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At least 19 recordsLinked to original sources
PubMedDate not supplied

Brain edema and blood-brain barrier permeability following quantitative cerebral microembolism.

Cerebral microemboli were formed in rats by injecting 4,000 carbonized microspheres, 50 +/- 10 mu in diameter, 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. The microspheres were mainly distributed in the cerebral hemisphere on the side of the injection. In 61 rats this hemisphere contained 582 +/- 20 microspheres against 99 +/- 9 in the contralateral hemisphere. Brain edema was assessed by measuring brain content of water, sodium and potassium. Blood-brain barrier (BBB) permeability was determined by brain accumulation of 125I-albumin. In the ipsilateral hemisphere brain edema and an increase in BBB permeability appeared 6 hours after embolization and progressed up to 48 hours. Twenty-four hours after embolization, significant correlations were observed between the microsphere content of the cerebral hemispheres and 1) the increases in water and sodium levels, 2) the decrease in potassium level, 3) the increase in BBB permeability. The study of these correlations should make it possible to ignore the poor reproducibility of embolizations and to analyze with increased accuracy the results of various experiments.

Animals↗
PubMed1979

Dynamics of cerebral edema. The role of an intact vascular bed in the production and propagation of vasogenic brain edema.

Brain edema was produced in cats by a standardized cortical freezing lesion. With a careful microsurgical tehnique, the injured cortex was removed as a single piece, either immediately after induction or at 2, 4, or 8 hours after lesion production. The injured brain was either discarded or replaced in its bed. Brain edema and the defect in the blood-brain barrier were assessed by determining percent dry weight, increase in volume of white matter, and spread of Evans' blue by planimetry. The results indicate that 1) if the lesion is removed immediately after production, formation of the expected vasogenic brain edema is completely abolished; 2) replacement of the frozen brain is unable to induce significant increase in permeability of the surrounding blood-brain barrier or a significant amount of brain edema; and 3) if the lesion is removed at 2, 4, or 8 hours with or without replacement, advancement of the edema front and increase in the amount of edema is stopped. It appears that an intact vascular bed is necessary for the extracellular fluid component of brain edema, and that no edemagenic factors exist within the injured brain in this model that influence either the production or propagation of the increased extracellular fluid volume.

Animals↗
PubMed1979

Tissue albumin and water content in the early stages of vasogenic brain edema formation.

Brain edema (BE) research lacks quantitative regional methods. We modified the method of Pappius and McCann (1969), who used radioactive iodinated I125 serum albumin (RISA) as a label for vasogenic BE fluid. To correct for intravascular plasma volume we used Cr51 labelled red blood cells and calculated equivalent extravascular plasma volume (EVPV). The modified RISA method was compared with a standard method for measuring increased tissue water, i.e. the change in wet:dry weights. Anesthetized rabbits were subjected to unilateral cortical freeze injury and sacrificed three hours later. The lesion corresponding to the area of blood brain barrier (BBB) breakdown was delineated by Evan's blue staining. That area and the two adjacent poles were sectioned. The contralateral hemisphere was used as the control. Good agreement was found between the two methods. By the modified RISA method, 4.08% of the wet weight of the injured hemisphere was EVPV while the decrease in dry weight corresponded to 5.56% edema. In the freeze lesion, however, where BBB breakdown occurred extravascular (EV) protein exceeded EV water, while adjacent to the lesion in the area with intact BBB, EV water exceeded EV protein. This suggests that the diffusion rate for water through brain tissue exceeds that of albumin in the early stages of vasogenic BE formation. We conclude that the modified RISA method is a satisfactory measure of regional vasogenic BE in acute animal experiments.

Animals↗
PubMed1979

The effect of intracerebral ouabain administration on the composition of edema fluid isolated from cats with cold-induced brain edema.

Brain edema fluid was collected from cats with a freezing lesion in the left parietal cortex by the insertion into the brain of needles containing nylon wicks and connected to polyethylene tubes. The edema fluid samples which accumulated in the polyethylene tubes were regularly analyzed for Na+ and K+ content, colloid osmotic pressure, lactate dehydrogenase and creatine phosphokinase activity, and 99mTc-albumin radioactivity; the albumin tracer being introduced intravenously at the time of cold-injury. One series of cats received an intracerebral injection of ouabain solution, the control series an intracerebral injection of saline, at 100 min after the cold-injury. The ouabain injection was followed by an increase of K+ content, LDH and CPK activities but a decrease of Na+ concentration in the edema fluid, attributable to a concentration of solutes in the edema fluid as presumably water and Na+ were shifted into the cells and hence the extracellular space was reduced.

Animals↗
PubMed1979

[Effect of nootropil and contvykal on the structural changes in the central nervous system in hypoxic brain edema].

The brain cortex of rabbits exposed to 15-minute ishemia in the presence of monitored hypotonia was studied in 27 experiments in order to verify the efficacy of nootropil and contrykal as agents intended for the treatment of posthypoxic edema of the brain. The therapeutic efficacy was assessed on the basis of the evidence obtained with the aid of light and electron microscopy. It was found that nootropil exerts a favourable action on the ultrastructure of intracellular organella of the neuron: mitochondria, lysosomes, ribosomal apparatus, nuclear envelope, etc. Under the effect of nootropil and contrykal the posthypoxic microcirculatory changes showed signs of compensation and proved reversible. Manifestations of posthypoxic edema of the brain were less pronounced. It is suggested that the efficacy of the treatment regimen offered is related to the normalizing effect of nootropil on metabolic and repair processes in neurons and cellular elements pertaining to the microcirculatory system as well as with a direct action of contrykal on the local factors of capillary permeability.

Animals↗
PubMed1979

Effects of dexamethasone on tumor-induced brain edema and its distribution in the brain of monkeys.

A human choriocarcinoma was successfully adapted to grow in the brain of monkeys (Macaca mulatta), thus providing a model of tumor-induced brain edema. Four animals were given dexamethasone (3 mg/kg/day) during 3 to 5 days after the onset of clinical signs, and the other five received no treatment for the same period. Tissue water and electrolyte content of treated and untreated animals were compared in cortex and white matter at various distances from the edge of the tumor. In untreated animals, 67.9% and 23.6% swelling was detected in adjacent and remote white matter, respectively, but only 11.8% swelling was noted in adjacent cortex. In animals treated with dexamethasone these percentages of swelling were improved to 32.4% and 11.9% in the corresponding white matter, and to 4.9% in adjacent cortex. The electrolyte changes shown in edematous brain of control animals also demonstrated significant improvement in the dexamethasone-treated group. Tissue radioactivity of 3H-dexamethasone at 60 minutes after intravenous injection was high in the periphery of tumor, adjacent cortex, and white matter, but low in the center of tumor, remote cortex, and white matter. The sites with high concentrations of dexamethasone also showed significant improvement of brain edema after dexamethasone treatment, suggesting that dexamethasone may act directly at these loci.

Animals↗
PubMed1979

Electroencephalography in brain edema (127 cases of brain tumor investigated by cranial computerized tomography).

Cranial computerized tomography (CCT) in permitting visualization of cerebral edema in live patients, allows for the first time valid studies concerning the role of reactional edema in the generation of EEG abnormalities related to expanding processes. The authors analyze the results of EEG and CCT in 127 patients presenting cerebral tumor(s), 84 of which were accompanied by reactional edema. The study leads to the conclusion (also demonstrated by certain animal work) that edema per se is only rarely responsible (9.5%) for the EEG abnormalities.

Brain Edema↗
PubMed1979

Composition of isolated edema fluid in cold-induced brain edema.

Edema fluid isolated from cats with cold-induced brain edema was subjected to analysis of electrolyte content, enzyme activities, colloid osmotic pressure and the radioactivity of intravenously injected 99mTc-labeled albumin. The findings corroborate the essential features of vasogenic edema, such as its origin from the blood plasma, its rapid propagation into the white matter of the brain as contrasted with the delayed spread into gray matter, and its contribution to composition of cerebrospinal fluid. Moreover, the elevated activities of cellular enzymes and K+ content of edema fluid point to the admixture with cellular contents due to the freezing damage.

Albumins↗
PubMed1977

Osmotic opening of the blood-brain barrier in the rhesus monkey without measurable brain edema.

The blood-brain barrier in the rhesus monkey was opened to intravascular Evans blue-albumin, without causing brain edema or altering brain electrolytes, by perfusing 2.5 molal recrystallized D,L-lactamide into the internal carotid artery for 20--30 sec. Gross neurological and behavioral sequelae were absent in 7 of 8 animals with barrier opening, and 2 days after perfusion no statistically significant changes were observed in sodium, potassium or water contents of perfused as compared to unperfused gray and white matters of brains of the 7 normal animals. Brain endema may not have developed because parenchymal albumin was excreted or metabolized by 2 days. It is suggested also that closure of the barrier after several hours prevents salt from accompanying plasma fluid into the brain. Entry of fluid without salt would reduce, before measurable edema developed, any transcapillary osmotic gradient established by prior entry of plasma albumin.

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↗
PubMed1978

Therapy of ischemic brain edema.

With corticosteroids and diuretics, glycerol treatment may be an effective therapy of early edema accompanying focal brain ischemia. The suggested regimen for intravenous infusion is 500 ml of 10% glycerol solution during at least 2 h, twice a day, starting as soon as possible after stroke onset and continuing thereafter for 5--7 days.

Brain Edema↗
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↗
PubMedDate not supplied

Report of Joint Committee for Stroke Resources. IV. Brain edema in stroke.

A classification of brain edema is provided as well as an extensive review of the animal models from which we have derived most of the basic information we have about the formation and resolution of edema. The clinical aspects of cerebral edema in stroke are discussed and also modern methods for identifying cerebral edema in the human. Attention is given to computed tomography and enhanced CT and advances in their application to this condition. Treatment of cerebral edema in the stroke patient using glycerol, dextran 40, mannitol, steroids, and other drugs is discussed and the need pointed out for controlled clinical trials of the therapeutic effectiveness of these agents.

Adrenal Cortex Hormones↗
PubMed1979

Influence of hypoxia on the composition of isolated edema fluid in cold-induced brain edema.

The isolation of edema fluid from cats with cold-induced cerebral edema allowed the study of changes of Na+ and K+ content, lactate dehydrogenase and creatine phosphokinase activity, colloid osmotic pressure and the level of intravenously administered 99mTc-albumin in the edema fluid during a period of hypoxia. The changes consisted of an increase of all mentioned parameters, except Na+; and could be interpreted as a concentration of solutes (but for Na+) in the extracellular edema fluid, concomitant to a reduction of the extracellular space, as the oxygen deficiency caused improper functioning of the cellular Na+-K+ pump, with a resulting shift of fluid (including Na+) into the cellular elements.

Albumins↗
PubMedDate not supplied

Brain edema during ischemia and after restoration of blood flow. Measurement of water, sodium, potassium content and plasma protein permeability.

The left cerebral hemisphere of Mongolian gerbils was used to elucidate the mechanisms of brain edema which develop during cerebral ischemia and after restoration of cerebral blood flow following temporary ischemia. Water content was measured by the tissue-drying method. Sodium and potssium ion concentration was measured by flame photometry. Passage of 131I-albumin (RISA) from blood to the cerebral parenchyma was measured on a gamma scintillation counter. Our findings indicate that pure cytotoxic edema develops during ischemia and during a short period after restoration of cerebral blood flow. Vasogenic edema, which is accelerated by the leakage of plasma constitutents from blood due to blood-brain barrier damage, developed after restoration of the cerebral blood flow. After less than 1 hr of ischemia, restoration of the cerebral blood flow drastically reduced the degree of brain edema. However, restoration of the cerebral blood flow greatly worsened the brain edema following more than 3 hr of ischemia.

Animals↗