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PubMed2003

Thrombin preconditioning upregulates transferrin and transferrin receptor and reduces brain edema induced by lysed red blood cells.

Pretreatment with a low dose of thrombin reduces brain edema after both hemorrhagic and ischemic stroke. We call this phenomenon thrombin preconditioning (TPC) or thrombin-induced brain tolerance. The present study examines whether TPC can attenuate the brain edema induced by lysed red blood cells (RBCs) to determine whether thrombin production early in an intracerebral hemorrhage (ICH) might alter potentially injurious events associated with clot resolution. It also examines whether TPC might be protective by altering iron handling within the brain, particularly through modulating transferrin (Tf) and transferrin receptor (TfR) levels. Brain edema was measured by wet/dry weight. Western blot analysis and immunohistochemistry were used for Tf and TfR measurements. We found that TPC reduces lysed RBC-induced brain edema and upregulates both Tf and TfR levels in the brain. Thrombin formation after an ICH may be part of a signaling cascade that acts to limit potentially injurious events associated with clot resolution through altering iron-handling proteins.

Animals↗
PubMed1994

Sequential change of brain edema by semiquantitative measurement on MRI in patients with hypertensive intracerebral hemorrhage.

The progression of brain edema in seven patients with hypertensive intracerebral hemorrhage (ICH) was evaluated. Five were of putaminal and two were of thalamic hemorrhage. The hematoma volume in the patients was 4 approximately 40 ml (18.9 +/- 8.0 ml). Sequential MRI (SE: 2000/40) was performed at one, two and four weeks after onset. The edema volume (EV) was calculated as 1/2.(long diameter).(short diameter).(thickness) of the high intensity area (HIA) on MRI. In comparison with the EV at one week after onset, the EV at two weeks was increased and the EV at four weeks returned to the same level of that at one week (132.3 +/- 26.1%, 100 +/- 10.6%, respectively). In contrast, the consciousness level and motor weakness of the patients had already improved at two weeks after onset. Our results demonstrate that progression of brain edema after small or medium size ICH may not bring about a deterioration of the clinical course. Moreover, progression of brain edema to the cerebral cortex and ventricle as indicated by MRI suggested an absorption pathway for the edema fluid, and implying that brain edema following ICH could play a part in the healing process after ICH.

Aged↗
PubMed1989

Effect of a superoxide dismutase derivative on cold-induced brain edema.

Although the involvement of reactive oxygen species has been suggested in the pathogenesis of brain edema, direct evidence supporting this concept is lacking. To elucidate a critical role of oxygen radicals, effect of a superoxide dismutase (SOD) derivative that circulated bound to albumin with a half-life of 6 h on the occurrence of cold-induced brain edema was studied in the rat. When animals were challenged with brain injury by applying a liquid-nitrogen-cold probe to one side of the cerebral hemisphere over the bony skull for 20 s, the vascular permeability of the underlying tissue increased significantly and unilateral brain edema occurred as determined by the accumulation of intravenously injected Evan's blue and the increase in brain weight. Intravenous administration of the SOD derivative markedly suppressed the increase in vascular permeability and the occurrence of brain edema, particularly at their early stages. These and other results suggest that superoxide anion and/or its metabolite(s) might play a critical role in the pathogenesis of traumatic brain injury.

Animals↗
PubMed2005

The pathophysiology of brain edema in acute liver failure.

Brain edema leading to intracranial hypertension is a cause of death in acute liver failure (ALF). The pathogenesis of this unique complication has been investigated in man, in experimental models and in isolated cell systems. From this experience, an integrated view has emerged, pointing at several mechanisms that contribute to cerebral swelling; an osmotic derangement in astrocytes, changes in cellular metabolism as well as alterations of cerebral blood flow. The ability of mild hypothermia to counteract each of these changes in experimental systems has supported the organization of a clinical trial of mild cooling in this disease. Such an advance can be viewed as the clinical translation of 20 years of research in this area.

Animals↗
PubMed1994

Severe brain edema associated with cumulative effects of hyponatremic encephalopathy and ischemic hypoxia.

Hyponatremia in cats produced brain edema, detectable by both magnetic resonance imaging (MRI) and increased brain water, with a compensatory decrease of brain sodium. Sodium transport was measured in synaptosomes from hyponatremic cat cerebral cortex. The sodium efflux via Na(+)-K(+)-ATPase was significantly higher (144%) than control, while sodium influx via the Na+/H+ antiporter was significantly decreased (74%). Both responses tend to decrease brain intracellular sodium and thus, brain cell osmolality. Ischemia following unilateral middle cerebral artery occlusion also resulted in brain edema. However, the efflux of sodium via both Na(+)-K(+)-ATPase and sodium channels actually decreased, both maladaptive responses. Furthermore, when ischemia was superimposed upon hyponatremia, all of the cerebral adaptive changes which had been induced by hyponatremia alone were rendered ineffective. This resulted in further elevations of brain water and sodium. Hyponatremia superimposed upon ischemia thus worsens the brain edema associated with ischemia alone. Thus, ischemia impairs the ability of the brain to adapt to hyponatremia, probably by eliminating the compensatory mechanisms of brain sodium transport initiated by hyponatremia.

Animals↗
PubMed1993

Local cerebral blood flow and glucose metabolism in hydrostatic brain edema.

This study investigated the effect of hydrostatic pressure gradient on the cerebrovascular dynamics and metabolism during the development of brain edema. Hydrostatic brain edema was induced by bolus injection of autologous blood through the common carotid artery in Sprague-Dawley rats. Rats were divided into two groups, with craniectomy (Cr+ group) and without (Cr- group). Animals were sacrificed 0, 24, and 48 hours after hypertensive insult. Brain water content was determined by the gravimetric method. Regional cerebral blood flow and local cerebral glucose utilization were measured by the quantitative autoradiographic method using [14C]iodoantipyrine and [14C]deoxyglucose, respectively. Hypertensive insult produced multifocal lesions stained by Evans blue. Brains from the Cr- group showed a transient increase in water content and no significant change in cerebrovascular dynamics and metabolism. Brains from the Cr+ group showed a pronounced increase in water content which persisted 48 hours later. Misery perfusion was also observed 24 hours after the insult and the cerebrovascular dynamics and metabolism were significantly decreased after 48 hours. These results indicate that an increased hydrostatic pressure gradient enhances tissue damage and causes reopening of the blood-brain barrier.

Animals↗
PubMedDate not supplied

Ischemic brain edema: comparative effects of barbiturates and hypothermia.

The effect of pentobarbital and hypothermia on the development of ischemic brain edema was studied in 23 rhesus monkeys undergoing transorbital middle cerebral artery occlusion. Fifteen additional animals served as unclipped controls. Regional cortical cerebral blood flow (rCBF), arteriovenous oxygen content difference (AVDO2), and regional cortical metabolic rate of O2 (rCMRO2) were measured hourly until sacrifie 11 hours postocclusion, at which time ischemic cerebral edema was measured. In 8 animals no treatment followed the occlusion, and these developed edema. In 7 animals pentobarbial 14 mg/kg was administered intravenously 30 min after occlusion and 7 mg/kg every 2 hours thereafter. In this group ischemic brain edema was negligible. In 8 animals, hypothermia to 25.9 +/- 0.5 degrees C was started 30 min after occlusion and maintained until sacrifice; ischemic brain edema was not significantly altered from untreated-clipped animals. On the basis that both pentobarbital and hypothermia produced similar changes in rCBF, AVDO2, and rCMRO2, but only pentobarbital prevented edema, it is postulated that the mode of action of barbiturates in preventing ischemic brain edema is not entirely related to their known effect on blood flow and metabolism.

Animals↗
PubMedDate not supplied

Influence of various agents on the development of brain edema in the rat following microembolism. Protective effect of gamma-butyrolactone.

Brain edema was induced in rats by injecting 50 mu microspheres, 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. Edema was assessed 12 or 24 h after embolization by measuring brain water content and, in some experiments, sodium and potassium. Pretreatments with dexamethasone, parachlorophenylalanine (an inhibitor of 5-hydroxytryptamine synthesis), mepyramine and metiamide (H1 and H2 histamine receptor antagonists) or aminophylline did not influence significantly the development of brain edema evaluated 24 h after embolization. Aminophylline treatment (100 mg/kg) markedly increased mortality following embolization. Gamma-butyrolactone (300 mg/kg, every 2 h) inhibited significantly the development of brain edema evaluated 12 hours after embolization. Increases in water and sodium in the embolized cerebral hemisphere were reduced by about 50%. This protective effect may be related to the known depressant action on brain metabolism.

4-Butyrolactone↗
PubMed1991

Mechanism of action of arginine vasopressin on acute ischemic brain edema.

The purpose of this experiment is to study the role of arginine vasopressin (AVP) in acute cerebral ischemic edema in Mongolian gerbils. The results show that intracerebroventricular injection (ICV) of AVP exacerbates acute ischemic brain edema, while ICV of AVP antiserum significantly decreases the ischemic brain edema. Nimodipine (calcium antagonist) cannot block this role of AVP in brain edema. In addition, the cortical Na(+)-K+ ATPase activity is significantly decreased, while the cAMP content of ischemic cortex and hypothalamus and the cGMP content of the hypothalamus are markedly increased after AVP ICV. These suggest that AVP may play an important role in the pathophysiologic process of ischemic brain edema by inhibiting the Na(+)-K+ ATPase activity of the cerebral cell membrane and the AVP receptors mediated by cAMP and cGMP.

Animals↗
PubMed2007

In vivo brain edema classification: New insight offered by large b-value diffusion-weighted MR imaging.

PURPOSE: To assess the role of large b-value diffusion weighted imaging (DWI) in the characterization of the physicochemical properties of the water in brain edema under experimental and clinical conditions. MATERIALS AND METHODS: Vasogenic brain edema was induced in mice by means of cold injury. A total of 17 patients with extensive peritumoral brain edema were also investigated. The longitudinal relaxation time (T(1)) and apparent diffusion coefficient (D) were measured in the edematous area both in humans and in mice. D was calculated by using both mono- (D(mono)) and biexponential (D(fast) and D(slow)) approaches in the low and overall range of b-values, respectively. The D values were correlated with the T(1) values. RESULTS: A strong linear correlation was found between T(1) and D(mono) in vasogenic brain edema, both in humans and in mice. After breakdown of D(mono) into fast and slow diffusing components, only D(fast) exhibited a strong correlation with T(1); D(slow) was unchanged in vasogenic brain edema. CONCLUSION: Large b-value DWI can furnish a detailed characterization of vasogenic brain edema, and may provide a quantitative approach for the differentiation of edema types on the basis of the physicochemical properties of the water molecules. Application of the DWI method may permit prediction and follow-up of the effects of antiedematous therapy.

Animals↗
PubMed1995

Vascular endothelial growth/permeability factor expression in human glioma specimens: correlation with vasogenic brain edema and tumor-associated cysts.

Peritumoral vasogenic brain edema (PVBE) is a common accompaniment of malignant gliomas. It results from microvascular extravasation of plasma fluid and proteins through the interendothelial spaces. Tumor-associated cysts (TACs) are observed more commonly with benign gliomas that are not associated with PVBE. This study investigates the hypothesis that these morphologically distinct epiphenomena of microvascular extravasation are linked by a common pathophysiological mechanism involving vascular endothelial growth/permeability factor (VEG/PF), which has been implicated in vascular leak phenomena including ascites, malignant effusions, and brain edema. Furthermore, VEG/PF has been isolated from cultured glioma cells, and both VEG/PF protein and messenger RNA transcripts are expressed in brain tumor tissue. To further elucidate the relationship of VEG/PF to PVBE and TACs, the authors examined 34 pathological specimens for VEG/PF expression. Nineteen primary low-grade tumors, 11 primary high-grade tumors, and four gliosis controls were immunostained with a polyclonal anti-VEG/PF immunoglobulin G antibody. Magnetic resonance imaging was used to quantitate PVBE and to determine the presence of TACs and tumor enhancement. The study revealed that eight VEG/PF-negative specimens exhibited no significant edema, whereas 26 VEG/PF-positive tumors exhibited either significant PVBE or TACs. Notably, eight of nine benign TACs that were not associated with PVBE immunostained positive for VEG/PF. These data indicate a high degree of correlation between VEG/PF expression by gliomas and the occurrence of PVBE or TACs, irrespective of tumor grade, thus supporting VEG/PF's pivotal role as the common pathophysiological link between these processes.

Antibodies, Neoplasm↗
PubMed1994

High colloid oncotic therapy for contusional brain edema.

We investigated whether prolonged high colloid oncotic therapy for two weeks can suppress contusional brain edema. Eighteen patients with cerebral contusion were randomly divided into two groups of patients receiving high oncotic pressure (HOP; 26-30 mmHg) treatment and those receiving normal oncotic pressure (NOP; 22-26 mmHg) treatment. Oncotic pressure was maintained for two weeks with administration of a 25% albumin solution with additional use of furosemide. Edema volume was calculated by summation of all measured low-density areas in each CT slice multiplied by 1.0 cm of slice of thickness. We expressed contusional brain edema volume as a percent increase based on each patient's initial CT. The mean percent increase of contusional brain edema in the NOP group was significantly higher than that in the HOP group at 9-15 days (208.9% and 14.0%, respectively) and 16-25 days (188.8% and 10.0%, respectively). There were no complications such as heart failure or renal failure during treatment. All the patients in the HOP group recovered with minimal or no neurological deficit. On the other hand, 30% of patients in the NOP group remained in poor condition. With frequent measurement of oncotic pressure and adjustment of fluids and electrolytes, continuous oncotic therapy for two weeks effectively and safely reduced contusional brain edema.

Adolescent↗
PubMed1985

Magnetic resonance imaging of experimental brain edema in cats.

The authors observed the natural course of experimental brain edema in vivo using magnetic resonance (MR) imaging. To detect and qualify the edematous lesion, they obtained images by the spin echo technique (repetition time, 2100 ms; echo time, 80 ms). These showed the maximal brain edema on the 1st to 3rd days after the operation, as evidenced by a pixel density study and a finding of mass effect. On MR images enhanced with manganese, the inversion recovery technique (repetition time, 2100 ms; inversion time, 500 ms) demonstrated the edematous lesion as a high signal intensity area with good spatial resolution. Moreover, the follow-up inversion recovery images with manganese suggested that there was a system for absorption of edema fluid between blood vessels and the edematous lesion. The authors think that MR imaging is an important technique for observation of the dynamics of experimental brain edema.

Animals↗
PubMed1989

Neurotransmitter amines in brain edema of a rat glioma model.

The effect of vasogenic brain edema on amine neurotransmitter concentrations was studied in rats bearing transplanted glioma C6 brain tumors. In comparison with sham-operated and nonoperated controls, the tumor-implanted animals showed significant decreases in both dopamine (DA) and norepinephrine (NE) in the hypothalamus, cortex, and striatum. Treatment with dexamethasone (DEX) tended to restore these monoamines to the levels measured in sham-operated controls. In the nonoperated controls, DEX significantly increased NE but not DA. In tumor-bearing rats there was no increase in hypothalamic or striatal water content, and DEX had no effect on the water content of these structures. However, there was a significant increase in the cortical water content, which was reduced by DEX to the control levels. The water content within the tumor was also significantly decreased by DEX. In the nonoperated controls, there was no difference in water content between DEX-treated and nontreated animals. These findings suggest that tumor-induced brain edema reduces noradrenergic and dopaminergic activities. DEX administration resulted in normalization of the water content in edematous regions and of the DA and NE concentrations, and brought about marked symptomatic improvement.

Animals↗
PubMed2000

[Effect of baicalin and dexamethasone on cytokines in brain tissue of infectious brain edema].

OBJECTIVE: To explore the effect of baicalin(BC) and dexamethasone(DXM) on interleukin-1 beta (IL-1 beta) and tumor necrosis factor alpha(TNF-alpha) in brain tissues of infectious brain edema. METHODS: The infectious brain edema model induced by pertussis bacilli(PB) was used. Brain water content(WC), content of Na+ and the levels of IL-1 beta, TNF-alpha were determined, and the morphological changes were observed under the light microscope. RESULTS: The results showed that the levels of WC, Na+, IL-1 beta and TNF-alpha in group PB were higher than those in group of normal saline(NS) (P < 0.01). And they were lower in groups BC and DXM than those in group PB(P < 0.05). In groups BC and DXM, there were no significant difference in the contents of water, Na+, IL-1 beta and TNF-alpha(P > 0.05). The water contents were positive linar correlated with IL-1 beta or TNF-alpha(P > 0.05). The water contents were positive linear correlated with IL-1 beta or TNF-alpha contents(r = 0.9381, 0.8349, P < 0.01). The structure of brain tissues in group NS was normal. In group PB, there were severe edema in brain tissues. In groups BC and DXM, the edema of brain tissues was reduced. CONCLUSIONS: The results suggest that the protective effect of BC and DXM against infectious brain edema were similar, the mechanism may be associated with the reduction of TNF-alpha and IL-1 beta.

Animals↗
PubMedDate not supplied

Proton NMR relaxation times in ischemic brain edema.

The state of water in cerebral ischemia was studied by using the proton nuclear magnetic resonance (1H-NMR) method. Cerebral ischemia was induced experimentally in Mongolian gerbils by unilateral ligation of the common carotid artery. Longitudinal (T1) and transverse (T2) relaxation times of the ischemic brain were measured with a pulse FT-NMR spectrometer and the water content was determined by the wet/dry method. Quantitative analysis of the relaxation times was performed sequentially during the initial 7 hours following ligation and the data were compared with those of brain edema previously reported by S. Naruse in the rat. Characteristic findings in brain ischemia include prolongation of the slow component of T2 and increase in the water content. A quantitative comparison of relaxation rate and water content demonstrates that ischemic brain edema in Mongolian gerbils is different from cytotoxic and vasogenic types of brain edema. When R2 (1/T2) was plotted against the water content, the slope value of ischemia in the gerbil was between the slope values of the TET intoxication and cold injury induced edemas reported previously. From these results, it might be said that ischemic brain edema includes both the cytotoxic and vasogenic types of brain edema. Glycerol was demonstrated to affect brain ischemia by decreasing the water content and by shortening the slow component of T2. By analysis of the relaxation times and water content, we examined the pathophysiological characteristics of water molecules in ischemic brain tissue.

Animals↗
PubMed1990

Evaluation of brain edema using magnetic resonance proton relaxation times.

Experimental and clinical studies on the evaluation of water content in cases of brain edema were performed in vivo, using MR proton relaxation times (longitudinal relaxation time, T1; transverse relaxation time, T2). Brain edema was produced in the white matter of cats by the direct infusion method. The correlations between proton relaxation times obtained from MR images and the water content of white matter were studied both in autoserum-infused cats and in saline-infused cats. The correlations between T1 as well as T2 and the water content in human vasogenic brain edema were also examined and compared with the data obtained from the serum group. T1 and T2 showed good correlations with the water content of white matter not only in the experimental animals but also in the clinical cases. The quality of the edema fluid did not influence relaxation time and T1 seemed to represent almost solely the water content of the tissue. T2, however, was affected by the nature of existence of water and was more sensitive than T1 in detecting extravasated edema fluid. It seems feasible therefore to evaluate the water content of brain edema on the basis of T1 values.

Animals↗