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

1979 ◽  
Vol 50 (3) ◽  
pp. 361-367 ◽  
Author(s):  
Kazuo Yamada ◽  
Alfonso M. Bremer ◽  
Charles R. West
Keyword(s):  
White Matter ◽  
Brain Edema ◽  
Macaca Mulatta ◽  
Clinical Signs ◽  
Treated Group ◽  
Dexamethasone Treatment ◽  
Tissue Water ◽  
Content Type ◽  
High Concentrations ◽  
The Brain

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

Composition of isolated edema fluid in cold-induced brain edema

1979 ◽  
Vol 51 (1) ◽  
pp. 70-77 ◽  
Author(s):  
Jurjen Gazendam ◽  
K. Gwan Go ◽  
Annie K. van Zanten
Keyword(s):  
Cerebrospinal Fluid ◽  
White Matter ◽  
Brain Edema ◽  
Vasogenic Edema ◽  
Colloid Osmotic Pressure ◽  
Freezing Damage ◽  
Content Type ◽  
Edema Fluid ◽  
The Brain ◽  
Fine Print

✓ Edema fluid isolated from cats with cold-induced brain edema was subjected to analysis of electrolyte content, enzyme activities, colloid osmotic pressure and the radioactivity of intravenously injected 99mTc-labeled albumin. The findings corroborate the essential features of vasogenic edema, such as its origin from the blood plasma, its rapid propagation into the white matter of the brain as contrasted with the delayed spread into gray matter, and its contribution to composition of cerebrospinal fluid. Moreover, the elevated activities of cellular enzymes and K+ content of edema fluid point to the admixture with cellular contents due to the freezing damage.

A simple gravimetric technique for measurement of cerebral edema

1978 ◽  
Vol 49 (4) ◽  
pp. 530-537 ◽  
Author(s):  
Anthony Marmarou ◽  
Werner Poll ◽  
Kenneth Shulman ◽  
Hemmige Bhagavan
Keyword(s):  
White Matter ◽  
Specific Gravity ◽  
Brain Edema ◽  
Cerebral Edema ◽  
Tissue Water ◽  
Simple Method ◽  
Content Type ◽  
Adult Cats ◽  
Automated Technique ◽  
Fine Print

✓ A simple method was developed for the laboratory preparation of gradient columns of specific gravity used in measurement of brain-tissue water. By this automated technique, virtually linear and repeatable density gradients were obtained from which values of tissue specific gravity could be determined. The specific gravity of both solid and fresh cortex and white matter from adult cats was measured and converted to units of percent water per gram tissue using conversion factors derived for this purpose and applicable to studies of brain edema.

Correlations between the apparent diffusion coefficient, water content, and ultrastructure after induction of vasogenic brain edema in cats

1999 ◽  
Vol 90 (3) ◽  
pp. 499-503 ◽  
Author(s):  
Toshihiko Kuroiwa ◽  
Tsukasa Nagaoka ◽  
Masato Ueki ◽  
Ichiro Yamada ◽  
Naoyuki Miyasaka ◽  
...  
Keyword(s):  
White Matter ◽  
Water Content ◽  
Brain Edema ◽  
Nerve Fibers ◽  
Tissue Water ◽  
Content Type ◽  
Deep White Matter ◽  
Vasogenic Brain Edema ◽  
Apparent Diffusion ◽  
Fine Print

Object. The authors examined the correlation between changes in the apparent diffusion coefficient, regional water content, and tissue ultrastructure after vasogenic brain edema.Methods. Vasogenic edema was induced in the white matter of six cats by cortical cold lesioning. The trace of diffusion tensor (Trace[D]) obtained from magnetic resonance imaging to measure the orientationally averaged water diffusibility was compared with the corresponding tissue water content determined by gravimetric studies and with ultrastructural water localization. Edema fluid had spread to the subcortical and deep white matter by 4.5 hours postlesioning. The increase in Trace(D) showed a significant linear correlation with the increase in tissue water content, both in the subcortical and deep white matter as follows: y = 45.5x − 2367 (r = 0.94) and y = 37.0x − 1769 (r = 0.93), respectively, where x is the water content (gram water/gram tissue) and y the Trace(D) (× 10−6 mm2/second). On histological examination, nerve fibers were found to be dissociated in the white matter and the extracellular space was markedly enlarged with protein-rich fluid. No noticeable hydropic swelling of the cellular components was observed.Conclusions. A linear correlation was observed between increases in Trace(D) and increases in extracellular water volume in in vivo vasogenic brain edema. A similar correlation between the subcortical and deep white matter showing different arrangements of nerve fibers (parallel compared with intermingled, respectively) indicated that measurement of Trace(D) is a suitable parameter for the evaluation of vasogenic brain edema.

Experimental delayed radiation necrosis of the brain

1979 ◽  
Vol 51 (5) ◽  
pp. 587-596 ◽  
Author(s):  
Albert N. Martins ◽  
Ralph E. Severance ◽  
James M. Henry ◽  
Thomas F. Doyle
Keyword(s):  
Rhesus Monkeys ◽  
Radiation Necrosis ◽  
Clinical Signs ◽  
Control Group ◽  
Content Type ◽  
Brain Irradiation ◽  
Primate Brain ◽  
High Doses ◽  
The Brain ◽  
Male Rhesus

✓ The authors have designed an experiment to detect a hitherto unrecognized interaction between high doses of the glucocorticoid, dexamethasone, and brain irradiation. Eighteen juvenile male rhesus monkeys received 1800 rads to the whole brain in 8.5 minutes. For 1½ days before and 10½ days after the irradiation, nine animals received approximately 2.9 mg/kg/day of dexamethasone intramuscularly in addition to irradiation, while the remaining nine animals served as the control group and received saline. All animals eventually developed a progressive neurological syndrome, and died of delayed radiation necrosis of the brain. The two groups were compared with regard to latency to onset of clinical signs, survival time, and number, distribution, and location of lesions of radionecrosis. Large doses of dexamethasone did not alter the susceptibility of the primate brain to delayed radiation necrosis. Detailed morphological study of the radionecrotic lesions supports the hypothesis that most, if not all, of the lesions develop as the consequence of injury to blood vessels.

Complement activation in the brain after experimental intracerebral hemorrhage

2000 ◽  
Vol 92 (6) ◽  
pp. 1016-1022 ◽  
Author(s):  
Ya Hua ◽  
Guohua Xi ◽  
Richard F. Keep ◽  
Julian T. Hoff
Keyword(s):  
Brain Edema ◽  
Complement Activation ◽  
Autologous Blood ◽  
Complement Cascade ◽  
Edema Formation ◽  
Content Type ◽  
Erythrocyte Lysis ◽  
The Brain ◽  
Brain Edema Formation ◽  
Fine Print

Object. Brain edema formation following intracerebral hemorrhage (ICH) appears to be partly related to erythrocyte lysis and hemoglobin release. Erythrocyte lysis may be mediated by the complement cascade, which then triggers parenchymal injury. In this study the authors examine whether the complement cascade is activated after ICH and whether inhibition of complement attenuates brain edema around the hematoma.Methods. This study was divided into three parts. In the first part, 100 µl of autologous blood was infused into the rats' right basal ganglia, and the animals were killed at 24 and 72 hours after intracerebral infusion. Their brains were tested for complement factors C9, C3d, and clusterin (a naturally occurring complement inhibitor) by using immunohistochemical analysis. In the second part of the study, the rats were killed at 24 or 72 hours after injection of 100 µl of blood. The C9 and clusterin proteins were quantitated using Western blot analysis. In the third part, the rats received either 100 µl of blood or 100 µl of blood plus 10 µg of N-acetylheparin (a complement activation inhibitor). Then they were killed 24 or 72 hours later for measurement of brain water and ion contents. It was demonstrated on Western blot analysis that there had been a sixfold increase in C9 around the hematoma 24 hours after the infusion of 100 µl of autologous blood. Marked perihematomal C9 immunoreactivity was detected at 72 hours. Clusterin also increased after ICH and was expressed in neurons 72 hours later. The addition of N-acetylheparin significantly reduced brain edema formation in the ipsilateral basal ganglia at 24 hours (78.5 ± 0.5% compared with 81.6 ± 0.8% in control animals, p < 0.001) and at 72 hours (80.9 ± 2.2% compared with 83.6 ± 0.9% in control animals, p < 0.05) after ICH.Conclusions. It was found that ICH causes complement activation in the brain. Activation of complement and the formation of membrane attack complex contributes to brain edema formation after ICH. Blocking the complement cascade could be an important step in the therapy for ICH.

The kallikrein-kinin system as mediator in vasogenic brain edema

1986 ◽  
Vol 64 (2) ◽  
pp. 269-276 ◽  
Author(s):  
Andreas Unterberg ◽  
Claudia Dautermann ◽  
Alexander Baethmann ◽  
Werner Müller-Esterl
Keyword(s):  
Brain Edema ◽  
Vasogenic Edema ◽  
Specific Inhibition ◽  
Kinin System ◽  
Content Type ◽  
Cold Lesion ◽  
Highly Active ◽  
Mediator Role ◽  
Kallikrein Kinin System ◽  
The Brain

✓ Evidence has previously been provided that administration of kinins to the cerebrum causes edema and opening of the blood-brain barrier. It has further been shown that these highly active compounds are formed in the brain under pathophysiological conditions. Their formation was enhanced when cerebral blood flow became compromised by an increase in intracranial pressure. Final evidence, however, was not available as to whether specific inhibition of the kallikrein-kinin (KK) system has a therapeutic function in acute head injury. The authors have demonstrated in rabbits that inhibition of the activating enzyme kallikrein by aprotinin or by aprotinin plus soybean trypsin inhibitor (SBTI), which interfere with plasma and tissue kallikrein, is associated with a decrease in formation of posttraumatic swelling after a standardized cold lesion to the brain. Saline-treated control animals with cerebral cold-induced injury had an increase in hemispheric weight 24 hours later of 13.0% ± 0.8% (standard error of the mean) in the damaged hemisphere compared to the contralateral nondamaged hemisphere. Administration of aprotinin or aprotinin plus SBTI led to a significant reduction of hemispheric swelling of 10.1% ± 0.7% or 10.4% ± 0.7%, respectively. In animals receiving SBTI only, hemispheric swelling evolving from cold injury was not significantly reduced. Therapeutic reduction of brain edema by aprotinin cannot be attributed to a nonspecific effect on the blood pressure, which in the experimental groups remained almost normal as compared to the control animals. Failure of SBTI to influence posttraumatic brain swelling may have resulted from disturbances in intravascular coagulation. Measurements of aprotinin in plasma and tissue demonstrate that the inhibitor doses employed are within an effective therapeutic range. Attenuation of brain edema by specific inhibition of the KK system provides evidence for a mediator role of kinins in vasogenic edema. Clinical trials with inhibitors of the KK system in acute forms of traumatic lesions associated with vasogenic edema appear worthwhile.

scholarly journals Glutamine synthetase expression in the brain during experimental acute liver failure (immunohistochemical study)

2021 ◽  
Vol 11 (10) ◽  
pp. 342-356
Author(s):  
T. Shulyatnikova ◽  
V. Tumanskiy
Keyword(s):  
White Matter ◽  
Glutamine Synthetase ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Caudate Nucleus ◽  
Immunohistochemical Study ◽  
Clinical Signs ◽  
Brain Regions ◽  
Progressive Increase ◽  
The Brain

The aim of the study was to determine the immunohistochemical level of glutamine synthetase (GS) expression in different brain regions in the conditions of experimental acute liver failure in rats. Materials and methods. The study was conducted in Wistar rats: 5 sham (control) animals and 10 rats with acetaminophen induced liver failure model (AILF). The immunohistochemical study of GS expression in the sensorimotor cortex, white matter, hippocampus, thalamus, caudate nucleus/putamen was carried out in the period of 12-24 h after acetaminophen treatment. Results. Beginning from the 6th hour after acetaminophen treatment all AILF-animals showed the progressive increase in clinical signs of acute brain disfunction finished in 6 rats by comatose state up to 24 h - they constituted subgroup AILF-B, “non-survived”. 4 animals survived until the 24 h - subgroup AILF-A, “survived”. In the AILF-B group, starting from 16 to 24 hours after treatment, a significant (relative to control) regionally-specific dynamic increase in the level of GS expression was observed in the brain: in the cortex – by 307.33 %, in the thalamus – by 249.47%, in the hippocampus – by 245.53%, in the subcortical white matter – by 126.08%, from 12th hour – in the caudate nucleus/putamen, by 191.66 %; with the most substantive elevation of GS expression in the cortex: by 4.07 times. Conclusion. Starting from the 16th hours after the acetaminophen treatment (from the 12th h in the caudate nucleus/putamen region) and up to 24 h, it is observed reliable compared to control dynamic increase in GS protein expression in the cortex, white matter, hippocampus, thalamus, caudate nucleus/putamen of the rat brain with the most significant elevation in the cortex among other regions. The heterogeneity in the degree of GS expression rising in different brain regions potentially may indicate regions more permeable for ammonia and/or other systemic toxic factors as well as heterogeneous sensitivity of brain regions to deleterious agents in conditions of AILF. Subsequently, revealed diversity in the GS expression reflects the specificity of reactive response of local astroglia in the condition of AILF-encephalopathy during specific time-period. The dynamic increase in the GS expression associated with impairment of animal state, indicates involvement of increased GS levels in the mechanisms of experimental acute hepatic encephalopathy.

scholarly journals Butin attenuates brain edema in a rat model of intracerebral hemorrhage by anti inflammatory pathway

2018 ◽  
Vol 9 (1) ◽  
pp. 7-12 ◽  
Author(s):  
Peiyu Li ◽  
Cheng Jiwu
Keyword(s):  
Intracerebral Hemorrhage ◽  
Brain Edema ◽  
Treated Group ◽  
Control Group ◽  
Lesion Volume ◽  
Dependent Manner ◽  
Neurological Score ◽  
Factor Α ◽  
The Brain ◽  
Brain Tissues

Abstract Background This study evaluates the effect of butin against brain edema in intracerebral hemorrhage (ICH). Methodology ICH was induced by injecting bacterial collagenase in the brain and all the animals were separated into four groups such as control group, ICH group treated with vehicle, Butin 25 and 50 mg/kg group receives butin (25 and 50 mg/kg, i.p.)60 min after the induction of ICH in all animals. One day after neurological score, hemorrhagic injury and expressions of protein responsible for apoptosis and inflammatory cytokines were assessed in the brain tissue of ICH rats. Result Neurological scoring significantly increased and hemorrhagic lesion volume decreased in butin treated group of rats compared to ICH group. However, treatment with butin significantly decreases the ratio of Bax/Bcl-2 and protein expression of Cleaved caspase-3 than ICH group in dose dependent manner. Level of inflammatory mediators such as tumor necrosis factor-α (TNF-α) and interlukin-6 (IL-6) in the brain tissues were significantly decreased in the butin treated group than ICH group. In addition butin attenuates the altered signaling pathway of NF-κB in the brain tissues of ICH rats. Conclusion Our study concludes that butin attenuates the altered behavior and neuronal condition in ICH rats by reducing apoptosis and inflammatory response.

Evaluation of periventricular hypodensity in experimental hydrocephalus by metrizamide CT ventriculography

1982 ◽  
Vol 56 (2) ◽  
pp. 235-240 ◽  
Author(s):  
Hideo Hiratsuka ◽  
Hitoshi Tabata ◽  
Shin Tsuruoka ◽  
Masaru Aoyagi ◽  
Kodai Okada ◽  
...  
Keyword(s):  
White Matter ◽  
Specific Gravity ◽  
Iodine Concentration ◽  
Periventricular White Matter ◽  
Hounsfield Units ◽  
Content Type ◽  
Experimental Hydrocephalus ◽  
Enhanced Ct ◽  
Kaolin Injection ◽  
The Brain

✓ Hydrocephalus was induced in 13 dogs by injecting kaolin into the cisterna magna and was evaluated by computerized tomography (CT) scans. Modification of periventricular hypodensity was observed by metrizamide-enhanced CT ventriculography. Periventricular hypodensity was seen as early as 12 hours after kaolin injection. On CT ventriculography, metrizamide stayed longer in the ventricles of hydrocephalic dogs than in those of normal dogs, and migrated into the areas of periventricular hypodensity; the changes became significant within 12 to 24 hours. Four of the dogs were killed immediately after CT ventriculography, and the iodine concentration was measured. Iodine concentration was highest in the periventricular white matter, followed by the basal ganglia, and it was low in the cerebral and cerebellar cortex. When the change in Hounsfield units found by CT ventriculography at the regions of interest was compared to the actual iodine concentrations, the figures were quite compatible. Similarly, the specific gravity was measured in tissue from various parts of the brain of two hydrocephalic dogs, and compared against the value of that from five normal dogs. The specific gravity values were particularly low in the periventricular white matter of the hydrocephalic brains, suggesting a higher water content in that region. Since the increased migration of metrizamide occurred at the same region, it is suggested that development of periventricular hypodensity is due to increased transit of cerebrospinal fluid from the ventricles to the white matter.

Contribution of edema and cerebral blood volume to traumatic brain swelling in head-injured patients

2000 ◽  
Vol 93 (2) ◽  
pp. 183-193 ◽  
Author(s):  
Anthony Marmarou ◽  
Panos P. Fatouros ◽  
Pal Barzó ◽  
Gennarina Portella ◽  
Masaaki Yoshihara ◽  
...  
Keyword(s):  
Brain Edema ◽  
Brain Tissue ◽  
Blood Volume ◽  
Cerebral Blood Volume ◽  
Brain Swelling ◽  
Tissue Water ◽  
Content Type ◽  
Head Injured ◽  
Injured Patients ◽  
Fine Print

Object. The pathogenesis of traumatic brain swelling remains unclear. The generally held view is that brain swelling is caused primarily by vascular engorgement and that edema plays a relatively minor role in the swelling process. The goal of this study was to examine the roles of cerebral blood volume (CBV) and edema in traumatic brain swelling.Methods. Both brain-tissue water and CBV were measured in 76 head-injured patients, and the relative contribution of edema and blood to total brain swelling was determined. Comparable measures of brain-tissue water were obtained in 30 healthy volunteers and CBV in seven volunteers. Brain edema was measured using magnetic resonance imaging, implementing a new technique for accurate measurement of total tissue water. Measurements of CBV in a subgroup of 31 head-injured patients were based on consecutive measures of cerebral blood flow (CBF) obtained using stable xenon and calculation of mean transit time by dynamic computerized tomography scanning after a rapid bolus injection of iodinated contrast material. The mean (± standard deviation) percentage of swelling due to water was 9.37 ± 8.7%, whereas that due to blood was −0.8 ± 1.32%.Conclusions. The results of this study showed that brain edema is the major fluid component contributing to traumatic brain swelling. Moreover, CBV is reduced in proportion to CBF reduction following severe brain injury.

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