[Therapy of space-occupying intracranial processes (brain edema, brain tumor) and low cerebrospinal fluid pressure].
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Adrenal Cortex Hormones↗
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Blood-to-brain sodium transport in ischemic brain edema.
Brain edema is a frequent complication of cerebral ischemia; however, its mechanism of formation is not well understood. Sodium is known to accumulate in brain during the early stages of partial ischemia. Therefore, the present studies were undertaken to determine the relation among BBB sodium transport, integrity of the BBB, and development of brain edema during the first 24 hr after the onset of cerebral ischemia. Partial cerebral ischemia was produced in gerbils by ligation of the left common carotid artery under ether anesthesia. After recovery from the anesthetic, animals were scored for the presence of symptoms, and those with scores greater than 10 of 25 (n = 87) were chosen for this study. Measurements of tissue water, sodium, and potassium contents, and brain uptake of 22Na and 3H-mannitol were made in each group at 1.5, 3, 6, 12, and 24 hr after carotid ligation. Accumulation of sodium and water in the ischemic compared with the nonischemic cerebral cortex was progressive. This edema formation was not of the vasogenic type because the permeability of the BBB to mannitol was unchanged. Blood-to-brain sodium transport was reduced by 30% to 40% at all time points in the ischemic cortex. Nevertheless, the remaining sodium transport activity appeared to play a role in the development of brain edema because Na accumulated in the tissue at a rate that was approximately the same as the rate of 22Na uptake from blood.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
[Physiopathology of brain edema].
Brain edema (BE), defined as an increase in tissue water content leading to an increase in tissue volume, is a common histopathologic response associated with a number of acute and subacute brain lesions. In some cases BE is a result of an unbalance of physical forces, hydrostatic or osmotic gradients driving the water in the tissue (hypertensive encephalopathy, hydrocephaly, plasma hypoosmolarity). In most cases however BE is associated with complex brain tissue alterations. According to Klatzo (1967) two physiopathological types can be described: vasogenic edema follows a breakdown of blood brain barrier to proteins. Edema fluid enlarges the extra-cellular space and spreads within the white matter; cytotoxic edema is an intra-cellular retention of water due to various disorders of ionic balance across the plasmic cell membrane. In both cases the hydrostatic gradient between the vascular lumen and the tissue plays a major role in the amount and spread of the edema fluid. In both cases also, toxic substances produced by tissue destruction act as factors of secondary damage causing more blood brain barrier lesions and/or cellular membrane alterations and eventually enhance edema. In various pathological conditions vasogenic and cytotoxic edema are associated: edema around circumscribed lesions such as hematomas, traumatic contusions, tumors, abscesses is basically a vasogenic edema with a secondary cytotoxic component. Ischemic edema is initially a pure cytotoxic phenomenon with a secondary osmotic edema and lately a vasogenic component. The formation of BE leads to an increase in tissue pressure which may reduce local cerebral blood flow. If blood supply is already impaired this can lead to energy shortage and further tissue destruction. If the bulk of edema is large enough intracranial pressure rises up, brain shifts and herniations may occur. Hypertonic solutions and corticoids are the more widely used drugs against brain edema. Hypertonic solutions remove water from the normal brain and hence may reduce intracranial pressure rather than treat edema. Corticoids, through various discrete mechanisms interfere with some toxic substances, enhance energetic metabolism and allow tissue restitution with a rather limited effect on edema itself.
Brain Edema↗
[Effect of glycerol administration on experimental cerebral ischemia--Part 1. Studies on lipid peroxides, prostaglandins, brain edema and brain metabolites].
Using two different models of non ischemic and transient cerebral ischemia in SHR, the effect of hyperosmolar solution with intravenous 10% glycerol on serum lipid peroxides, plasma prostaglandins (TXA2, PGI2), brain water content and brain metabolites were studied. Glycerol did not influence the levels of lipid peroxides, plasma prostaglandins and brain water content in the non ischemic rats. In the transient ischemia group, on the other hand, serum lipid peroxides were significantly reduced in the glycerol administrated group. On the study of plasma prostaglandins, there was no difference of TXA2 levels between two groups, but PGI2 levels were significantly increased in the glycerol administrated group. Brain water content was significantly decreased. And on the study of brain metabolites, ATP concentrations remained higher and lactate concentrations were lower in the glycerol administrated group compared with those in the control group. But there was no difference with pyruvate concentrations between two groups, furthermore L/P ratio improved in the glycerol administrated group. Besides the effect on reduction of brain edema as for hyperosmolar solution, glycerol may indicate improvement of ischemic impediments on brain by the action of antioxidation and reinforcement of PGI2.
Animals↗
Transport of sodium from blood to brain in ischemic brain edema.
Brain water and sodium increase during ischemia, suggesting that the blood-brain barrier permeability to sodium is increased. To test this hypothesis we measured the permeability-surface area products of 22Na and [3H]sucrose in gerbils following 3 hours of unilateral ischemia. In animals with neurologic symptoms, unilateral carotid occlusion reduced the cerebral blood flow in the ipsilateral cerebral hemisphere to 13 +/- 4 ml/100 g/min (n = 6). The water content of the ischemic hemisphere increased from 79.0 +/- 0.6 to 80.8 +/- 0.2% (n = 7, p less than 0.001) and tissue sodium content increased from 231 +/- 17 to 359 +/- 23 mEq/kg (p less than 0.0001). However, there was a 40% reduction in the sodium permeability-surface area product of the ischemic hemisphere compared with the control side (1.65 +/- 0.44 vs 2.79 +/- 0.29 microliter/g/min, n = 6, p less than 0.001). The sucrose permeability-surface area product, a measure of blood-brain barrier integrity, was unchanged. Although ischemia was less severe in the diencephalon, the tissue water and sodium contents increased significantly on the ischemic side. In contrast to the cerebral hemisphere, however, the permeability-surface area products for both sodium and sucrose were unchanged in the ischemic diencephalon. These results suggest that the increase in tissue sodium seen in ischemic edema is not due to enhanced sodium uptake; we speculate that it results, in part, from a reduction in sodium and water clearance from the tissue.
Animals↗
Ultrasonic diagnosis of subdural hematomas, epidural hematomas, brain edema and brain atrophy.
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Atrophy↗
The role of bradykinin in the etiology of vasogenic brain edema and perilesional brain dysfunction.
The feline infusion model of brain edema was used to evaluate the role of bradykinin in the etiology and pathophysiology of vasogenic brain edema. Bradykinin (3 or 90 ug in 600 microL saline) did not alter normocapnic regional cerebral blood flow (rCBF) nor induce specific changes in either the somatosensory (SEP) or motor (MEP) evoked potentials. The mean increases in ICP (from 4.5 to 16.1 mmHg) and peri-infusion white matter water content (from 69.4 to 79.8 ml/100 g tissue), mean decrease in lumped craniospinal compliance (from 0.040 to 0.014 ml/mmHg) and local histological changes were all similar to those after 600 microL saline infusion. The interstitial bradykinin infusion caused focal blood-brain-barrier (BBB) opening to Evans Blue dye and was chemotaxic for granulocytes. After the infusion there was a global loss of rCBF CO2 reactivity but there was no ischemia at normocapnia. These results show that bradykinin in brain edema fluid, at concentrations greater than those found in neuropathological conditions, can open the BBB of normal cerebral parenchymal capillaries and cause vascular dysregulation. In neuropathological conditions bradykinin may therefore potentiate formation of vasogenic brain edema but does not contribute to perilesional brain dysfunction.
Animals↗
Effect of atrial natriuretic peptide on ischemic brain edema: changes in brain water and electrolytes.
The effects of intraventricularly administered atrial natriuretic peptide (ANP) on the brain water, sodium, and potassium contents in ischemic brain edema were investigated. By use of a three-vessel occlusion model, ischemic brain edema was produced in the rat brain by 15 minutes of global ischemia followed by recirculation. Water content was measured by means of a drying/weighing method; sodium and potassium contents were measured by means of flame photometry. The effects of intraventricular administration of ANP were evaluated by a comparison between the groups given 2 and 5 micrograms of atriopeptin II (treated) and those given 0.9% NaCl (sham-treated). The treated groups showed significant decreases in brain water (P less than 0.02) and sodium (P less than 0.01) contents at 15 and 30 minutes after recirculation, whereas the brain potassium contents remained unaltered. Before ischemia and immediately after 15 minutes of ischemia, intraventricularly administered ANP did not significantly change the brain water, sodium, or potassium contents. There was no significant difference in the effect on the amount of brain water and sodium between the two doses (2 and 5 micrograms). These effects of ANP were thought not to be mediated by primary changes in serum osmolality and sodium and potassium concentrations, because intraventricular administration of ANP did not change them significantly. The present results reveal that, in ischemic brain edema, ANP may act directly on the central nervous system to inhibit brain water and sodium accumulation.
Animals↗
Mediators of brain edema and secondary brain damage.
Progress is our understanding of the roles of vasogenic and cytotoxic brain edema in secondary brain damage can be expected from studies of the ability of biochemical factors to open the blood-brain barrier, derange the microcirculation, and cause cell swelling and necrosis. Mediator compounds are considered to form or to become released in an area of primarily damaged brain (necrosis) and to enter the cerebral parenchyma through the broken blood-brain barrier from the intravascular space. Many biochemical factors must be considered. We suggested three criteria for determining the roles of mediators: a) they must inflict brain tissue damage, b) they must occur in pathologic concentrations or in compartments not normally present, and c) specific inhibition should attenuate secondary brain damage. These requirements are met by the kallikrein-kinin system and by glutamate. In the case of arachidonic acid and its many metabolites, the concept is difficult to test because fatty acids may be active only if not bound to proteins, and therapeutic inhibition might be difficult. A variety of mediators may enhance each other in a cascade manner by various initiating reactions that might be amenable for pharmacologic inhibition.
Animals↗
Neuropharmacologic control of cerebral capillary permeability: current implications for therapy of vasogenic brain edema.
Vasogenic brain edema occurs as a result of a diverse spectrum of central nervous system pathology. The fundamental physiologic abnormality of vasogenic brain edema is an increase in cerebral capillary permeability. It is hypothesized that the recent development of new, potent, synthetic vasopressin antagonists will make it possible to impede the formation of vasogenic brain edema by the intraventricular administration of such agents with the subsequent inhibition of the neural control of brain capillary permeability by the locus ceruleus. The action of the vasopressin antagonists should be synergistic with the anti-edema effects of central alpha-adrenergic blockade produced by phentolamine. The combination of these two modes of therapy is expected to produce an increase in intracranial pressure which will require additional forms of medical therapy to control, in spite of the overall decrease of brain parenchymal water content.
Blood-Brain Barrier↗
Brain edema, autoregulation, and calcium antagonism. An experimental study with nimodipine.
We investigated the effects of the calcium entry blocker nimodipine on cerebral autoregulation, BBB, and vasogenic edema in animal experiments. In the first series of rats, ICBF was measured with H2 clearance using a balanced multiwire surface electrode. Variations in blood pressure (SAP), which was measured via femoral catheter, were induced by infusion of norfenefrine (pressure increase) and by hemorrhage (pressure decrease). The effect of SAP on the cerebral microcirculation was evaluated. In control animals receiving nimodipine, a typical autoregulation plateau was found. In rats treated with nimodipine infusion (12-14 micrograms/kg/min), 1CBF was considerably elevated at all blood pressure levels above 50 mm Hg, and in the steep 1CBF/SAP correlation, the autoregulation plateau was almost suspended. In a second series of randomized rats, the effect of nimodipine on BBB was investigated after Evans blue infusion. When a SAP of 180 mm Hg systolic was maintained for 6 min, a diffuse Evans blue staining was seen in 70% of the nimodipine animals (break-through of BBB). In the third series of rats, the effect of nimodipine on cold injury edema was investigated. Nimodipine (1 mg i.p.) considerably decreased the SAP; Edema formation measured by water and Na+ content 24 hr after trauma was then reduced. However, if the decrease in SAP was in part prevented by norfenefrine application, the rats receiving nimodipine developed significantly more edema. Brain water and sodium contents were markedly increased in both hemispheres. The results indicate an interference of nimodipine with cerebral autoregulation, and a BBB disruption may occur at lower SAP. If the BBB is impaired, nimodipine may considerably intensify edema formation. Nimodipine and similar calcium entry blockers should therefore only be used with caution in acute brain damage.
Animals↗
The effects of glucosteroids upon cold-induced brain edema. 3. Prevention of gliosis following brain edema.
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Animals↗
Brain edema and the blood brain barrier in galactosamine-induced fulminant hepatic failure rats. An animal model for evaluation of liver support systems.
Rats with galactosamine-induced fulminant hepatic failure (FHF) have been a popular animal model for the evaluation of liver support systems. Because development of brain edema is a major and frequent complication during FHF, it was studied for this report. The degree of hepatocyte necrosis closely paralleled the severity of coma. Abnormalities in the orientation of hepatocellular organelles were evident as early as grade I hepatic coma, 24 hr after galactosamine-induced liver damage. Galactosamine caused a characteristic pattern of hepatocyte necrosis such that the endoplasmic reticulum completely surrounded the nucleus to cause karyolysis and subsequent cell death. Quantitative measurements of brain water content revealed evidence of brain edema with increasing severity of coma. Brain edema resulted in a greater than 4% swelling of the brain during this period. Light microscopy showed increasing cerebral and cerebellar edema during progressive stages of FHF. Electron microscopy studies revealed evidence of progressive cerebral edema, particularly in the perivascular region of cerebral capillaries. Marked swelling of perivascular astrocytes was evident as early as 24 hr after galactosamine-induced FHF when the animals were in Grade I hepatic coma. Abnormal swelling and distortion of astroglia, including its subcellular organelles, and the presence of cytoplasmic vacuoles, was clearly evident during the deeper stages of hepatic coma (Grades II-IV). Trypan blue dye infusion studies revealed evidence of extensive blood-brain barrier (BBB) breakdown beginning in Grade III coma.
Animals↗
[Ultrastructure of capillary permeability in human brain tumor--Part 6: Metastatic brain tumor with brain edema].
Metastatic brain tumors very often cause severe brain edema. We examined ultrastructural findings of capillaries of these tumors and discussed the causes of cerebral edema as compared with those of glioblastoma which were previously reported. Four specimens were examined: two adenocarcinomas from the lung, one squamous cell carcinoma from the lung and one adenocarcinoma from the breast. These replicas and ultrathin sections were examined by transmission electron microscope. The following characteristic structures were detected; the capillary endothelium was proliferated, had marked infolding, and an increased number of pinocytotic vesicles and vacuoles. Short and elongate intercellular junctions were present. No open junction was detected. The basal lamina lost its three layered appearance and was irregular in width. Among these, an appearance of capillary fenestration was the most conspicuous features and observed in almost all capillaries. Two different pathogenesis for making vasogenic edema are proposed in metastatic brain tumor and glioblastoma. The frequent fenestration of the former and activated pinocytotic vesicles of the latter are responsible for extravasation of the edema fluid. The differences in distribution patterns of fenestration in metastatic brain tumor cannot be identified with respect to histological types.
Adenocarcinoma↗
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↗
[Distribution and constitutional changes of edema fluid in cytotoxic brain edema analyzed by electron microscopy and differential scanning calorimetry].
To understand the pathogenesis of brain edema, we studied distribution and constitutional changes of brain-tissue water by morphological and thermoanalytical methods in cytotoxic brain edema induced by 6-aminonicotinamide (6-ANA). Ninety-two Wistar rats were divided into three groups; Group I rats receiving physiological salt solution intraperitoneally served as controls. Group II and III animals were intraperitoneally given 120 mg/kg and 36 mg/kg of 6-ANA respectively. All animals were starved after injection of drugs to exclude differences in water intake. Then they were decapitated at 3, 6, 12, 24, 36 or 48 hours to measure specific gravity (SG) of large brain tissue (1.1-1.5 g), and to evaluate water content (WC) and free water ratio (FWR) of small brain-tissue samples (15-35 mg) taken from the frontal cortex; WC was measured by a drying-weighing method, and FWR was analyzed with a differential scanning calorimeter. Moreover morphological changes of the frontal cortex of the brain were studied in Group II (n = 12) at 3, 6, 12, 24 and 48 hours with an electron microscope. Neurological status of animals administered 6-ANA (Group II and III) deteriorated with time. Morphological studies showed that perivascular astrocytes and astrocytic processes in the cerebral cortex were swollen most remarkably at 48 hours. However neuronal and endothelial cells were almost intact. The FWR of Group I decreased significantly about four per cent (p less than 0.001) after being starved for 48 hours. But the SG and WC of the group showed little change.(ABSTRACT TRUNCATED AT 250 WORDS)
6-Aminonicotinamide↗
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↗
Stimulation of astrocytes affects cytotoxic brain edema.
Cytotoxic brain edema has been produced in rats by subacute intoxication with triethyltin (TET). Some animals were allowed to recover spontaneously, others were post-treated with an extract of Ginkgo biloba (EGB) for 1 to 4 weeks, beginning 3 days after intoxication was stopped. The time course of the resolution of the edema was studied biochemically and morphologically by light microscopy, histochemistry and electron microscopy (EM). Morphometric evaluation showed that the spontaneous reabsorption of TET-induced edema was very slow: it was evident only 2 weeks after ending TET administration and it required more than 4 weeks to be completed. EGB therapy markedly decreased the vacuolation, as well as the abnormal levels of water and sodium contents, 1 week after beginning the treatment. Less influence of EGB was observed at the later stages. During spontaneous recovery, astroglial cells in the edematous white matter of TET-intoxicated animals showed short and swollen processes containing few organelles, low levels of NADH- and NADPH-tetrazolium reductase activities and glial fibrillary acidic protein (GFAP)-immunofluorescence for about 2 weeks. During EGB therapy the astrocytes regained their cellular processes, containing intense oxidative enzyme activities and GFAP-immunofluorescence as early as after 1 week of treatment. In the EM, astrocytes often appeared hypertrophic, surrounding myelin vacuoles and displaying phagocytosis of myelin debris. We conclude that EGB can accelerate the reabsorption of TET-induced cerebral edema and improve the astroglial reaction.
Animals↗