Factors affecting the extension of peritumoural brain oedema. A CT-study

Summary In human brain tumours the extension of peritumoural brain oedema may vary considerably. 37 brain tumours of various pathology and 2 abscesses were examined to identify the factors and mechanisms responsible for the oedema spreading. Peritumoural oedema profiles were determined towards the white matter and ventricle by measuring the CT-numbers of consecutive tissue blocks of 3.0–3.6 mm from the tumour to the normal white matter or the ventricle. It was found that neither the size of the tumour nor the histology has a close relationship to the amount of peritumoural oedema. The distance of oedema spreading rather is determined by the amount of fluid accumulation in the white matter immediately bordering the tumour. This relationship corresponds to a semilogarithmic function and represents the relation between the tumour-adjacent accumulation of extracellular fluid volume and the distance of extracellular fluid movement. The analysis of this relation leads to the suggestion that pressure gradients and bulk flow are involved in the development of human peritumoural oedema.     

A study on peritumoural brain oedema around meningiomas by CT and MRI scanning

Summary There is a great variability in the amount of peritumoural brain oedema accompanying meningiomas. In a previous study it was found that the degree of brain oedema in the white matter around meningiomas correlated with disruption of the layers (especially the cerebral cortex), which separate the tumour from the white matter, as well as with the size and histological subtype of the tumour.In the present study comprising 9 meningiomas, the volume of oedema was calculated by integration of the cross-sectional oedematous areas on serial MRI slices. The volume of oedema was zero in 3 cases and ranged from 11 to 176.4 ml in the other 6 cases. The MRI-scans also showed disruption of the cortex in all cases, ranging from slight to severe. T₁ and T₂ measurements were made at the level of maximum extension, using a mixed sequence at a field strength of 1.5 T. From the T₂ values tissue water content in % was calculated using the equations: WC=39.36/(R₂ + 37.2) for cortex, and WC=29.63/(R₂ + 27.8) for white matter. These had been obtained by correlating water content with relaxation rates, measured in vitro on human brain autopsy specimens which were subjected to hydration with distilled water or dehydration by hyperosmolar solutions. Mean water content amounted to 82.53% for normal cortex, 74.72% for normal white matter, and 84.59% for oedematous white matter around the tumour.On the assumption that the spread of contrast agent marks the advancement of the front of oedema produced by the tumour, CT-studies were made before, and at 1 1/2, 3 and 6h after contrast infusion. The increase in diameter of the contrast-stained area on the CT-scan allows calculation of the excess of oedema production per unit tumour volume. Of 6 tumours with oedema (mean peritumoural water content of 91% and mean volume of oedema of 69.2 ml) the production excess at the steady-state was 0.18–1.08 ml/h/cm³ tumour volume, whereas 3 tumours without associated oedema had a production excess of 0.03–0.12 ml/h/cm³. Moreover, penetration of the cortex seems to constitute a separate factor determinig the spread of oedema.     

Experimental transplantation gliomas in the adult cat brain

Summary In adult cats experimental brain tumours were produced by stereotactical xenotransplantation of the rat glioma clone F 98 into the internal capsule of the left hemisphere. Two to four weeks after transplantation tumours and peritumoural oedema were investigated by magnetic resonance imaging (MRI), electrophysiological recording and analysis of tissue content of water, electrolytes and extravasated serum proteins.Spherical tumours with a diameter of about 10 mm developed at the injection site and were surrounded by massive white matter oedema. Water content in peritumoural white matter increased from 2.63 ± 0.17 to 3.65 ± 0.19 ml/g d.w. (means ± SD), sodium from 187±11 to 351±55 eq/g d.w. and calcium from 7.4±1.1 to 13.3 ± 1.3 ± 1.3 eq/g d.w. Potassium and magnesium did not change. Oedema development was associated with the extravasation of 18.0 ± 16.8mg/g d.w. albumin and 15.8 ± 12.2 mg/g d.w. immunoglobulin. The calculated electrolyte content of oedema fluid approximated that of plasma but the serum protein content was about 40% lower. The ratio of low (albumin) to high (immunoglobulin) molecular weight proteins was the same in blood and oedema fluid. It is, therefore, concluded that peritumoural oedema consist of two components,a whole plasma extravasate and a protein-free ultra-filtrate.Peritumoural oedema could be clearly detected by MRI but differentiation between tumour and oedema was only possible after contrast enhancement with gadolinium-DTPA. The ratios of the intensities of the MR signal correlated linearly with the water content within white matter. MRI, in consequence, allows quantification of oedema provided a reference area with normal water content is present.     

Corticosteroid therapy of experimental tumour oedema

Summary Experimental brain tumours were produced in cats by stereotactic implantation of 4 million suspended cells of a rat glioma clone into the internal capsule. Three weeks after implantation a spherical tumour developed with a diameter of up to 10 mm which was surrounded by vasogenic white matter oedema. In untreated animals water content in the peritumoural white matter increased from 69.1 ± 0.9 to 80.0 ± 0.8 ml/100 g w. w., and regional blood flow reciprocally decreased from 32.2. ± 5.6 to 18.9 ± 0.05 ml/100 g/min. A single injection of a crystalline suspension of 10 mg/kg dexamethasone given intramuscularly one week before the animals were killed, led to a significant amelioration of brain oedema. Peritumoural white matter water content decreased to 73.0 ± 0.5 ml/100 g w. w. and blood flow rose to 35.7 ± 2.8 ml/100 g/min. These changes were accompanied by parallel shifts of electrolyte content but they did not correlate with EEG activity, as assessed by Fourier frequency analysis. Corticosteroids did not prevent extravasation of peroxidase or Evans blue across the tumour vessels. The beneficial effect, therefore, is attributed to either an acceleration of resorption or an inhibition of the spread of oedema from the tumour into the peritumoural brain tissue.     

Brain swelling and brain oedema in acute head injury

Summary Chronological changes in diffuse brain swelling and brain oedema were studied in repeated CT studies following a closed head injury. These findings were compared with changes in intracranial pressure (ICP). The grades of diffuse brain swelling were classified into mild, moderate and marked according to the CT findings. Planimetry of low density areas of brain oedema was carried out on repeated CT images. Diffuse brain swelling was recognized in 71 of patients shortly after the head injury and subsided within days 3–5. Brain oedema first appeared 24 hours post injury and did not reach its maximum size and distribution before days 5–8. Thus, these two events can be clearly separated. The intracranial pressure reflected the course of the brain swelling and was not very high during the presence of maximum oedema.     

Technical Note: A new Model for Quantitative Analysis of Brain Oedema Resolution Into the Ventricles and the Subarachnoid Space

Summary  Objective. The aim of the current study was to develop an experimental animal model for quantitative analysis of oedema resolution via the subarachnoid space and the ventricular system using fluorescent oedema markers.  Methods. Artificial cerebrospinal fluid (CSF) containing TRITC-albumin (MW 67.000D) and Na⁺-fluorescein (MW 376D) was continuously infused into the white matter of the left frontal lobe of New Zealand white rabbits (n=6) at a rate of 100 μl/h for 3 hrs. A closed cranial window for superfusion of the brain surface with artificial CSF fluid (3 ml/h) was implanted above the left parietal cortex for measurement of the fluorescence markers in the subarachnoid space. Uptake of the fluorescence indicators into the ventricles was quantified by ventriculo-cisternal perfusion (3 ml/h). The effluates were collected at 30 min intervals for 3 hrs after the start of infusion. Clearance of the oedema fluid into the perfusates was measured by fluorescence spectrophotometry.  Results. At an intracranial pressure of 15.0±1.7 mm Hg (mean±SEM) both indicators started to accumulate in the subarachnoid and ventricular perfusates at 90 min following onset of oedema fluid infusion. The concentrations of the indicators in the ventricular system increased to 7.7±5.1% of Na⁺-fluorescein and 16.1±13.0% of TRITC-albumin of the total amount infused were recovered in the ventricular system at 3 hours after start of the oedema infusion, while 3.4±3.2% of Na⁺-fluorescein and 3.7%± 3.2 of TRITC-albumin, respectively, were found in the effluates of the subarachnoid space.  Conclusion. The present study demonstrates that resolution of vasogenic brain oedema into the cerebral ventricular system and the subarachnoid space following its entry into cerbral white matter can be quantitatively analysed using fluorescence markers, which serve as oedema fluid indicators. The results indicate that the oedema fluid is cleared not only into the ventricular system but also via the subarachnoid space.     

Peritumoural brain oedema in intracranial meningiomas: Influence of tumour size, location and histology

Summary Peritumoural brain oedema was examined retrospectively in 175 patients with 179 intracranial meningiomas. The influence of tumour size, location and histology were investigated.Tumour volume and localization, and the presence of peritumoural brain oedema (PTBOe) were determined by computed tomography (CT). The oedema-tumour volume ratio was defined as Oedema Index (Oel). All patients underwent microsurgical removal of the tumour. Surgically resected meningiomas were classified histopathologically based on criteria of the new World Health Organization (WHO) classification. A close relationship was found between the tumour size and the incidence of peritumoural oedema: with increasing size of the tumour the incidence of oedema also rises, the oedema index, however decreases. Frontobasal and temporobasal meningiomas showed a significant increase in the oedema incidence and the mean oedema index. If major parts of the surface of meningiomas were adjacent to subarachnoid cisterns only a slight tendency for the development of oedema was observed. WHO-III-meningiomas showed a significantly higher oedema incidence (61.1% vs. 94.4%; p<0.004) and mean oedema index (Oel=2.7 vs. 3.7; p<0.0009) than WHO-I-meningiomas. Brain tissue was affected in 59 cases. 19 meningiomas with infiltration into adjacent brain parenchyma revealed a statistically significant increase in oedema incidence (94.7% vs. 51.7%; p<0.0003) and mean oedema index (Oel=3.9 vs. Oel=2.2; p<0.0001) when compared to tumours without any brain tissue involvement in the histopathological specimens. Tumours with large volume, fronto-temporo-basal location and anaplastic histology were not only associated with the highest incidence of oedema formation but also presented with an overproportionate infiltrative growth. Thus, a disruption of the arachnoid or a true brain infiltration may be an essential factor for the development of a PTBOe.     

The contribution of arachidonic acid to the aetiology and pathophysiology of focal brain oedema; studies using an infusion oedema model

Summary Arachidonic acid solution (2 to 15 mg/ml) was infused into the right forebrain white matter of anaesthetised cats over three hours to evaluate its contribution to the genesis and pathophysiology of vasogenic brain oedema.The 0.6 ml infusion increased local white matter water content by a mean of 11.3 ml/100 g tissue but did not increase cortical water content. Histological studies revealed local expansion and trabeculation of the white matter with aggregations of granulocytic neutrophils in the venules and perivenular brain. The adjacent cortical cytoarchitecture was normal. The white matter around the infusion site was stained lightly and over a variable area (15–20 mm²) by intravenously administered Evans Blue dye 2%.Regional cerebral blood flow (rCBF) adjacent to the frontal infusion did not change significantly during the period of infusion and remained similar to rCBF in the contralateral hemisphere. Following the arachidonic acid infusion regional CBF CO₂ reactivity was normal and three was no asymmetry of either cortical somatosensory evoked potential (SEP) or motor evoked potential (MEP) waveforms.The increase in brain water content and changes in the ICP and ICP related biodynamics (pressure-volume index, lumped craniospinal compliance and CSF outflow resistance) were similar to those seen following infusion of 0.6 ml saline. These studies suggest that free intraparenchymal arachidonic acid, at concentrations exceeding those occurring in most neuropathological conditions, can increase the normal brain parenchymal capillary permeability but does not disrupt focal cerebrovascular and electrophysiological function. The clinical implications of these findings are discussed.Presented in part at Brain Oedema VIII, Bern, Switzerland, June, 1990.     

Measurement of changes in brain water in man by magnetic resonance imaging

John Hunter was undoubtedly aware of the water content of normal brain tissue, and described cerebral oedema. The advent of nuclear magnetic resonance (NMR) shed new light on brain water, and the derivation of spatial information and hence images from NMR signals, has permitted studies of regional brain water in man in vivo. The initial study described here tested whether NMR longitudinal relaxation time (T1) correlates with brain water content in the cerebral cortex and white matter in man, and significant relationships have been demonstrated in cortex (r = 0.65, P less than 0.002) and white matter (r = 0.94, P less than 0.0001), the latter having narrow 95% confidence limits. The residual variance allows the prediction of water content from the T1 of white matter, measured from the image of a single patient, with an accuracy of +/- 4% of total tissue water with 95% confidence. In the further study described, the effects of dexamethasone and an infusion of 20% mannitol on brain water content has been assessed in patients with intrinsic cerebral tumours. Dexamethasone had no significant effect on the T1 of normal brain, oedematous peritumoural white matter, or tumour tissue. It must be concluded that the water content of these tissues is not changed by dexamethasone and that the clinical improvement seen in patients with cerebral tumours immediately after dexamethasone has to be explained by some mechanism other than a reduction in cerebral oedema. Mannitol did reduce the T1 of oedematous peritumoural white matter, and the T1 of tumour tissue, but did not change the T1 of normal brain significantly.(ABSTRACT TRUNCATED AT 250 WORDS)     

Rebound of ICP after brain compression

Summary The rebound of intracranial pressure (ICP) occurring after decompression of an intracranial mass lesion was studied in an epidural balloon compression model. Intracranial morphology and brain tissue water content were assessed with magnetic resonance imaging (MRI). Fast and slow components of the transverse relaxation time (T2) were used as indicators of brain oedema development.During balloon compression a progressive prolongation of both the fast and the slow T2 components took place. Following deflation of the balloon both components increased rapidly, particularly the slow-T2. The MR scans displayed progressive occlusion of the aqueduct, and obliteration of the ambient and pontine cisterns. The changes in morphology and in water content after decompression had largely the same time course as the development of the rebound of ICP. In contrast, no changes in morphology and tissue water content occurred after hydrostatic brain compression achieved by subarachnoid fluid infusion.The findings suggest that the intracranial pressure rebound is caused by cerebral oedema accumulated during and particularly in the recirculation phase after an ischaemic injury of adequate intensity and adequate duration.     

Cerebral oedema associated with WHO-I,WHO-II,and WHO-III-meningiomas: Correlation of clinical,computed tomographic,operative and histological findings

Summary Meningiomas were studied in 60 patients retrospectively. Clinical, operative and histological findings were correlated with the occurrence and extension of peritumoural oedema as measured by computerized tomography. A relationship was found between both oedema and seizures and between oedema and tumour location. No relationship between tumour size, arachnoid breaching, WHO-grade or tumour vascularity and oedema was detected. In four patients with severe pre-operative oedema, cerebral signs and symptoms persisted despite uncomplicated tumour removal.The present study shows that peritumoural oedema is not only epileptogenic but that it can also cause irreversible cerebral damage as well. Since this study purports to demonstrate that meningiomas with intact leptomeninges can show severe peritumoural oedema, the blood barrier breakdown theory cannot be considered as the only aetiological factor.     

The importance of protein content in the Oedema fluid for the resolution of brain Oedema

Summary The infusion model of oedema is developed in the rat. Unilateral, constant volume, intracerebral infusions of oedema fluid of varying protein (bovine albumin) concentrations are performed. Brain tissue is analyzed for water content using the gravimetric technique. The authors find significant differences in the spatial distribution of brain water in the different infusion groups at 48 and 72 hours post infusion. The control infusate (mock cerebrospinal fluid) clears by 72 hours. However, infusates containing protein (32.5 and 65.0mg/ml albumin) are not completely cleared until 5 to 8 days post infusion, with the less concentrated solution clearing more rapidly in the area of infusion at 72 and 96 hours post infusion. The data support the hypothesis that the rate of clearance of vasogenic brain oedema is dependent on the amount of extravasated protein.This work was supported by NIH Grant 5RO1NS19235-03.     

Resorption of peritumoural oedema in cerebral gliomas during dexamethasone treatment evaluated by NMR relaxation time imaging

Summary Peritumoural brain oedema is a prominent feature of malignant brain tumours. Glucocorticoids diminish the neurological symptoms and signs caused by the oedema and reduce the abnormally high cerebral water content. The exact mechanisms of action of the glucocorticoids are unknown.The present study investigates the influence of dexamethasone on NMR relaxation time T₁ in peritumoural oedema in 13 patients with gliomas. It is shown that NMR T₁ images can be used as a potent monitor of brain oedema, and that dexamethasone significantly reduces mean T₁ after 1, 3, and 7 days of treatment by 2%, 6%, and 13% respectively.Using an image histogram analysis technique the term superoedema was defined as the 50% of the total oedema area with the highest t₁, corresponding to the highest water content. It is shown, that with this technique the treatment effect of steroids on superoedema was a reduction of 13%, 33%, and 57% after 1, 3, and 7 days of treatment respectively. The mean change after 24 hours of treatment was statistically significant (p < 0.01).The method can be used in all situations where the anti-oedematous effect of a given treatment is to be monitored.     

Angiogenesis and Brain Oedema in Intracranial Meningiomas: Influence of Vascular Endothelial Growth Factor

Summary The correlation between angiographic neovascularization, peritumoural brain oedema (PTBOe) and the expression of vascular endothelial growth factor (VEGF) , was analysed in 30 patients with intracranial meningiomas. Pre-operative angiograms were examined for the existence of either an exclusively dural tumour blush or an additionally pial tumour supply from cerebral arteries. Furthermore the presence of macroscopic tumour-neovascularization and dysplastic changes of tumour-draining cerebral veins was evaluated. VEGF expression was investigated on histological tissue samples, using immunohistochemical techniques. VEGF immunohistochemistry and neuroradiological evaluations were performed in double blind fashion. Tumour volume and the amount of oedema were calculated by computerized tomography (CT) or magnetic resonance imaging (MRI). The oedema-tumour volume ratio was defined as oedema index (OeI). Compared to VEGF-negative meningiomas, tumours with striking VEGF staining revealed a significant higher mean oedema index (OeI=4,2 vs. OeI=1,5; p<0.018), and a higher oedema incidence (91,7% vs. 44,4%; p<0.046). Equally, meningiomas with additionally tumour supply from cerebral arteries were associated with a significant higher mean OeI (OeI=4.1 vs. OeI=1.2; p<0.01) and oedema incidence (94,7% vs. 20,0%; p<0,0023) than meningiomas with exclusively tumour supply from dural arteries. All meningiomas with striking VEGF-expression were associated with vascular tumour supply from cerebral arteries, but VEGF-negative tumours only in 50% (p<0.029). These data suggest a link between VEGF-expression, arterial tumour supply and peritumoural brain oedema. The development of tumour supply from cerebral arteries may be important for formation of meningioma-related oedema. Therefore, VEGF may represent a potent mediator in the evolution of this type of vascularization in meningiomas.     

Attenuation of cryogenic induced brain oedema by arginine vasopressin release inhibitor RU51599

Summary Centrally released arginine vasopressin (AVP) has been implicated in the regulation of the brain water content and is elevated in the cerebrospinal fluid of patients with ischaemic and traumatic brain injuries. The protective effect of RU51599, which is a selective kappa opioid agonist as an AVP release inhibitor, on brain oedema was examined. Male Wistar rats, weighing 300 to 400 g each, were used. The cortical cryogenic injury was produced by application of a previously prepared metal probe cooled with dry ice to the dura of the right patietal region. Animals were separated into three groups. Group 1: sham operated rats without lesion production. Group 2: saline-treated rats with lesion production. Group 3: RU51599-treated rats with lesion production. In Group 3, rats were treated with RU51599 (0.1–3 mg/kg) at 30 minutes before lesion production, 1 hour, 2 hours, and 4 hours after lesion production. After 6 hours, animals were decapitated and brain water contents were measured using the dry-wet weight method. The extent of blood brain barrier (BBB) disruption was determined by assessment of Evans blue uptake based on extraction from tissue using dimethylformamide. The primary injured infarcted area was determined by 2,3,5-triphenyltetrazolium chloride (TTC) staining. Sodium and potassium contents in serum and brain tissue were measured using atomic absorption spectrophotometry. The antagonism of naloxone against protective effects of RU51599 on cryogenic induced brain oedema and on antinociceptive effects in acetic-acid treated animals was examined. Statistical analysis was performed using Dunnett-test and U-test following Kruskal-Wallis test. RU 51599 significantly reduced the brain water contents on the injured side and the contralateral non-injured side (p<0.01) after 4 administration of 1 and 3 mg/kg. RU51599 neither significantly inhibited BBB disruption nor reduced the primary injured infarcted area. RU51559 significantly increased brain sodium and potassium contents in the injured brain and also increased serum sodium levels (p<0.01). Naloxone antagonized the anti-oedema effects and antinociceptive effects of RU51599. These findings indicate that the AVP release inhibitor, RU51599 posssibly mediated by opioid receptors, has a potential protective effect on cryogenic-induced brain oedema and that centrally released AVP plays an important role in the progression of vasogenic brain oedema.     

Intracranial hypertension and brain oedema in albino rabbits. Part 3: Effect of acute simultaneous diuretic and barbiturate therapy

Summary Increased intracranial pressure due to brain oedema was produced in albino rabbits by combining a cryogenic lesion in the left hemisphere with the intraperitoneal administration of 6-aminonicotinamide (cytotoxic agent). The following parameters were assessed: intracranial pressure (ICP), systolic arterial pressure (SAP), central venous pressure (CVP), EEG, brain water and electrolyte content, gross pathology, and blood brain barrier integrity. Acute therapy to reduce ICP was performed by administering a bolus of mannitol (1 gm/kg) and 30 minutes later, also in bolus, frusemide (5 mg/kg). Immediately following the administration of mannitol an infusion of pentobarbitone was commenced; this was continued for one hour so that a total of 10 mg/kg was administered.There was a 50% reduction of ICP at one hour from initiation of treatment. The brains of the animals were extracted immediately upon cessation of therapy (pentobarbitone) and they revealed a significant reduction of water content for the right, uninjured, hemisphere only, when compared to controls; a slight but not significant reduction of the brain sodium and potassium was noted in both hemispheres. There was no change noted in the gross pathology and extent of blood brain barrier breakdown. In all animals epinephrine infusion had to be administered for between 20 and 30 minutes to maintain a SAP over 80 torr. There seems to be no advantage in the simultaneous administration of barbiturates and diuretics for the control of ICP due to brain oedema.     

Decompressive frontal lobe resections and brain oedema

Summary Thirteen patients with expanding mass lesions underwent postoperative serial CT scanning after frontal lobe resection. Cases with malignant tumours and significant preoperative oedema showed a rapid postoperative filling of the resection cavity which presumably reflects increased intracranial pressure. Cases with more benign lesions without significant preoperative oedema continuously maintained an empty resection cavity. The results suggest that the clinical outcome after frontal lobe resection can be predicted from preoperative CT scans.     

Spatial and quantitative distribution of human peritumoural brain oedema in computerized tomography

Computerized tomography (CT) was used to study the pathways of oedema spreading in man. Based on the assumption that local changes in CT numbers in oedematous white matter closely correspond to changes in tissue water content, CT numbers of consecutive tissue blocks of 3.0-3.6 mm were examined in the main directions of oedema spreading: towards the deep white matter, towards the cortex and towards the ventricle. Tumours with oedema grade II and III showed a reduction of CT number of 10 +/- 1.8. The corresponding increase in water content of about 10-12% seems to be an upper limit of fluid accumulation in the white matter. From this oedema centre, water content very slowly and gradually decreased along the oedema projection into the deep white matter. In contrast, if oedema reached the cortex of adjacent gyri, the decline in water content was very sharp. A similar observation was made in the external capsule where oedema sharply declined at the border to the adjacent grey matter, putamen and claustrum. Oedema projection towards the ventricle showed a nearly uniform magnitude from the centre to the ventricular lining, suggesting a certain resistance by a limited capacity of transependymal drainage of oedema fluid. It is assumed that the spatial distribution and extension of oedema around a brain tumour is determined by a system of differential resistance to fluid movement in the following order: grey matter--ventricular lining--white matter.     

Experimental transplantation gliomas in the adult cat brain

Experimental brain tumours were produced in adult cats by stereotactic xenotransplantation of the rat glioma clone F98. Regional ATP, glucose and lactate were measured after 2-4 weeks on coronal cryostat sections by substrate-induced bioluminescence, potassium content was imaged by the histochemical sodium cobaltinitrite method, and regional pH by incubating cryostat sections with the fluorescent pH-indicator umbelliferone. The regional biochemical alterations were correlated with magnetic resonance imaging and tissue water content. Biochemical changes were heterogeneous in tumours but exhibited a rather uniform pattern in peritumoural oedema. ATP was consistently reduced, glucose and lactate were increased and pH was more alkaline than in normal white matter. The decrease of ATP matched the increase of water, indicating that ATP decline represents fractional dilution in the oedematous tissue rather than break-down of energy metabolism. The increased lactate levels, therefore, may originate from the tumour and not from a metabolic disturbance in the peritumoural oedematous tissue. The implications of this interpretation for the pathogenesis of peritumoural oedema are discussed.     

Determination of endogenous serum proteins in normal and oedematous brain tissue of cat by rocket and crossed immunoelectrophoresis

Summary A quantitative method for determination of endogenous serum proteins has been established and tested in an experimental model of peritumoural brain oedema in cats. Rocket and crossed immunoelectrophoresis were applied for determination of total serum proteins, albumin, IgG and haemoglobin in blood and brain homogenates. Modifications such as the use of non-ionic detergents and of antisera with different specificity were established for each antigen under investigation. The content of total serum proteins, albumin and IgG was substantially higher in tumour and peritumoural brain tissue than in the non-oedematous brain. The measurement of haemoglobin allowed the calculation of blood volume and, in consequence, the differentiation between intra- and extravascular serum proteins. The results are in line with earlier measurements obtained by different analytical methods and demonstrate that the present technique provides a reliable approach for the quantitative assessment of serum protein extravasation.