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PubMed2006

TIMP-1/MMP-9 imbalance in brain edema in rats with fulminant hepatic failure.

BACKGROUND: Fulminant hepatic failure (FHF) is a devastating disease. When coma sets in, brain edema develops, changing FHF into a lethal condition. Liver transplantation is the definitive treatment. However, a third of these patients die as the result of brain edema before a donor becomes available. Tissue inhibitor of matrix metalloproteinase (MMP), or TIMP, and MMP-9 are implicated in ischemic brain edema. We thus hypothesized that an imbalance in TIMP-1/MMP-9 relationship plays a role in the development of increased brain extravasation and edema in FHF. MATERIALS AND METHODS: FHF was induced with a single intraperitoneal injection of D-galactosamine (250 mg/kg). Control rats received saline. GM6001, a synthetic MMP inhibitor, was administered (30 mg/kg) every 12 h for 3 doses starting at 12 h after D-galactosamine injection. MMP-9 was assayed with standard gelatin zymography. Brain extravasation, a measurement of the blood-brain barrier permeability, was determined with Evans blue. Brain edema was determined using specific gravity method. RESULTS: The active MMP-9 in the systemic circulation was significantly increased in the comatose FHF as compared to the precoma FHF and control animals (6.5 +/- 0.7 versus 4.6 +/- 0.4 versus 2.6 +/- 0.5 pg/microg, respectively; P < 0.05). Conversely, TIMP-1 was steadily decreased in precoma and coma FHF rats by 35% and 45%, respectively. Blocking MMP-9 activity with GM6001 significantly attenuated brain extravasation and edema in rats with FHF. CONCLUSIONS: Our study strongly supports that the perturbation of decreased TIMP-1 and increased MMP-9 contributes to the pathogenesis of brain edema in FHF. Our findings present a potential therapeutic approach to effectively increase the window of opportunity for life-saving liver transplantation.

Animals↗
PubMed2004

Aquaporin-4 facilitates reabsorption of excess fluid in vasogenic brain edema.

Aquaporin-4 (AQP4) is the major water channel in the brain, expressed predominantly in astroglial cell membranes. Initial studies in AQP4-deficient mice showed reduced cellular brain edema following water intoxication and ischemic stroke. We hypothesized that AQP4 deletion would have the opposite effect (increased brain swelling) in vasogenic (noncellular) edema because of impaired removal of excess brain water through glial limitans and ependymal barriers. In support of this hypothesis, we found higher intracranial pressure (ICP, 52+/-6 vs. 26+/-3 cm H2O) and brain water content (81.2+/-0.1 vs. 80.4+/-0.1%) in AQP4-deficient mice after continuous intraparenchymal fluid infusion. In a freeze-injury model of vasogenic brain edema, AQP4-deficient mice had remarkably worse clinical outcome, higher ICP (22+/-4 vs. 9+/-1 cm H2O), and greater brain water content (80.9+/-0.1 vs. 79.4+/-0.1%). In a brain tumor edema model involving stereotactic implantation of melanoma cells, tumor growth was comparable in wild-type and AQP4-deficient mice. However, AQP4-deficient mice had higher ICP (39+/-4 vs. 19+/-5 cm H2O at seven days postimplantation) and corresponding accelerated neurological deterioration. Thus, AQP4-mediated transcellular water movement is crucial for fluid clearance in vasogenic brain edema, suggesting AQP4 activation and/or up-regulation as a novel therapeutic option in vasogenic brain edema.

Animals↗
PubMed1985

[The pathomechanism underlying ischemic brain edema: the role of Na+, K+-ATPase of the brain microvessels].

In the present study, the anti-edema effect of AVS [1,2-bis (nicotineamide)-propane] was evaluated using the cat MCA occlusion model with or without recirculation. In the prolonged ischemia (PI) group, cortical edema as assessed by the changes in specific gravity, developed in those cortical areas where the mean 1-CBF was less than 25-30 ml/100 g/min during MCA occlusion (4 hours). In the recirculation group (2 hours' ischemia followed by 2 hours' recirculation: RC group), the ischemic threshold for edema development was almost the same as in the PI group. In both groups, the drop in cortical specific gravity was significantly suppressed by AVS. Regarding the time-course of 1-CBF, there was no difference between the PI-AVS-treated and PI-saline-treated groups. In the RC group, however, the postischemic hypoperfusion was significantly ameliorated by AVS. Based on the present and previous data showing the antiedema effect of AVS, the mechanism of action of AVS was discussed in relation to the pathomechanism underlying ischemic brain edema. Our new concept of ischemic brain edema is briefly stated below. Related in vitro studies have shown the followings: (i) the influx of sodium not of proteins is the principal cause of ischemic brain edema: (ii) the eicosanoid synthetic capacity of the brain microvessel (MV) is increased simultaneous to edema development (iii) an elevation in the level of hydroperoxides enhances the activities of Na+, K+-ATPase as well as the arachidonate cascade of MV. These data suggest that free fatty acids and free radicals liberated following cerebral ischemia stimulate the activity of the MV-Na+, K+-ATPase, which results in increased sodium influx across the BBB. AVS was shown to scavenge hydroxyl radicals and to inhibit the stimulatory effects of a lipid hydroperoxide (15-HPAA) on the activities of Na+, K+-ATPase and the arachidonate cascade of the MV. These actions of AVS may be linked to its antiedema effect.

Animals↗
PubMed1978

Therapy of ischemic brain edema.

With corticosteroids and diuretics, glycerol treatment may be an effective therapy of early edema accompanying focal brain ischemia. The suggested regimen for intravenous infusion is 500 ml of 10% glycerol solution during at least 2 h, twice a day, starting as soon as possible after stroke onset and continuing thereafter for 5--7 days.

Brain Edema↗
PubMedDate not supplied

[Effect of phenothiazine derivatives on the development of experimental traumatic brain edema].

The effect of levomepromazin, propazin, diprazin and dyphenhydramine on the development of traumatic edema of the brain has been studied. Phenothiazine derivatives with an unbranched dialkylaminoalkyl side chain at the nitrogen atom (propazin) have been found to produce the most remarkable antiedematic action. The drugs that have a branched dialkylaminoalkyl chain (levomepromazin, diprazin) do not return brain water content to normal.

Animals↗
PubMed1982

[Nuclear magnetic resonance studies of effects of glycerol on brain edema].

Effects of glycerol on the state of water in edematous brain tissues were studied by the pulse FT NMR technique. Brain edemas were induced experimentally by cold injury and triethyl tin (TET) intoxication in Wistar rats. Ten percent w/v glycerol (1 g/kg body weight) were injected intravenously at 30 minutes before decapitation for the NMR measurements. Transverse relaxation times (T2) in the cerebral gray and white matter were measured by Meiboom-Gill pulse sequence at the resonant frequency of 100 MHz. Water content was calculated from the difference between wet and dry weight after heating in an oven at 95-100 degrees C for 72 hours after the NMR measurements. In the normal brain T2 value was 76.4 msec and 75.4 msec in the gray and white matter respectively. In the edematous brain, T2 separated into two components, one slow and one fast, corresponding with the increase of water content. Values of the slow component (slow T2) were characteristic of both types of brain edema. In the cold injury edema, slow T2 values became 105 msec in the gray matter and 96 msec in the white matter, while in the TET induced edema, it became 450 msec in the white matter. After glycerol infusion, slow T2 became faster in these regions in both types of brain edema, showing 92.1 msec in the gray matter and 88.1 msec in the white matter of the cold injury edema, and 388 msec in the white matter of TET induced edema. The degree of the changes of slow T2 values per unit change of water content was greater in the cold injury edema than in the TET induced edema. Serum osmolality elevated 23.8 mOsmol greater than the control value after glycerol infusion in this experiment. It is concluded from these findings that glycerol retracts free mobile water molecules from the edema fluid by osmotic pressure gradient.

Animals↗
PubMed1987

[The effects of hyperglycemia on ischemic brain edema].

The effects of hyperglycemia on ischemic brain edema in rats were studied by measuring the local changes in water content of brain and cerebrovascular permeability using a transient middle cerebral artery (MCA) occlusion model. Rats, fasted except for water for 12-16 hours, were used. They were anesthetized with halothane and the stem of the left MCA was occluded for 2 hours by a microclip. Reperfusion was performed by removal of the clip. The rats were allowed to awake from anesthesia after removal of the clip. Hyperglycemia was induced by intraperitoneal injection of 50% glucose and same volume of physiological saline was injected intraperitoneally 20 minutes before MCA occlusion in control rats. Cerebrovascular permeability was measured by quantitative autoradiography using 14C-alpha-amino-isobutyric acid (14C-AIB) 2 hours after reperfusion. The specific gravity of cerebral tissue, determined by the gradient column with bromobenzene and kerosene, was used to study local changes in brain water content 2 hours after MCA occlusion and 2 hours after reperfusion. In hyperglycemic rats, plasma glucose content-ration rose to over 500 mg/dl at the peak and then declined. A hyperglycemic state around 300 mg/dl was maintained during the experiments. Elevation of hematocrit and plasma osmolarity were observed in hyperglycemic rats. At 2 hours after MCA occlusion, specific gravity of the brain was decreased in the left MCA territory, especially in the frontal cortex, in both groups. The decrease in the frontal cortex in hyperglycemic rats was statistically significant compared with that in the control rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2004

Noninvasive quantification of brain edema and the space-occupying effect in rat stroke models using magnetic resonance imaging.

BACKGROUND AND PURPOSE: Brain edema is a life-threatening consequence of stroke and leads to an extension of the affected tissue. The space-occupying effect due to brain edema can be quantified in rat stroke models with the use of MRI. The present study was performed to test 2 hypotheses: (1) Can quantification of the space-occupying effect due to brain edema serve as a noninvasive measure for brain water content? (2) Does morphometric assessment of brain swelling allow determination of true infarct size on MRI after correction for the space-occupying effect of edema? METHODS: Thirty rats were subjected to permanent suture middle cerebral artery occlusion. MRI was performed after 6 or 24 hours, and hemispheric swelling was assessed morphometrically. Interobserver and intraobserver agreements were determined for MRI measurements. In study I, the space-occupying effect due to brain edema was correlated with the absolute brain water content by the wet/dry method. In study II, lesion volumes corrected and uncorrected for edema were calculated on MRI and on TTC staining and compared. RESULTS: Interobserver and intraobserver agreements for MRI measurements were excellent (r>or=0.97). Brain water content and hemispheric swelling correlated well after 6 and 24 hours (r>or=0.95). Corrected lesion volumes correlated with r=0.78 between TTC staining and MRI. Without edema correction, lesion volumes were overestimated by 20.3% after 6 hours and by 29.6% after 24 hours of ischemia. CONCLUSIONS: Morphometric assessment of hemispheric swelling on MRI can determine the increase in absolute brain water content noninvasively and can also provide ischemic lesion volumes corrected for brain edema.

Animals↗
PubMedDate not supplied

Experimental brain infarcts in cats. II. Ischemic brain edema.

In cats, the early development of ischemic brain edema was studied 1 to 4 hours after transorbital occlusion of the left middle cerebral artery (MCA). Two groups of animals were compared: those in which blood flow in the territory of the MCA decreased below the threshold of 10--15 ml/100 g/min (critical ischemia) and those in which it remained above this level (non-critical ischemia). In animals with critical ischemia, water content in the cortex of the MCA territory increased from 80.7 +/- 0.4 to 83.0 +/- 0.3 vol. % (means +/- SE) within 4 h. Edema was associated with an increase in tissue osmolality by 16--22 mosm/kg w.w., and a rise of sodium from 262 +/- 9 to 454 +/- 13 meq/kg d.w. and a decrease of potassium from 442 +/- 20 to 305 +/- 32 meq/kg d.w. The sodium/potassium ratio rose from 0.60 +/- 0.03 to 1.55 +/- 0.17. The water and electrolyte disturbances were accompanied by a major shift of extracellular fluid into the intracellular compartment, as evidenced by the increase in cortical impedance from 282 to 660 ohm/cm within 2 h. According to the Maxwell equation, this reflects a narrowing of the extracellular space from 19.8 to 11.4%. Brain volume was continuously monitored using an induction transducer; swelling began within a few minutes of vascular occlusion, and it continued throughout the 4 h observation period. During this time the blood-brain barrier remained intact as evidenced by the absence of Evans blue staining. Edema was associated with disturbances of the energy producing metabolism, but there was no strict correlation with either lactate or the concentration of high energy phosphates. In animals without critical ischemia, i.e. in which blood flow remained above 10--15 ml/100 g/min, edema was absent despite a distinct deterioration of the energy state of the brain. Edema was also absent in the border zone, in the territory of the posterior cerebral artery and in the contralateral hemisphere of animals with both critical and non-critical ischemia. It is concluded that the early ischemic brain edema following middle cerebral artery occlusion is of the cytotoxic type, that it develops at a flow rate below 10--15 ml/100 g/min, and that it is not strictly correlated with the energy state of the brain.

Animals↗
PubMed2003

Vasopressin accelerates experimental ammonia-induced brain edema in rats after portacaval anastomosis.

BACKGROUND/AIMS: Cerebral hyperemia is an important contributor to the development of brain edema in fulminant hepatic failure. Rats receiving an ammonia infusion after portacaval anastomosis (PCA) demonstrate a rise in cerebral blood flow (CBF) with brain edema at 180 min. Vasopressin (VP), a systemic vasoconstrictor which in the rat dilates cerebral vessels through V(2) receptors, was used to ascertain the effects of increasing CBF. METHODS: Changes in CBF were measured with Laser Doppler flowmetry (LDF). Absolute CBF was measured with radioactive microspheres to calculate oxygen and ammonia uptake. RESULTS: Compared to the NH(3)+Vehicle group, VP+NH(3) infusion accelerated the rise in CBF (117+/-21 vs. -6+/-12%, P<0.01), and the development of brain edema (81.09+/-0.17 vs. 80.29+/-0.06%, P<0.01). Radioactive microspheres confirmed these results (254+/-44 vs. 106+/-9.5 ml/min/100 g, P<0.01). Oxygen uptake was similar. Ammonia uptake was more than twofold higher in the VP+NH(3) group. A V(1) antagonist negated the higher mean arterial pressure (MAP) that occurs with VP but cerebral hyperemia still occurred. A V(2) antagonist resulted in similar systemic pressures, CBF and brain water compared to the VP+NH(3) group. CONCLUSIONS: In this model, an increase in CBF with VP hastens the development of brain edema while increasing ammonia delivery to the brain.

Ammonia↗
PubMed2004

Aquaporins and brain edema.

Aquaporins are a family of transmembrane proteins that selectively allow the passage of water through the plasma membrane. Their importance is highlighted by their ubiquitous presence from bacteria to mammals. In humans, they are found throughout the body and recent work has highlighted their function within the brain. They are intimately involved in the production of cerebrospinal fluid and the control of water movement at the blood-brain barrier. Aquaporin levels are up-regulated in animal models of trauma, stroke and water intoxication as well as around human malignant brain tumors. They have thus been implicated in the formation of brain edema. Knockout mice, without the aquaporin gene, appear to have reduced brain edema compared to their wild type brethren in models of brain edema. Currently, the clinical treatment of brain edema is limited. Increased knowledge of the aquaporins may open new targeted therapies for brain edema.

Aquaporin 4↗
PubMed2000

[Protective effects of baicalin, mannitol and dexamethasone on infective brain edema in rats].

OBJECTIVE: To compare the therapeutic effects of baicalin, mannitol and dexamethasone on infective brain edema(IBE) in rats. METHODS: Forty normal Sprague-Dawley(SD) rats (200 +/- 30) g by weight were divided into 5 groups randomly: (1) normal saline control group(NS, n = 8); (2) infective brain edema group (BE, n = 8); (3) mannitol treatment group(MAN, n = 8); (4) dexamethasone treatment group(DXM, n = 8); and (5) baicalin treatment group(BC, n = 8). Pertussis bacilli(PB, contained bacilli in 10.8 x 10(9), 0.2 ml-1.kg-1) were injected into the left carotid arteries through the left common carotid arteries by puncture to obtain BE models. The contents of brain water, sodium ion, potassium ion and Evans blue in brain tissues were observed too. RESULTS: The contents of brain water, sodium ion, and EB in BE group were higher than those in BE group(P < 0.01), they decreased in MAN, DXM, BC groups and were lower than those in BE group(P < 0.01). In MAN, DXM, BC groups, there were no significant difference in the contents of brain water and sodium ion(P > 0.05). The EB content in BC group was higher than that in MAN and DXM groups(P < 0.01). The content of potassium ion in BE group was higher than that in MAN and DXM groups, the content of potassium ion was similar to that in NS group, but lower than that in BC group. Light microscope inspection in MAN, DXM and BC groups showed lessened brain edema, slight increase of perivascular space, and occasional nerve cell pyknotic nucleus. We found on nerve cell vacuolar degeneration in DXM group. CONCLUSION: Baicalin, mannitol and dexamethasone all have similar protective effects on infective brain edema in rats.

Animals↗
PubMed2005

Intraventricular albumin: an optional agent in experimental post-traumatic brain edema.

HYPOTHESIS: Human albumin may be effective in the treatment of posttraumatic brain edema due to its hyperoncotic features. Therefore, the aim of the experimental study presented in this paper has two points: the first is to evaluate the efficacy of intraventricular hyperoncotic human albumin on post-traumatic brain edema and the second is to try to show the appropriate posttraumatic time window for albumin administration. METHOD: Traumatic brain injury and subsequent edema was formed by a model of impact acceleration injury in rats. Human albumin was administered via intraventricular route by using a stereotactic head holder. All animals in each group were decapitated 24 hours after the procedure and the effect of albumin was evaluated by measurement of tissue specific gravity. RESULTS: Tissue specific gravity decreased in edematous tissue (trauma indicator), increased after albumin administration at the 12th (p < 0.001), and both at the 1st and 12th hour of the trauma (edema treatment; p < 0.001). On the other hand, albumin administered at the 12th, and at both the 1st and 12th hours in the rats without trauma has caused the formation of the brain edema. CONCLUSION: We conclude that human albumin is effective in cytotoxic, but not in vasogenic edema and exerts its best anti-edematous effect at the 12th hour of severe head trauma and this study may help future studies that will try to show the effects of albumin with different time modalities after severe head injury.

Analysis of Variance↗
PubMed2002

Effects of brain hypothermia on brain edema formation after intracerebral hemorrhage in rats.

Patients with intracerebral hemorrhage (ICH) may deteriorate progressively after the initial ictus because of the brain edema around the hematoma. Recently, thrombin has become known to play an important role in the brain edema formation after ICH. In this study, we examined the effect of brain hypothermia on brain edema formation after hematoma and thrombin injection into the brain in rats and clarified the mechanism of hypothermia on brain damage. Anesthetized Sprague-Dawley rats received an injection of 100 microL of autologous blood or 10 units of bovine thrombin into the basal ganglia. Animals were divided into the normothermic and hypothermic groups, which were housed in a room at 25 degrees C and in a cold room at 5 degrees C respectively, for 24 hours. Brain water content was significantly reduced with hypothermia in the cortex (80.8 vs. 79.7% p < 0.05) after hematoma induction. After thrombin injection, brain water content was also significantly reduced with hypothermia in the basal ganglia (84.5 vs. 82.2%; p < 0.01), accompanied by a significant reduction in blood-brain barrier (BBB) permeability to Evan's blue (29.4 vs. 11.6 ng/g tissue; p < 0.05) and in accumulation of polymorphonuclear leukocytes (3.03 vs. 0.27 U of myeloperoxidase/g tissue; p < 0.01). This study indicates that brain hypothermia significantly reduces brain edema formation after hematoma and thrombin injection into the brain in rats. Inhibition of thrombin-induced BBB breakdown and inflammatory response with hypothermia appear to contribute to brain protection in this model.

Animals↗
PubMed1988

Treatment of tyramine-induced brain edema with anion transport inhibitor L-644,711.

Tyramine induces coma in phenelzine-treated dogs. Development of coma in these animals is associated with brain edema, abnormal brain scans of Tc-99m-diethylene-triamine-penta-acetic acid (Tc-99m-DTPA), and elevated levels of CSF catecholamines. We found that the intravenous administration of 6-7 mg/kg of a single dose of L-644,711 given fifteen minutes after the oral administration of tyramine to phenelzine-pretreated animals followed by an infusion of normal saline containing 6-7 mg/kg of the drug given over a period of 2 hr caused reversal of brain injury. This was accompanied by full recovery within a period of 24 hr of all the animals tested. A follow-up study revealed that 24 hr after treatment with L-644,711 CSF levels of catecholamines and brain images of Tc-99m-DTPA were indistinguishable from normal controls. Animals that received no drug died from unresolved coma within 4 to 24 hr. Animals that had recovered due to therapy with L-644,711 were given 10-14 days rest followed by a repetition of the phenelzine and tyramine treatment but denied L-644,711 therapy. These animals also died of unresolved coma within 24 hr. This preliminary study suggest that the use of L-644,711 may constitute an important advance in treatment of brain edema of a wide range of neurological disorders.

Animals↗
PubMed2003

Matrix metalloproteinases are not involved in early brain edema formation after cardiac arrest in rats.

INTRODUCTION: Resuscitation from cardiac arrest (CA) often results in a poor neurological outcome possibly due to an incomplete understanding of the pathophysiology of brain injury following CA-induced global cerebral ischemia. Brain edema is an important manifestation after CA and is associated with significant morbidity and mortality. The matrix metalloproteinases (MMPs) contribute to brain edema formation following focal cerebral ischemia. The objective of this study was to investigate the role of an MMP inhibitor, GM6001, in CA-elicited brain edema. METHODS: Eighteen rats were subjected to normothermic (37.5 +/- 0.5 degrees C) CA induced by eight minutes of asphyxiation and assigned to a CA-control group (CA), an alcohol-placebo group (CA + ETOH), or a GM6001-treated group (CA + GM6001). GM6001 in 100% alcohol or a vehicle was given i.v. before CA to achieve a whole blood concentration of 10 microM. Animals were resuscitated with CPR, ventilation and epinephrine. Brain edema was determined by brain wet-to-dry weight ratio at one hour after resuscitation. FINDINGS: Brain wet-to-dry weight ratio was 4.86 +/- 0.09 in CA, 4.76 +/- 0.12 in CA + ETOH (p = 0.30 vs. CA), and 4.72 +/- 0.03 in CA + GM6001 (p = 0.17 vs. CA and 0.42 vs. CA + ETOH). INTERPRETATION: MMPs are not involved in brain edema formation one hour following CA.

Animals↗
PubMed1990

Some mechanisms of brain edema studied in a kainic acid model.

Kainic acid (KA) is a potent neuroexcitatory drug widely used in the experimental study of seizure activity. Subcutaneous injection of KA into rats (10 mg/kg in saline 10 mg/ml; pH 7.0) induced longlasting status epilepticus followed by damage of CNS tissue in the entorhinal/pyriform cortex and in the hippocampus. The studies covered by this report demonstrated the formation of cytotoxic brain edema characterized by massive swelling of perineuronal and perivascular astroglia with microcirculation disturbance after KA injection, resulting in parenchymal necrosis of the affected region; furthermore perivenous hemorrhages and necroses corresponding to herniation lesions of the brain appear. Tracer studies with Na-fluorescein, Evans blue, albumin, and horseradish peroxidase revealed only a mild increase in the permeability of cerebral vessels, topographically unrelated to areas of brain edema. Treatment of brain edema with dexamethasone did not influence the incidence and severity of edematous brain damage. Treatment with mannitol, however, completely prevented the lesion in 54% of animals injected with KA. The present results indicate that brain edema plays an important role in the pathogenesis of epileptic brain damage following systemic KA intoxication. It is suggested that in this model brain edema develops due to massive ionic imbalance caused by KA induced persistent neuronal excitation. In addition the model demonstrates the possible pathogenetic role of selective astrocytic swelling in the production of local hippocampal ischemia followed by herniation and its sequels. Such pathology originating from astrocytes probably may occur also in closed brain injury.

Animals↗
PubMed1992

Cytotoxic brain edema: assessment with diffusion-weighted MR imaging.

To determine whether cytotoxic brain edema is associated with a decrease in diffusion, it was induced in rats, in the absence of ischemia, with an established model of acute hyponatremic encephalopathy. Cytotoxic brain edema secondary to acute hyponatremia was induced with intraperitoneal injections of 2.5% dextrose in water and subcutaneous injection of arginine-vasopressin. Coronal spin-echo magnetic resonance (MR) images were obtained with and without strong diffusion-sensitizing gradients before and after induction of acute hyponatremia. The apparent diffusion coefficient (ADC) was measured at two coronal section locations. In hyponatremic rats, the brain ADC was significantly reduced (P = .0153 and .0001) and was positively correlated with increased total brain water content (P = .0011). Plots of ADC versus total brain water showed a statistically significant inverse linear relationship between ADC and increasing brain water at the anterior coronal section location. The results indicate that the ADC may be a sensitive indicator of cytotoxic brain edema and thus may enable quantitative evaluation of such edema with diffusion-weighted MR imaging.

Animals↗