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PubMed2002

Decreased hemispheric Aquaporin-4 is linked to evolving brain edema following controlled cortical impact injury in rats.

The cerebral Aquaporin-4 (AQP4) water channel is suggested to be involved in brain edema formation aggravated by reduced cerebral blood flow early after traumatic brain injury (TBI). Therefore, the temporal profile of brain edema formation, AQP4 expression, and cortical perfusion were investigated following focal TBI in rats. Brain edema was maximal by 24 h. Concurrently, AQP4 protein expression was decreased in both hemispheres, being more pronounced in the traumatized hemisphere (-50%) 48 h after trauma. Cortical perfusion was only decreased in the ipsilateral cortex (-40%) between 4 and 8 h after trauma, reaching baseline values at 24 h. Globally reduced AQP4 expression following induction of a focal contusion coincides with edema development and seems to be independent of changes in cortical perfusion.

Animals↗
PubMed1997

Occurrence of apoptosis following cold injury-induced brain edema in mice.

Apoptosis has been known to contribute to neuronal death following a variety of brain insults. However, the role of vasogenic brain edema in neuronal apoptosis is unknown. We studied the temporal pattern of brain edema and neuronal apoptosis following cold injury. Cold injury-induced brain edema, which was detected by the increased water content in the injured hemisphere, reached its maximum level at 24 h and remained there at 72 h, whereas the blood-brain barrier breakdown detected by Evans Blue extravasation returned to the control value by 24 h after injury. Terminal deoxynucleotidyl transferase-mediated uridine-5'-triphosphate-biotin nick end labeling (TUNEL)-positive apoptotic cells were scattered in the center of the lesion at 1 h and were dispersed over the cold lesion at 24 h. The number of these TUNEL-positive cells was maximized in the periphery but decreased in the center at 72 h after cold injury. We postulate that secondary neuronal damage occurred not only through necrotic, but also apoptotic pathways, and that apoptotic neuronal death may result from vasogenic edema development and may contribute to the expansion of the lesion in both the acute and delayed phases after cold injury.

Animals↗
PubMed2002

Bench to bedside: brain edema and cerebral resuscitation: the present and future.

Sudden cardiac arrest (CA) claims approximately 1,200 lives daily in the United States. Cardiopulmonary resuscitation attempts have so far achieved suboptimal results, and even when restoration of spontaneous circulation (ROSC) is achieved, about 30% of survivors suffer permanent brain damage. This illustrates the need for an improved basic scientific understanding of the pathophysiology of global cerebral injury caused by whole-body ischemia/reperfusion (I/R) injury following CA. Brain edema has been recently documented in experimental CA followed by one hour of ROSC. Brain edema has also been documented in CA and stroke patients by computed tomography or magnetic resonance imaging scanning, and has been shown to predict a poor neurologic outcome. The mechanisms underlying brain edema formation elicited by CA are unclear. New scientific findings of the roles of blood-brain barrier (BBB) permeability, matrix metalloproteinases (MMPs) of a family of proteases, aquaporin 4 (AQP4) of a family of membrane water-channel proteins, and the N-methyl-D-aspartate (NMDA) receptors in the mechanisms underlying CA-elicited brain edema were reviewed. By defining the roles of BBB permeability, MMPs, AQP4, and NMDA receptors in CA-induced brain edema formation, effective new therapeutic strategies to extend cellular and tissue survival, and preserve neurologic function following CA may be feasible.

Animals↗
PubMed1998

CT diagnosis of non-traumatic subarachnoid haemorrhage in patients with brain edema.

The aim of the study is to prove, retrospectively, that it is unlikely that the computerized tomography (CT) diagnosis of subarachnoid haemorrhage (SH) accompanies the CT diagnosis of generalized brain edema. A total of 100 comatose patients underwent CT of the brain. Of this number, 42 underwent an enhanced CT scan. In 26 patients, lumbar puncture was also performed. A control group of ten patients diagnosed with headache and having a normal CT scan underwent NECT and ECT. Measurements of the white and gray matter density in Hounsfield units (HU) were performed in all 110 cases, including the controls. The brain tissue density and the difference between the densities of the white and gray matter were lower in the cases with brain edema than in the controls. The data values were statistically significant. Small cerebral ventricles, sulci and cisterns and small differences between white and gray matter measurements were observed in the CT scans of the brain edema cases. All 100 patients had CT diagnosis of brain edema and SH. There was no bloody or xanthochromic CSF in any of the 26 lumbar punctures performed. In the enhanced CT scans, there was poor or no filling of the lateral sinuses. The compression of the lateral sinuses by the edematous brain tissue most probably results in their stenosis or obstruction due to disturbed brain venous drainage which can mimic CT findings of SH.

Adolescent↗
PubMed1982

Brain edema and gliopathy induced by 6-aminonicotinamide intoxication in the central nervous system of rats.

Brain edema was produced by 6-aminonicotinamide (6-AN) in the rat with accompanying metabolic disturbance due to the accumulation of an antimetabolite of nicotinamide in the CNS. Twenty-four hours after intraperitoneal administration of 6-AN, significant (P less than 0.01) increases of sodium and water in the medulla oblongata were observed. By electron microscopy, the lesion was characterized by swelling of the perivascular neuroglial processes, producing disturbances of the active transport in the cell membrane and increased pinocytosis in the endothelial cells, especially of the arterioles and venules. The metabolic inhibitor was shown to produce not only an increased water and sodium uptake in neuroglias, which is characteristic of cytotoxic brain edema, but also produced protein-rich edema in the extracellular space, ie, vasogenic brain edema. The protein transport in the metabolic disturbance caused by 6-AN was traced, using horseradish peroxidase, revealing that it occurred from the vasculature into the extracellular spaces via pinocytotic vesicles due to the change in the cerebrovascular permeability.

6-Aminonicotinamide↗
PubMed2000

[A canine model of brain edema established in the early postburn stage].

OBJECTIVE: To establish a canine model of brain edema in the early stage of severe burn. METHODS: Mongrel dogs were inflicted by napalm with 50% TBSA III degree burn. The dogs were randomized into normal control (C), burn (B), burn with balanced salt solution (S) and burn with glucose (G) groups. The macropathological, histopathological and ultrastructural changes of brain tissue and brain water (%) were examined at 6, 12, 18 and 24 postburn hours (PBH), respectively, with simultaneous evaluation of blood brain barrier by (99) TC -- ECD. RESULTS: Pathological evidence of brain edema exhibited at as early as 6 PBH in B, S and G groups, which included cellular swelling of partial endothelia and pericapillary astrocytes, and ischemic necrosis of endothelia, neurons and axons to varying degrees. All the changes exhibited more and more obvious with the elapse of postburn time. The brain water content in each burn group, especially in G group at 24 PBH, was more than that in C group. It was indicated by nuclide imaging that there appeared gradual increasing of the concentration of (99) TC -- ECD in brain tissue in B and C groups since 6 PBH. CONCLUSION: This model was established for the convenience of burn scholars to study the pathogenesis and management of postburn brain edema.

Animals↗
PubMed1999

A novel Na+ and Ca2+ channel blocker, T-477, prevents brain edema following microsphere-induced permanent occlusion of cerebral arterioles in rats.

One of the most common acute complications of stroke is brain edema. Treatment of edema is recommended when the condition of the patients is deteriorating. The present study was undertaken to evaluate the effect of T-477 [(R)-(+)-2-(4-chlorophenyl)-2,3-dihydro-4-diethyl aminoacetyl-4H-1,4-benzorthiazine hydrochloride], a novel neuronal Na+ and Ca2+ channel blocker, on brain edema in rats. Cerebral ischemia was induced by intra-arterial infusion of 1000 microspheres into the forebrain of freely moving rats, resulting in brain edema. T-477 was intravenously infused continuously for 24 h or twice for 3 h with a 3-h interval between infusions immediately after microsphere injection. T-477 dose-dependently inhibited the increase in brain water content by both infusion procedures; the inhibition was statistically significant at doses of 25 mg/kg per 24 h and 14 mg/kg per 9 h. Additionally, infusion of T-477 at a dose of 14 mg/kg per 9 h significantly inhibited the decrease in K content and the increase in Ca content of the forebrain. In conclusion, T-477 prevents brain edema following microsphere-induced cerebral embolism in rats.

Animals↗
PubMed1990

Is postischemic hypoperfusion related to brain edema?

The effect of reversible cerebral ischemia on brain edema development was studied with a gravimetric method. CBF changes after ischemia were correlated with alterations in brain SG. Forebrain ischemia (15 min) was induced in rats by reversible bilateral ligation of both carotid arteries plus induction of controlled hypotension to 50 mm Hg. The SG of different brain structures was determined in a Percoll column up to 24 hr after ischemia. In addition, rCBF was measured by [14C]iodoantipyrine autoradiography. Cerebral ischemia resulted in reduction of CBF to less than 1% of normal in cortical structures and the caudatoputamen. One hour after the end of ischemia, blood flows were still reduced to 30% to 50% of the control level indicative of DPH. SG in cortex and hypothalamus reached a maximal decrease 10 min after the end of the ischemia and was still significantly reduced at 1 hr, although it was normal again 6 hr later. Regression analysis revealed a significant correlation between CBF obtained during ischemia and the corresponding SG found at 10-min recirculation, which could also be established at 1-hr recirculation. Therefore, a causal relation between the development of the DPH and the formation of ischemia might be considered.

Animals↗
PubMed1978

Clearance of edema fluid into cerebrospinal fluid. A mechanism for resolution of vasogenic brain edema.

The authors present the results of an investigation studying the resolution of vasogenic brain edema using cold injury in cats. The appearance of RISA-I131 and sucrose-C14 lebeled edema fluid in the ventricular cerebrospinal fluid (CSF) was assessed by means of ventriculocisternal perfusion. The effect of low- or high-pressure perfusion on edema spread was determined by measuring the water, sodium, RISA-I131, and sucrose-C14 content of serial tissue blocks taken from the injured cortex through the white matter to the ventricular ependyma. The findings indicate that increasing the hydrostatic pressure gradient between edematous brain and CSF enhances the clearance of edema fluid into the ventricular CSF. This was conclusively demonstrated with low-pressure ventricular perfusion which markedly diminished the amount of edema close to the ventricles compared to the controls. The concentration of albumin, sodium, and potassium to the fluid removed from the tissue during low-pressure perfusion indicates that bulk flow was the primary method of edema movement through the extracellular space. With high-pressure perfusion the concentration profiles suggested alternative mechanisms of edema resolution, such as diffusion and reabsorption into capillaries.

Animals↗
PubMed2006

Brain edema after intracerebral hemorrhage in rats: the role of inflammation.

BACKGROUND: Intracerebral hemorrhage (ICH) results in secondary brain edema and injury that may lead to death and disability. ICH also causes inflammation. It is unclear whether inflammation contributes to brain edema and neuron injury or functions in repairing the brain tissue. AIMS: To understand the effect of inflammation in ICH, we have carried out an investigation on the various aspects and the dynamic changes of inflammation. SETTINGS AND DESIGN: An ICH model was generated by injecting 50 microl autologous tail artery blood stereotactically into the right caudate nucleus of 30 rats, which were randomly divided into five ICH groups. Similarly, five Sham control groups were generated by inserting the needle to the right caudate nucleus of rats. MATERIALS AND METHODS: Rat behavior was evaluated over the time course (6 h, 24 h, 48 h, 72 h and 7 d) in each group. The rats were then killed by administering an overdose of pentobarbital. Following the euthanasia, the brain water content, neuronal loss, glia proliferation, inflammatory infiltration and brain morphology of the rats were measured. Additionally, the expression of TNF-alpha, IL-6, ICAM-1, VEGF, NF-kappaB, C3 and CR2 was analyzed by immunohistochemistry. STATISTICAL ANALYSIS: The data were analyzed by student's t test. RESULTS: Rat brain water content increased progressively over the time course and reached its peak at 48 h followed ICH. The maximum of inflammatory infiltrate (especially neutrophils) and immunopositive cells of TNF-alpha, IL-6 and NF-kappaB, were at 48 h. The expression of C3 and CR2 reached their peaks at 48-72 h, while the expression ICAM-1 and VEGF were at maximum at 72 h followed ICH. CONCLUSIONS: The results suggested that the inflammatory cytokines, complement system and VEGF may have a function in the development of the brain edema and neuron injury followed ICH.

Animals↗
PubMed1984

Effects of pre-ganglionic decentralization or post-ganglionic excision of the superior cervical ganglia on brain edema and heat stroke in rats.

The preventive effect of pre-ganglionic decentralization (Sympathetic trunk resectioN) or postganglionic excision (ganglionectomy) of the superior cervical ganglia on thermal injury induced brain edema or the development of heat stroke was assessed in rats. Brain edema was induced by cold or heat injury to the cortex in 24 rats. The results showed that decentralization, but not excision, of the superior cervical ganglia greatly inhibited the formation of brain edema which was subsequently induced. When heat stroke was induced by exposing 24 rats to an ambient temperature of 41 degree C, the latency for the onset of the heat stroke and the survival time after the heat stroke were greatly prolonged by the former surgical procedure, but shortened by the later one. The present study demonstrates the potential benefit to brain edema and heat stroke of the pretreatment with decentralization of the superior cervical ganglia.

Animals↗
PubMed1990

Importance of protein content in the edema fluid for the resolution of brain edema.

This study shows that there is a quantitative relation between the protein content of edema fluid and the rate of fluid clearance. Minimal clearance takes place during the first 3 days in the high albumin group. Thereafter, the majority of the fluid is cleared, and tissue water returns to normal values by 8 days. This appears to support an idea that the rate of clearance is in direct proportion to protein concentration. This also supports the findings of Kuroiwa et al. who showed a direct relation between protein extravasation and the increase of water in extracellular vasogenic edema. However, the rate of clearance does not in fact appear to be linear with time as the greater percentage of protein edema fluid is cleared after 3 days. This may be explained by the observations of Rasmussen and Klatzo and Bodsch and Hossmann who indicate that the composition of the extracellular protein may undergo various changes, similar to fragmentation, hence increasing the number of osmotically active particles so the pre-existing edema would remain stable or slightly increase. In conclusion, this study demonstrates that the infusion model of edema can be applied to the rat for study of resolution dynamics. We have also shown that in this model, there is a proportional relation between protein concentration of the edema fluid and time necessary for clearance.

Albumins↗
PubMed1999

[Effect of baicalin and tetramethylpyrazine on intracranial hypertension of infectious brain edema in rabbits].

OBJECTIVE: To evaluate the effects of mannitol (MN), baicalin (BC) and tetramethylpyrazine (TMPZ) on intracranial hypertension (ICH) of infectious brain edema induced by Pertussis bacilli (PB) in rabbits. METHODS: Forty-five rabbits were divided randomly into five groups: the normal saline group (A); the pertussis bacilli group (B); the MN treated group (C); the TMPZ treated group (D) and the BC treated group (E). PB was injected into the left internal carotid artery of rabbits to establish the infectious brain edema model, their intracranial pressure (ICP) was monitored continuously by fiberoptic ICP monitor. Treatments were given intravenously 1 hour after injecting PB, and changes of ICP, brain water content (WC), Evans blue (EB), Na+, K+ and morphology were observed within 4 hours after PB or NS injection. RESULTS: MN, TMPZ and BC all could reduce the brain edema and ICH in rabbits induced by PB, the effect of MN was the most rapid and obvious one, but it lasted for rather shorter time, while the effect of TMPZ and BC was initiated later but lasted for a longer time. The ICP of Group C in 2nd to 4th hour was higher than that of Group D and Group E, but lower than that of Group B. The ICP of Group E in 3rd to 4th hour was lower than that of group D. At the same time of lowering ICP, brain WC, EB, Na+ contents and pathologic morphologic change were also alleviated. CONCLUSION: Both BC and TMPZ could reduce ICP in infectious brain edema, the effect of BC was better than that of TMPZ.

Animals↗
PubMed1990

Effect of astrocyte-derived factors on ischemic brain edema induced by rat MCA occlusion.

To clarify whether astrocyte-derived factors may protect cerebral tissue from ischemia, we examined brain edema, demyelination and astrocyte proliferation in brains with focal ischemia and treated with astrocyte-cultured medium. We occluded the left middle cerebral artery of rats and implanted the Osmotic Minipump, which continuously infused the glial-cultured medium or control medium into the left lateral ventricle. Animals were sacrificed at 3 days or 7 days after occlusion. Brains of both groups were compared by several markers, i.e. extravasation of Evans blue, demyelination by Woelcke's staining and glial proliferation by GFAP staining. We found the astrocyte-cultured medium reduced leakage of Evans blue-plasma protein complex from ischemic lesions and reduced the size of demyelinated lesions. However, the degree of astrocyte proliferation was similar in both groups. From these data, we speculate that humoral factors derived from cultured astrocytes lessened the brain edema by modifying the blood-brain barrier. These factors might also induce proliferation of the microglia, and may protect the neurons from secondary injury by oxygen-free radicals.

Animals↗
PubMedDate not supplied

[The effect of neurotropic agents on the development of toxic brain edema in sexually immature animals].

It was established on two age groups of rats that toxic brain edema in one-month-old animals is prevented by dopegit (100 mg/kg) and aminazine (2.5 mg/kg). The pharmacological correction of the brain edema in two-month-old rats is similar to that in adult animals. The central adrenergic structures play the significant role in the development of the brain edema in sexually immature animals.

Aging↗
PubMed1992

[Effect of ulinastatin on postischemic brain edema in cats].

The effect of ulinastatin on postischemic brain edema was investigated in adult mongrel cats. Focal brain ischemia was produced by occlusion of the left middle cerebral artery (MCA) through the transorbital approach. Following two hours of occlusion, the brain was reperfused for two hours. In all seven animals of the ulinastatin-treated group, ulinastatin was administered intravenously at a dose of 50000 U/kg before and after occlusion. In the control group, six animals were given only vehicle. Measurements of regional cerebral blood flow (rCBF) were performed before MCA occlusion by the hydrogen clearance method, and then repeated every 30 minutes during and after occlusion. Following two-hour reperfusion, the animals were sacrificed by intravenous KCl injection. Specific gravity of the cortex, where rCBF was measured, was determined by microgravimetric method. In the analysis of specific gravity of the cortex, in which mean rCBF during ischemia was above 15ml/100g/min, no significant difference was found between the ulinastatin-treated and control groups. In the specimen with mean rCBF below 15ml/100g/min during ischemia, cortical specific gravity was reduced remarkably in the control group, while not decreased in the ulinastatin-treated group. The difference was statistically significant between two groups (p less than 0.001). These findings suggest antiedema effect of ulinastatin.

Animals↗
PubMed1988

Prevention of ischemic and postischemic brain edema by a novel calcium antagonist (PN200-110).

The effect of PN200-110, a novel calcium antagonist, on the formation of brain edema was examined with rats using a middle cerebral artery (MCA) occlusion model. PN200-110 was effective in preventing the formation of brain edema in 6-h ischemia and in 3-h reperfusion following 3-h ischemia, which were cases in which great accumulations of calcium were autoradiographically observed. Furthermore, PN200-110 diminished the excessive accumulation of calcium in the MCA area involved. These results indicate that an inhibition of the massive influx of calcium into brain cells by PN200-110 may partially ameliorate cell damage, resulting in prevention of brain edema.

Animals↗
PubMedDate not supplied

Role of Gd-DOTA in the evaluation and imaging of experimental blood-brain barrier disruption in brain edemas and their improvement after anti-inflammatory drugs treatment.

This study was carried out to evaluate the effect of new anti-inflammatory drugs in the treatment of brain edema in new models. Experimental brain edema was induced in rats by stereotaxic injection of phospholipase A2 into one hemisphere. Concentrations of intravenously injected gadolinium-DOTA in the lesioned hemisphere were three times as high as in normal rat hemisphere. Edema was reduced by treatment with anti-inflammatory drugs such as dexamethasone (P < 0.01) or an experimental benzamide drug (P < 0.02). Magnetic resonance imaging (MRI) was then used to evaluate edema reduction after administration of contrast medium. We observed weighted scans for control lesioned rats, a reduction of signal intensity after dexamethasone and no significant regression after the benzamide drug. For purposes of experimental brain edema research in rats, the MRI technique facilitates detection and evaluation of the anti-inflammatory activity of molecules crossing the blood-brain barrier.

Animals↗