear magnetic resonance (NMR) imaging of brain edema from sliced rat brain: preliminary report].

A series of the sliced rat brain were imaged by proton nuclear magnetic resonance (1H-NMR) using a Carr-Purcell-Meiboom-Gill sequence. The slices were obtained from the adult male Wistar rats, normal or suffering from vasogenic brain edema at 2, 6, 24Hr, 2Wk and 2Mo period after the application of cryo-injury. The imaging time was arranged 17 to 22 minutes dependently upon signal to noise ratio. The slice thickness was 1.2 mm, and pixel dimensions were 0.2 X 0.2 mm. Whereas a voxel size in our images is mere 1/1,200 compared to that reported about the prototype human NMR imaging devices, high resolution has been realized. The spatial resolution is very fine, as evidenced by the appearance of major internal structures of rat brain, and the object contrast is so high that cerebral white-gray contrast is excellent, although the difference in water concentration between them is only 7%. It has been impossible to measure serially in vivo change in water concentration of small organs as rat brain, NMR has the capability to generate images in response to tissue state of hydration, therefore we can easily recognize the extent and intensity of the brain edema, which has been defined as an expansion of the brain volume resulting from an increase in its fluid content. And in this study, using the prototype mini-NMR-CT of excellent spatial and contrast resolution, we have been able to show this advantage of NMR as a new tool for research in the field of neurological surgery.

Animals↗
PubMed1992

The effect of bolus methylprednisolone in prevention of brain edema in hypoxic ischemic brain injury: an experimental study in 7-day-old rat pups.

One of the major mechanisms responsible for tissue injury in hypoxic ischemic brain damage is the formation of free radicals. We studied the efficacy of methylprednisolone, which is claimed to cause rapid congealing of membranes, and to protect the cells against the free radicals present in the environment, in preventing the brain edema that occurs in hypoxic ischemic brain injury. Hypoxic ischemic brain injury to the right hemisphere in 7-day-old rat pups is produced by cauterization of the right common carotid artery followed by hypoxia in 8% oxygen and 92% nitrogen for 3 h. The animals were divided into the groups. One group received methylprednisolone at 30 mg/kg body weight and the other an equal volume of saline 40 min before hypoxia. At 42 h of recovery, some of the rats were killed for measurement of water content in the right and left hemispheres whereas others were killed at 40 days for neuropathological examination. The water content in the right hemisphere was significantly lower in the 19 methylprednisolone-treated pups than it was in 20 saline-treated pups, mean +/- S.E.M. was 83.913 +/- 0.313% and 86.681 +/- 0.377%, respectively. The differences between the means were significant (P less than 0.001) according to the Mann-Whitney U-test. The difference of the mean water contents between the two hemispheres was significantly higher in the saline-treated group (2.695 +/- 0.372%) than it was in the methylprednisolone-treated group (0.432 +/- 0.088%), P less than 0.0001 by independent samples t-test. Neuropathological study was performed on 4 rat pups.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗