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PubMed1999

Mediators of cerebral edema.

The blood-brain barrier (BBB) which is located in the continuous endothelial lining of cerebral blood vessels rigidly controls exchange of water soluble compounds under physiological conditions. Under pathological conditions such as trauma or ischemia, BBB permeability may increase thus allowing plasma constituents to escape into brain tissue. This "opening" of the BBB may, at least in part, be mediated by massive release of autacoids resulting in vasogenic brain edema. Five criteria have to be fulfilled by an individual autacoid to be considered a mediator candidate of cerebral edema: i) a permeability-enhancing action under physiological conditions, ii) a vasodilatory action, iii) the ability to induce vasogenic brain edema, iv) an increase of concentration in the tissue or interstitial fluid under pathological conditions, and v) a decrease of brain edema by specific interference with the release or action of a given autacoid. Among the mediator candidates considered, bradykinin is the only one to meet all criteria. Histamine, arachidonic acid and free radicals including nitric oxide may also be considered mediators of brain edema, but for each of these compounds evidence is less clear than for bradykinin. Although the concept of mediators inducing brain edema is well established by experimental studies, only a bradykinin receptor antagonist has so far gained entrance into clinical evaluation.

Animals↗

PubMed1999

High altitude cerebral edema and acute mountain sickness. A pathophysiology update.

The diagnosis, treatment and prevention of high altitude cerebral edema (HACE) are fairly well established. The major unresolved issues are 1) the pathophysiology, 2) the individual susceptibility, and 3) the relationship of HACE to acute mountain sickness (AMS) and to high altitude pulmonary edema (HAPE). In the context of the two types of cerebral edema, cytotoxic (intracellular) and vasogenic, a leaking of proteins and water through the blood-brain barrier (BBB), a recent MRI study in persons ill with HACE (16) suggested a predominantly vasogenic mechanism. Causes of increased BBB permeability might include mechanical factors (loss of autoregulation and increased capillary pressure), ischemia, neurogenic influences (adrenergic and cholinergic activation), and a host of permeability mediators. Once vasogenic edema develops, cytotoxic edema generally follows, and although likely in HACE, this is still unproven. Symptoms of HACE are related to increased intracranial pressure (ICP), and death is from brain herniation. Treatment is directed both to lowering ICP by reducing the volume of intracranial contents, and to stopping the vasogenic leak. Evidence is accumulating that established moderate to severe AMS is due to cerebral edema, but whether this is true for early AMS (headache) is unclear. New work suggests that the brain swells on ascent to altitude, but that this is unrelated to AMS. Preliminary data showing that those with less cerebrospinal fluid volume (a tighter fit of the brain in the cranium) were more likely to develop AMS supports the hypothesis of Ross that those with less ability to accommodate the increased brain volume are the ones that suffer AMS. The blood-brain barrier and intracranial hemodynamics are the two key elements in the pathophysiology of HACE and AMS.

Altitude↗

PubMed1999

High-altitude pulmonary edema: from exaggerated pulmonary hypertension to a defect in transepithelial sodium transport.

High-altitude pulmonary edema (HAPE) is a form of lung edema which occurs in otherwise healthy subjects, thereby allowing the study of underlying mechanisms of pulmonary edema in the absence of confounding factors. Exaggerated pulmonary hypertension is a hallmark of HAPE and is thought to play an important part in its pathogenesis. Pulmonary vascular endothelial dysfunction and augmented hypoxia-induced sympathetic activation may be underlying mechanisms contributing to exaggerated pulmonary vasoconstriction in HAPE. Recent observations by our group suggest, however, that pulmonary hypertension itself may not be sufficient to trigger HAPE. Based on studies in rats, indicating that perinatal exposure to hypoxia predisposes to exaggerated hypoxic pulmonary vasoconstriction in adulthood, we examined effects of high-altitude exposure on pulmonary-artery pressure in a group of young adults who had suffered from transient perinatal pulmonary hypertension. We found that these young adults had exaggerated pulmonary vasoconstriction of similar magnitude to that observed in HAPE-susceptible subjects. Surprisingly, however, none of the subjects developed lung edema. These findings strongly suggest that additional mechanisms are needed to trigger pulmonary edema at high-altitude. Observations in vitro, and in vivo suggest that a defect of the alveolar transepithelial sodium transport could act as a sensitizer to pulmonary edema. The aim of this article is to review very recent experimental evidence consistent with this concept. We will discuss data gathered in mice with targeted disruption of the gene of the alpha subunit of the amiloride-sensitive epithelial sodium channel (alpha ENaC), and present preliminary data on measurements of transepithelial sodium transport in vivo in HAPE-susceptible and HAPE-resistant mountaineers.

Adult↗

PubMed1981

Specific demonstration of albumin by immunohistological techniques in human vasogenic brain edema.

In the present study, the immunofluorescent and immunoperoxidase methods were applied to demonstrate the serum proteins in vasogenic brain edema (6). Using these techniques on paraffin embedded formalin fixed human brains with carcinoma metastases, albumin was identified specifically in the edema fluid, while human immunoglobulin (IgG, IgA, IgM) were not detectable. The localisation and spreading of edema fluid clearly show the presence of the vasogenic type of brain edema under human pathological conditions. The astrocytes containing albumin confirm the conception concerning their role in the resolution of brain edema in human pathology, as well. The immunohistological techniques seem to be useful to investigate the human brain edema on necropsy material.

Brain Edema↗

PubMed2003

Neuropeptide release influences brain edema formation after diffuse traumatic brain injury.

The mechanisms associated with edema formation after traumatic brain injury (TBI) have not been fully elucidated. In peripheral tissue injury, the neurogenic component of inflammation plays a significant role in increased vascular permeability and edema formation. However, few studies have examined the role of neuropeptide induced neurogenic inflammation following TBI. Adult male Sprague-Dawley rats were either left untreated, or pre-treated with capsaicin (125 mg/kg s.c.) or equal volume vehicle, and injured 14 days later using the 2-meter impact-acceleration model. Subgroups of animals were assessed for blood brain barrier (BBB) permeability (Evans Blue), brain edema (wet weight/dry weight) and functional outcome (Barnes maze and Rotarod) for up to 2 weeks post-trauma. Increased BBB permeability was present in untreated animals between 3 and 6 h after injury but not at later time-points. Edema was maximal at 5 h after trauma, declined and then significantly increased over the 5 days post-trauma. In contrast, capsaicin pre-treated, neuropeptide-depleted animals exhibited no significant increase in BBB permeability or edema compared to vehicle treated animals after injury. Notably, motor and cognitive impairments were significantly reduced in the capsaicin-pretreated animals. We conclude that neurogenic inflammation contributes to the development of edema and posttraumatic deficits after diffuse TBI.

Animals↗

PubMed2003

Effect of delayed argatroban treatment on intracerebral hemorrhage-induced edema in the rat.

Studies indicate that thrombin plays an important role in intracerebral hemorrhage (ICH) induced edema formation. However, the time window for administration of a thrombin inhibitor to reduce ICH-induced edema is unknown. Nor is it known whether this time window extends beyond the period when a thrombin inhibitor might exacerbate rebleeding. This study examines whether a thrombin inhibitor, argatroban, can reduce edema formation following intracerebral infusion of 100 microl of blood in the rat, the therapeutic time window for argatroban, and whether argatroban promotes rebleeding. Intracerebral injection of argatroban 3 hours after ICH caused a significant reduction in edema measured at 48 hours. The systemic administration of argatroban (0.9 mg/h) starting 6 hours after ICH also significantly reduced edema formation. There was no protection when the onset of argatroban administration was delayed to 24 hours after ICH. Argatroban did not increase collagenase-induced hematoma volume when given into the clot after 3 hours or given systemically at 6 hours. Our data suggest argatroban may be an effective therapy for ICH-induced edema.

Animals↗

PubMed2003

Overexpression of interleukin-1 receptor antagonist reduces brain edema induced by intracerebral hemorrhage and thrombin.

Recent studies indicate that inflammatory reaction occurs around hematoma after intracerebral hemorrhage (ICH). In this study the authors examine the hypothesis that overexpression of IL-1ra in the brain attenuate brain edema formation after ICH. Adenoviruses expressing IL-1ra (Ad.RSVIL-1ra) or LacZ (Ad.RSVLacZ) or saline were injected into the lateral ventricle. On the fifth day after virus injection, 100 microl of autologous blood or 5 U thrombin was infused into the right basal ganglia. Rats with ICH were killed 24 or 72 hours later for measurement of brain water content. Thrombin-treated rats were killed 24 hours later for edema measurements and an assessment of polymorphonuclear leukocyte (PMNL) infiltration by myeloperoxidase (MPO) assay. Compared with control groups, Ad.RSVIL-1ra treated rats had less brain edema formation in the ipsilateral basal ganglia 3 days after ICH (81.5 +/- 0.3% compared with 83.4 +/- 0.4% and 83.3 +/- 0.5% in control animals). Ad.RSVIL-1ra treated rats had also less brain edema following thrombin injection. The reduction of brain edema induced by thrombin was involved in the reduction of PMNL infiltration in basal ganglia, as assessed by MPO assay. Adenovirus-mediated overexpression of IL-1ra attenuated brain edema formation following ICH, perhaps by reduction of thrombin-induced brain inflammation.

Animals↗

PubMed2000

Induction of colligin may attenuate brain edema following intracerebral hemorrhage.

Brain edema plays an important role in the secondary brain injury following intracerebral hemorrhage (ICH). Edema formation after ICH has been linked to thrombin toxicity. Therefore, the induction of endogenous serine protease inhibitors, which inhibit thrombin prior to ICH may limit edema formation. This study examines whether injection of a low dose of thrombin upregulates such inhibitors and induces tolerance to subsequent ICH. Rats received intracerebral infusions of either one unit thrombin or saline into the right caudate nucleus. After seven days, the rats were either (A) used to examine colligin (a serine protease inhibitor) induction by Western blot analysis, immunohistochemistry and immunofluorescent double labeling, (B) to determine brain water content, or (C) they received a second injection of 50 microL blood and brain edema was determined one day later. Intracerebral infusion of thrombin caused a marked upregulation of colligin, a serine protease inhibitor, in the ipsilateral basal ganglia. Immunocytochemistry and immunofluorescent double labeling showed that colligin was induced in astrocytes. Infusion of this dose of thrombin alone did not affect brain water content but it significantly attenuated subsequent ICH-induced brain edema (79.0 +/- 0.5 vs. 81.4 +/- 0.9%, P < 0.01). Our results demonstrate that low doses of thrombin upregulate brain colligin levels and attenuate edema formation induced by ICH.

Animals↗

PubMed2000

Thrombin preconditioning, heat shock proteins and thrombin-induced brain edema.

Intracerebral injections of high concentrations of thrombin cause brain edema but, in vitro, low concentrations of thrombin may be neuroprotective. This study investigated whether a low dose of thrombin might induce tolerance to subsequent large doses of thrombin (thrombin preconditioning; TPC) in a manner analogous to ischemic preconditioning. The study involved five parts. The first tested the effect of intracerebral infusion of a small dose (1 U) of thrombin on brain water content. In the second part, the effect of such a small dose of thrombin on subsequent edema formation from a large dose of thrombin (5 U) was evaluated. The time course of TPC was examined in the third part. In the fourth part, heat shock protein (HSP) 27, HSP32 and HSP70 were quantitated by Western blotting analysis while the fifth identified the cell types expressing HSPs. Injection of a low dose of thrombin alone did not cause brain edema. However, TPC significantly attenuated the edema induced by a subsequent injection of a large dose of thrombin. This effect of TPC was abolished by co-injection of a thrombin inhibitor, hirudin. The maximal effect of TPC on edema formation was seven days after pretreatment. This time course was similar to that for a marked up-regulation in astrocytic HSP27. TPC also induced HSP32, but this effect occurred earlier than the effect on edema formation. TPC had no effect on HSP70. These results suggest that thrombin-induced brain tolerance may be related to HSP27 induction.

Animals↗

PubMed1994

Resolution of peritumoral brain edema following excision of meningioma.

We studied the resolution of peritumoral brain edema after meningioma excision. In twenty-nine patients with meningioma, the total volume of tumor and the peritumoral edema were measured planimetrically by serial CT scans and MRI with or without contrast enhancement. Four different patterns of postoperative resolution of hypodense volume on CT were observed: Group A: a large hypodensity rapidly decreased and disappeared, which may be related to the clearance of the real peritumoral edema in meningioma. Group B: a small hypodensity gradually disappeared. Group C: the hypodensity remained unchanged, which may result from the damaged brain tissue. Group D: the hypodensity progressively decreased but persisted, which may represent both the peritumoral edema and damaged brain tissue. We have calculated the resolution rate of edema fluid using the clearance curve of Groups A and D. The average resolution rate of edema fluid during the passage through 1 cm3 of the peritumoral white matter was 0.0493 ml/day. We speculate that 50% of edematous white matter, which presented as hypodensity on a CT scan, may be resolved in 4 days after total removal, and that 90% may be resolved in 14 days.

Blood-Brain Barrier↗

PubMed1994

Traumatic brain edema: an overview.

This article provides a brief summary of concepts describing the formation and resolution of traumatic brain edema. Recent laboratory and clinical data are reviewed targeted toward resolving the contribution of edema to the swelling process. These data, indicate that blood volume is reduced in areas of ischemia following traumatic injury and edema volume is increased. Thus, edema is the major contributor to the swelling process in diffuse injury. As clinical MRI studies have not revealed barrier compromise in the presence of swelling, it is considered that other forms of edema, primarily ischemic and neurotoxic, make a substantial contribution to the edema volume.

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↗

PubMed1994

Is the swelling in brain edema isotropic or anisotropic?

A study was conducted to examine whether swelling of the brain due to vasogenic-type and cytotoxic-type edema is isotropic or anisotropic. Vasogenic edema was induced by cryogenic injury in cats, and coronal sections of the brain were examined at 4-5 h after injury. The swelling of the edematous white matter longitudinal to and transverse to the subcortical neuronal fibers was 2.3% and 91.1%, respectively. Ischemic edema was examined using cortical tissue specimens of cat brain subjected to either middle cerebral artery occlusion for 3 h or immersion in saline after decapitation for 3 h. The swelling parallel to the left-right axis, caudo-rostral axis and antero-posterior axis was 9.6%, 10.1% and 8.5%, respectively. Neuroglial cell swelling was prominent in the ischemic cortex. Thus swelling of the white matter in vasogenic-type edema was anisotropic, whereas that of gray matter in cytotoxic-type (ischemic) edema was isotropic. This observed difference in the biomechanical properties of brain tissue should be taken into account when the etiology of edema-mediated tissue injury, such as herniation, secondary bleeding or ischemia is investigated.

Animals↗

PubMed1994

Formation and resolution of brain edema associated with brain tumors. A comprehensive theoretical model and clinical analysis.

The purpose of this study is to quantify the relative contribution of the mechanisms in the absorption of edema fluid. The convection/diffusion and the comprehensive bulk flow model were applied for the finite element analysis of peritumoral brain edema. For clinical analysis, 90 meningiomas studied by MRI were selected. Serial CT scan and MRI were performed at 0, 2, 4, 6 hours after injection of Iopamidol or Gadpenteic acid respectively. Then the tracer distributions in the edematous brain was analyzed. The tracer movement in the brain is well represented by the convection/diffusion equation. The absence of the preferential fluid flow directing toward the ventricle indicates that a limited role of CSF sink action into the ventricle. From capillary surface area (240 cm2/g brain), capillary hydraulic conductivity (1.8 x 10(-8) ml/cmH2O/cm2/min) and the simulated average tissue pressure of 9.8 mmHg, maximum absorption rate into capillaries was estimated to be 0.003 ml/h/cm3 brain tissue. Considering the limited role of edema fluid clearance into the ventricle, the results indicate a possible role of subarachnoid CSF space for the clearance of edema fluid. The clearance of edema fluid into subarachnoid CSF space should be studied quantitatively. Finally, unification of the convection/diffusion and the comprehensive bulk flow model will provide a more quantitative analysis of edema formation and resolution by using MRI and tracer studies.

Blood-Brain Barrier↗

PubMed1994

Peritumoral brain edema and cortical damage by meningioma.

Forty supratentorial meningiomas were analyzed to identify factors causing peritumoral brain edema. Parasagittal, sphenoid ridge, and olfactory groove meningiomas induced edema more frequently than those in other locations. Meningothelial meningiomas were more invasive than other types and were associated with more peritumoral edema. Brain edema correlated significantly with tumor size and histological evidence of leptomeningeal and cortical damage from the tumor. Larger tumors destroy the leptomeninges and cerebral cortex, allowing direct transmission of edema fluid into the white matter, resulting in vasogenic edema.

Adult↗

PubMed1988

Experimental drug therapy of peritumoral brain edema.

Four drugs with potential anti-peritumoral brain edema activity were studied using the VX2 rabbit brain tumor model. Meclofenamate and indomethacin were tested in an attempt to confirm recent reports of anti-edema activity in non steroidal anti-inflammatory drugs (NSAID's). The 'angiostatic' steroids 17 hydroxyprogesterone and epicortisol were tested because of their lack of glucocorticoid and mineralocorticoid effects and their structural similarity to glucocorticoids. The protein and water component of brain edema were indirectly quantitated. None of the test drugs demonstrated significant anti-edema activity. This work does not confirm reports that NSAID's have anti-edema activity and suggests that there may be no correlation between 'angiostatic' and anti-edema activity in certain steroid compounds.

17-alpha-Hydroxyprogesterone↗

PubMed1990

An immunocytochemical study of protein clearance in brain infusion edema.

The pathways and mechanisms by which edematous fluid accumulation in the extracellular space (ECS) clears from brain are poorly understood. The objective of this study was to explore, using immunocytochemical technique, the fate of a proteinaceous fluid added to the brain ECS and to study the clearance pathways. The protein movement of this edema fluid was investigated using the direct infusion model on rats. Rat albumin (20 microliters) was slowly infused into the caudate-putamen of anesthetized adult rats and the spread and clearance of the edema was followed in various brain regions using immunocytochemical and conventional light and electron microscopy at 0, 1, 2, 3, 4, 6, and 8 days post-infusion. Our studies showed that protein-rich edema fluid cleared slowly from the brain, with 8 days required for the infusion albumin to exit completely from the brain parenchyma. Immediately following infusion, the albumin was distributed in the ECS of the white matter and the overlying deep cortical layers related to the infusion site. During the next 24 h, more of the infused albumin traveled through the ECS to the cortical surface where the albumin passed through the glia limitans to reach the subarachnoid front. Additionally, at 48 h post-infusion, that albumin, which had migrated to the ventricular wall, cleared from the ECS of the subependymal white matter and the ependymal clefts to reach the ventricular cerebrospinal fluid (CSF). In edematous regions, the perivascular spaces of venules and veins were filled with reaction product. Continuity of this perivascular reaction product existed from the deep edematous area to the temporobasal subarachnoid space from where the reaction product gradually disappeared from the parenchyma. From these studies we infer that during the late state of the resolution process the edema front moves toward both the ventricle and the cortical surface to reach the CSF. Thus, among the potential routes for edema clearance, the pathways leading to CSF clearance of fluid predominated. During this clearance process, neither neurons, glia nor the vascular endothelium showed any endocytotic response to the infused albumin throughout the 8-day course. We conclude from these observations that the CSF pathway is the major route of protein-rich edema clearance, when such clearance is not complicated by any concomitant CNS perturbation.

Animals↗

PubMed1993

Cerebrovascular permeability and brain edema after cortical photochemical infarcts in the rat.

The importance of protein extravasation for the development of vasogenic brain edema is still controversial. We, therefore, assessed the cerebrovascular permeability to serum proteins in relation to the development and resolution of brain edema in a photochemical cortical lesion in the rat. Cortical infarction was induced by in situ thrombosis using an argon laser beam aimed at the exposed parietal bone in animals given rose bengal i.v. The histology and the cerebrovascular permeability to serum proteins were scrutinized from 2 h to 3 weeks after the insult. The presence of serum proteins was demonstrated by an immunoperoxidase technique. The cerebral water content was estimated by specific gravity measurements of the cortical tissue in a kerosene-monobromobenzene gradient column from 2 h to 7 days after infarction. The blood-brain barrier was permeable to proteins at 2 h following the insult and proteins spread into the medial and lateral tissue reaching a maximum at 24 h. The specific gravity did not deviate from control values at 2 h. After 8 h the specific gravity of the lesion decreased with smaller decreases in the immediately adjacent tissue. At 24 h the changes in specific gravities reached a maximum in all regions except the immediately lateral area. The edema was generally worse in tissue medial to rather than lateral to the infarct. The degradation of serum proteins and the resolution of the brain edema followed the same time course with partial resolution of 72 h. By 1 week serum proteins and edema were confined to the central necrotic core. The results suggest a relationship between cerebrovascular permeability and cerebral edema in photochemical cortical infarction.

Animals↗