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PubMed1994

Protective effect of dipfluzine on experimental brain edema in rats.

The effects of dipfluzine (1-diphenylmethyl-4-(3-(4-fluorobenzoyl))-piperazine, Dip), a new calcium antagonist developed in China, on experimental brain edema in female Wistar rats with bilateral carotid artery ligation were compared with those of cinnarizine (Cin). Dip 25-100 mg.kg-1 i.p. protected the rats against the characteristic signs of global cerebral ischemia that correlate well with the development of brain edema. Its effects were more potent than those of Cin; and the effects of both drugs were more potent by both pretreatment and posttreatment than those by posttreatment alone. Dip 50 mg.kg-1 i.p. attenuated the reduction in cerebral blood flow (CBF) and the infarct size after occlusion, but did not alter CBF before ischemia. These findings suggested that Dip may be potentially useful to treat ischemic brain edema in part by preserving CBF in the ischemic zone.

Animals↗
PubMed1978

Brain edema in immature animals. An experimental study in rats.

Applying several procedures to produce brian edema, the authors examined electron microscopically immature rat brains, and the findings were compared with those in adult rat brains. Using Na-fluorescein and ferritin as tracers, the authors also examined the blood brain barrier (BBB) functionally. It was clarified that immature rat brains showed resistance to the brain edema of the vasogenic type in spite of breakdown of the BBB. On the basis of these results the authors discussed on genesis of brain edema of the vasogenic type.

Age Factors↗
PubMed1978

The spreading of focal brain edema induced by ultraviolet irradiation.

Focal brain edema limited to one cerebral hemisphere was produced by ultraviolet irradiation of the exposed cortex. Tissue water content was determined by the gravimetric method which allows microsampling. Therefore, the spread of edema around the small necrotic area could be mapped more precisely than by determination of dry weight which calls for larger samples. As early as 30 min following irradiation, hyperemia and swelling of the brain are observed under the operating microscope. This correlates with venous stasis, hyperemia, and broadened perivascular spaces around venules and large capillaries accompanied by a marked rise in the specific weight of the tissue. After 4 h an edema front can be observed spreading from the perinecrotic zone in which there is a marked rise in endothelial cell vesicular activity. Edema reaches maximum levels in the deep white matter at 48 h post irradiation with normalisation of the tissue water content after 96 h. The velocity at which the edema front spreads from the cortex to the periventricular area lies in the range of 0.25 mm/hr. Edema reabsorption coincides with signs of retrograde micropinocytosis in endothelial cells.

Animals↗
PubMed1980

The application of immunofluorescent antibody method in research of human brain edema.

The direct and indirect immunofluorescent methods were used to demonstrate the serum proteins in vasogenic brain edema on paraffin embedded formalin fixed human brains with carcinoma metastases. Applying these techniques extravasated albumin was detected within the tumor and in the surrounding neuropil. In the remote part of the peritumorous area the cytoplasma of neurons and astrocytes were stained specifically. The specific immunostaining clearly demonstrates the plasma origin of proteins in human peritumorous edema similarly to the experimental vasogenic brain edema. The immunofluorescent technique seems to be very useful to investigate the human brain edema on necropsy material as well.

Blood Proteins↗
PubMed1990

Effects of fluosol-DA on brain edema, energy metabolites, and tissue oxygen content in acute cerebral ischemia.

Perfluorochemicals were developed as a blood substitute and were reported to have an advantage in oxygen transport compared with blood. The present study was undertaken to investigate the therapeutic effects of a perfluorochemical, FDA, on brain edema and metabolites in acute cerebral ischemia. Cerebral ischemia was induced in SHR by BLCO followed by recirculation. The FDA administration resulted in (a) the significant inhibition of brain edema as shown by brain water content in the treated group, and (b) significant amelioration of metabolic impairments as shown by lesser degree of ATP and pyruvate decrease and lactate accumulation. The TpO2 was compared between FDA-infused and nontreated group during ischemia. The FDA-infused group had significantly higher TpO2 than nontreated group. These results indicate that the improvement of brain edema and metabolite levels were due to alleviation of ischemic hypoxia by FDA under the same ischemic insult.

Animals↗
PubMed2000

Effects of hypothermia on intracranial pressure and brain edema formation: studies in a rat acute subdural hematoma model.

Acute subdural hematoma (SDH) is the most common mass lesion in severe head injury, and brain ischemia is the leading pathophysiological mechanism in the development of secondary brain damage following SDH. Hypothermia has been employed as an effective neuroprotective procedure in clinical and laboratory studies on cerebral ischemic and contusional injuries. In the present study, we used a rat acute SDH model to assess the effect of hypothermia on the intracranial pressure (ICP) and also on the brain edema formation at 4 h after hematoma induction. Mild (34 degrees C) and moderate (32 degrees C) hypothermia did not significantly affect the ICP or cerebral perfusion pressure, but they were associated with a significant lower cortical brain edema formation beneath the hematoma (81.09 +/- 0.49%, p<0.05; and 80.88 +/- 0.17%, p<0.01) when compared with the normothermic control group (81.65 +/- 0.52%). This reduction in brain edema formation was comparable to the results of MK-801 treatment (80.95 +/- 0.35%, p<0.01). The present findings indicate that hypothermia represents a potent neuroprotective strategy. The possible protective mechanisms of hypothermic protection afforded in this rat acute SDH model are discussed.

Animals↗
PubMed1981

[Nuclear magnetic resonance studies on brain edema--time course of 1H-NMR relaxation times (author's transl)].

1. The state of water in normal and edematous brain tissue was studied by measurement of proton longitudinal (T1) and transverse (T2) relaxation times using pulsed nuclear magnetic resonance (NMR) technique. 2. In control rats, T1 and T2 of water showed one component, which was more fast in white matter. Those values displayed 1.07-1.18 sec. of T1 and 75-76 msec. of T2. 3. When rat brain was injured by cold, T1 was observed to become more longer (1.18-1.27 sec.), and T2 was observed to be separated into two components, the faster T2 (45-50 msec.) and slower T2 (100-105 msec.), in body gray and white matter of the injured side. 4. In triethyltin (TET) induced brain edema, elongation of T1 (1.2 sec.) and remarkable separation of T2, faster T2 (75 msec.) and slower T2 (400-450 msec.), were observed in white matter. 5. In both cold and TET induced edema, slower T2 fraction is suggested to be the extracellular space and faster T2 fraction, intracellular. 6. T2 changes precede the water content changes in cold injury, and parallel in TET induced edema. Those changes of relaxation times are reversible. 7. T2 changes of water is more sensitive than the T1 for the detection of production and disappearance of brain edema. 8. These results disclose the dynamic movements of water during the course of brain edema and offered significant information of the clinical application of NMR-CT.

Animals↗
PubMed2000

Time course of trace of diffusion tensor [Trace(D)] and histology in brain edema.

We examined the correlation between changes in the trace of diffusion tensor [Trace(D)], regional water content and tissue ultrastructure relating to cellular (cytotoxic) and vasogenic brain edema. Cellular edema was induced by left middle cerebral artery occlusion in cats (Kuroiwa T et al., 1998). Vasogenic edema was induced in the white matter of cats by a cold lesion (Kuroiwa T et al., 1999). In cellular edema, the water content increase correlated linearly with the Trace(D) decrease in both the gray and white matter. However, both the slopes and intercepts of the correlation lines were significantly different. Hydropic astrocytic swelling was seen in both structures, and in the white matter, oligodendrocytic and myelinated axonal swelling were observed. In vasogenic edema, the increase in Trace(D) showed a significant linear correlation with the increase in tissue water content. Histologically, nerve fibers were dissociated and the extracellular space was markedly enlarged with protein-rich fluid. These result showed that the different slopes and intercepts of the water content--Trace(D) correlation lines for different subtype of brain edema, which reflect different ultrastructural localization of water, should be taken into account when evaluating brain edema using Trace(D) mapping.

Animals↗
PubMed1979

A specific immunofluorescence technique for the demonstration of vasogenic brain edema in paraffin embedded material.

Serum proteins as constituents of vasogenic brain edema were visualized both macroscopically and microscopically applying a double layer immunofluorescence technique to paraffin embedded material derived from three experimental series: peritumorous edema following xeno-transplantation of glioma cells, edema after cerebral embolization with micropheres, and edema after unilateral MCA occlusion. Exclusively cats were used as experimental animals. The staining procedures resulted in selective green fluorescence of vessel contents as well as edema protein, which was demonstrable even macroscopically at times, where edema formation reaches a maximum in each experimental series. Microscopically, serum protein could be traced up to the end of observation time ranging from 1 to 4 weeks, where the specific fluorescence was related to cellular structures. As compared to other techniques employed in brain edema localization, immunostaining mainly offers the following advantages: avoidance of in vivo tracing, better structural resolution in paraffin than in freeze sections, high specificity and sensitivity in antigen localization.

Animals↗
PubMed1986

Brain edema in rabbits with galactosamine-induced fulminant hepatitis. Regional differences and effects on intracranial pressure.

Brain edema and intracranial hypertension are major complications of fulminant hepatic failure. We investigated the development of brain edema and monitored intracranial pressure in rabbits with toxic hepatitis induced by galactosamine. Using a gravimetric technique to assay small tissue samples, we found that brain water was increased in cortical grey matter, but not in subcortical, mesencephalic, and pontine white matter, or in the cerebellum. The proportion of water in cerebral grey matter in control animals was 80.96% +/- 0.49% with significant elevations to 81.96% +/- 0.47% and 82.95% +/- 1.49% in mild and severe encephalopathy, respectively. This corresponds to mean increases in tissue volume of 5.5% and 11.7%. The hippocampal grey matter also accumulated water in severe encephalopathy with a 30% increase in mean tissue volume. The regional increase in brain water was confirmed by the wet-dry weight method. Neither hypotension, hypoxia, nor severe hypoglycemia were present to account for the edema. Intracranial pressure was monitored continuously in unanesthetized rabbits via an intraventricular cannula as encephalopathy developed. The pressure was normal in the mild stage, but was intermittently elevated in animals with severe encephalopathy. The normal range of intracranial pressure was 2-9 mmHg and the range of peak values in galactosamine-treated rabbits was 18-55 mmHg. The regional differences in brain water accumulation suggest that cellular swelling and abnormalities in the movement of water across the blood-brain barrier may account for the brain edema in this model.

Animals↗
PubMed1998

A phase I trial of human corticotropin-releasing factor (hCRF) in patients with peritumoral brain edema.

BACKGROUND: Human corticotropin-releasing factor (hCRF) is an endogenous peptide responsible for the secretion and synthesis of corticosteroids. In animal models of peritumoral brain edema, hCRF has significant anti-edematous action. This effect, which appears to be independent of the release of adrenal steroids, appears mediated by a direct effect on endothelial cells. We conducted a feasibility and phase I study with hCRF given by continuous infusion to patients with brain metastasis. PATIENTS AND METHODS: Peritumoral brain edema documented by MRI and the use of either no steroids or stable steroid doses for more than a week were required. MRIs were repeated at completion of infusion and estimations by dual echo-image sequence (Proton density and T2-weighted images) of the amount of peritumoral edema were performed. The study was performed in two stages. In the feasibility part, patients were randomized to receive either 0.66 or 1 microgram/kg/h of hCRF or placebo over 24 hours. The second part was a dose finding study of hCRF over 72 hours at escalating doses. RESULTS: Seventeen patients were enrolled; only one was receiving steroids (stable doses) at study entrance; dose-limiting toxicity (hypotension) was observed at 4 micrograms/kg/h x 72 hours in two out of four patients, while zero of five patients treated at 2 micrograms/kg/h developed dose-limiting toxicities. Flushing and hot flashes were also observed. Improvement of neurological symptoms and/or exam were seen in 10 patients. Only small changes were detected by MRI. Improvement in symptoms did not correlate with changes in cortisol levels, and changes in cortisol levels were not correlated with changes in peritumoral edema. CONCLUSIONS: hCRF is well tolerated in doses up to 2 micrograms/kg/h by continuous infusion x 72 hours. Hypotension limits administration of higher doses. The observation of clinical benefit in the absence of corticosteroids suggests hCRF may be an alternative to steroids for the treatment of patients with peritumoral brain edema. Further exploration of this agent in efficacy studies is warranted.

Adrenal Glands↗
PubMed1999

Treatment of brain edema with a nonpeptide arginine vasopressin V1 receptor antagonist OPC-21268 in rats.

OBJECTIVE: Recent experimental evidence suggests that centrally released arginine vasopressin plays a significant role in brain capillary water permeability as well as in pathogenesis of vasogenic brain edema. The purpose of this study was to examine the effects of orally administered OPC-21268, a nonpeptide arginine vasopressin V1 receptor antagonist, on cold-induced brain edema in rats. METHODS: Cold brain injury was induced for 1 minute in 140 rats. Treatment with OPC-21268, at dosages of 100 mg (n = 20), 200 mg (n = 20), and 300 mg/kg (n = 15), or with saline (n = 17) was started 1 hour after the induction of cold injury and was continued every 8 hours for 24 hours. Two percent Evans blue in saline (1 ml/kg) was administered intravenously before cold injury in another group of rats, 15 of which were saline-treated and 55 of which were OPC-21268-treated at the above dosages. After 24 hours, brain tissue water and electrolytes, brain tissue swelling, blood-brain barrier permeability to Evans blue, and plasma electrolytes and osmolality were determined. RESULTS: Compared with the saline-treated group, OPC-21268 treatment at the dosages of 200 and 300 mg/kg significantly reduced brain water content in both hemispheres (P<0.01). Swelling of the traumatized hemispheres was also significantly reduced at 200 and 300 mg/kg dosages (P<0.05). Brain tissue sodium content was significantly reduced at the dosage of 300 mg/kg (P<0.05). Blood-brain barrier permeability to Evans blue was significantly decreased in a dose-dependent manner compared with the saline-treated group (P<0.01). No significant changes were observed in other parameters. CONCLUSION: Our results indicate that OPC-21268 predominantly exerts a protective effect in areas where the maximum amount of blood-brain barrier breakdown occurs, and it is effective in the treatment of cold-induced vasogenic brain edema.

Administration, Oral↗
PubMed2003

[Heat shock protein 70 induction by heat stress suppress interleukin-1beta and tumor necrosis factor-alpha levels in the brain tissue in rats with infectious brain edema].

OBJECTIVE: To investigate the changes of interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha) in the brain tissue of rats with infectious brain edema (IBE) and their relationship with heat shock protein 70 (HSP70) by heat stress response (HSR). METHODS: Seventy-two SD rats were randomly divided into normal controls group (NS group), IBE group, and HSP group, each group was divided into three subgroups. The rats in subgroups were killed at 4 hours, 8 hours and 24 hours after the injections of IBE or normal saline respectively. HSP70 in brain tissues were determined by western blot analysis. The concentrations of IL-1beta and TNF-alpha in the brain homogenate of rats were determined by enzyme linked immunoadsorbent assay (ELISA). RESULTS: The results showed that HSP70 in brain tissues were elevated after heat shock. IBE group and NS group at 4 hours, 8 hours, 24 hours were induced to base levels of HSP70. The concentrations of TNF-alpha were significantly elevated in IBE group than in NS group at the various time points (P<0.01 or P<0.05), especially at 8 hours. The concentrations of IL-1beta were significantly increased in IBE group compared with NS group at 4 hours, 8 hours. HSR reduced the IL-1beta and TNF-alpha concentrations in the brain tissue in compared with IBE group (P<0.05 or P<0.01). CONCLUSION: IL-1beta and TNF-alpha are involved in infectious brain edema by IBE. HSP70 against infectious brain edema in rats may be associated with the reduction of IL-1beta and TNF-alpha in brain tissue.

Animals↗
PubMed1998

Regional cerebral blood flow in peritumoral brain edema during dexamethasone treatment: a xenon-enhanced computed tomographic study.

OBJECTIVE: Regional cerebral flood flow (rCBF) in peritumoral brain edema is assumed to be decreased because of increased interstitial pressure. Impaired blood flow might lead to local hypoxia, altered metabolism, and disturbed ion homeostasis, thus causing neurological sequelae. Steroid treatment is thought to positively influence the sequelae of brain edema. We aimed to determine the rCBF in peritumoral edema in humans receiving dexamethasone treatment and the relationship of rCBF to global CBF. METHODS: We measured rCBF in 11 patients with untreated anaplastic gliomas or glioblastomas that were World Health Organization Grade III or IV restricted to one hemisphere with significant peritumoral edema who were receiving a standard dose of dexamethasone. rCBF was determined using stable xenon-enhanced computed tomography in a stereotactic frame. Edema was defined both by means of actual histology (stereotactic biopsies) and by imaging criteria. RESULTS: rCBF in peritumoral edema was decreased by 32% as compared with contralateral normal white matter. In each patient, this reduction was linearly related to blood flow in nonaffected white matter and cortex. The flow ratio in the different compartments was 1 (edema):1.5 (contralateral white matter):2.7 (contralateral cortex). Absolute perfusion values in contralateral cortex (means +/- standard deviations) (29.9+/-7.1 ml/100 g/min) and contralateral white matter (16.1+/-3.7 ml/100 g/min) were significantly decreased as well. CONCLUSION: Our study demonstrated that rCBF in peritumoral brain edema during steroid treatment is still decreased and is in a range in which it may cause neurological sequelae. Also, global CBF was decreased in all patients.

Adult↗
PubMed2002

Delayed onset of brain edema and mislocalization of aquaporin-4 in dystrophin-null transgenic mice.

Cerebral water accumulation was studied during induction of brain edema in dystrophin-null transgenic mice (mdx-betageo) and control mice. Immunofluorescence and immunoelectron microscopic analyses of dystrophin-null brains revealed a dramatic reduction of AQP4 (aquaporin-4) in astroglial end-feet surrounding capillaries (blood-brain barrier) and at the glia limitans (cerebrospinal fluid-brain interface). The AQP4 protein is mislocalized, because immunoblotting showed that the total AQP4 protein abundance was unaltered. Brain edema was induced by i.p. injection of distilled water and 8-deamino-arginine vasopressin. Changes in cerebral water compartments were assessed by diffusion-weighted MRI with determination of the apparent diffusion coefficient (ADC). In dystrophin-null mice and control mice, ADC gradually decreased by 5-6% from baseline levels during the first 35 min, indicating the initial phase of intracellular water accumulation is similar in the two groups. At this point, the control mice sustained an abrupt, rapid decline in ADC to 58% +/- 2.2% of the baseline at 52.5 min, and all of the animals were dead by 56 min. After a consistent delay, the dystrophin-null mice sustained a similar decline in ADC to 55% +/- 3.4% at 66.5 min, when all of the mice were dead. These results demonstrate that dystrophin is necessary for polarized distribution of AQP4 protein in brain where facilitated movements of water occur across the blood-brain barrier and cerebrospinal fluid-brain interface. Moreover, these results predict that interference with the subcellular localization of AQP4 may have therapeutic potential for delaying the onset of impending brain edema.

Animals↗
PubMed2004

Reduced brain edema and matrix metalloproteinase (MMP) expression by pre-reperfusion infusion into ischemic territory in rat.

The aim in this study was to investigate whether our experimental model for stroke therapy, flushing the ischemic territory with saline prior to reperfusion, could ameliorate disruption of microvascular integrity by reducing matrix metalloproteinase (MMP) expression during reperfusion. Stroke in Sprague Dawley rats (n = 42) was induced by a 2-h right middle cerebral artery (MCA) occlusion using a novel intraluminal hollow filament. Prior to reperfusion, 24 of the ischemic rats received 6ml isotonic saline at 37 degrees C infused into the ischemic area through the filament. Brain edema was determined by comparing the percentage difference in brain volume between the right and left (contralateral to stroke site) hemispheres, while the expressions of MMP-2 and -9 mRNA were analyzed by real-time reverse transcriptase-polymerase chain reaction (real-time RT-PCR). A significant (p < 0.01) brain edema, determined by an increased brain volume of 19 +/- 4%, and overexpression of the mRNA encoding MMPs, determined by increased relative mRNA level ratio, were found in ischemic rats. The brain damage, in terms of brain edema (4 +/- 1%) and overexpression of MMPs, was significantly (p < 0.05) ameliorated as a result of saline flushing into the ischemic territory prior to reperfusion. This study has enhanced our understanding of the causal mechanisms by which the neuroprotective effect of ischemic area "flushing" can be achieved.

Animals↗
PubMed1984

The kallikrein-kinin system as mediator in vasogenic brain edema. Part 2: Studies on kinin formation in focal and perifocal brain tissue.

Vasogenic edema was induced in mongrel cats by cold injury to study uptake and activation of the plasma-kallikrein-kinin system in central nervous system (CNS) tissue. A method was developed for quantitative assessment of kinin formation in affected brain tissue areas. Gross disruption of the blood-brain barrier by focal trauma causes marked penetration of plasma kininogens into necrotic and edematous brain tissue. Moreover, the kallikrein-kinin (KK) system was activated in both necrotic and perifocal edematous areas, and was markedly enhanced by additional cerebral ischemia. Formation of kinins in necrotic brain tissue led to consumption of approximately 60% to 80% of the amount of kininogens being taken up. In perifocal edematous tissue, formation of kinins was less pronounced, or even absent. However, if cerebral ischemia evolved after severe intracranial hypertension, kinins were also formed in the perifocal edematous brain. The intravascular origin of kininogens found in pathological tissue areas secondary to injury was deduced from the observation that cerebral tissue of the contralateral hemisphere with an intact blood-brain barrier had no measurable quantities of kininogens. Consumption of plasma kininogens or formation of kinins were assessed as the difference of the total amount of plasma kininogens taken up into the tissue minus the amount of kininogens found in the brain at postmortem examination. The data indicate that uptake and activation of the plasma-KK system might occur under all pathological conditions in which blood-brain barrier damage permits cerebral penetration of plasma proteins, such as with cerebral contusion, focal ischemia, and tumors. The potent pathophysiological mechanisms induced by kinins in CNS tissue, such as formation of brain edema, microcirculatory dysfunction, and enhancement of blood-brain barrier permeability, together with their formation in focal and perifocal pathological brain tissue, provide further support for a mediator function of the KK system. Methods that specifically interfere with the formation of kinins in damaged brain should therefore be expected to attenuate vasogenic edema.

Animals↗
PubMed1983

[Influence of alpha-methyl-prednisolone on perifocal brain edema--CT observations in ten patients with circumscribed supratentorial brain tumours].

Under treatment of peritumoural brain oedema with 6-methyl-prednisolone, in most cases there are no significant density changes to be seen on the CT although there is undoubted clinical improvement. In order to get data for an optimal timing of pre-operative treatment with steroids we had to prove the effect of 6-methyl-prednisolone (Urbason, Hoechst) with intermittent measurements of the so-called CT "Region of interest" in always the same parts of the perifocal brain oedema for seven days pre-operatively. This study was carried out in ten patients with solitary supratentorial brain tumours. CT measurements on the first day without medication, continued with an initial dosage of 1000 mg Urbason, followed by 3 X 40 mg daily during the second to the fifth day, and finally on the seventh day after the steroid was stopped. In all cases we found increasing attenuation coefficients due to decreasing oedema with a peak on the fourth and fifth days.

Adult↗