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PubMed1997

Soluble transforming growth factor-alpha is present in the pulmonary edema fluid of patients with acute lung injury.

Recent in vivo and in vitro experimental evidence indicates that transforming growth factor-alpha (TGF-alpha) is an important growth factor in the process of recovery and remodeling that occurs after acute lung injury. However, there are very little clinical data on TGF-alpha in patients with acute lung injury. Therefore, the purpose of this study was to determine if TGF-alpha is present in biologically significant concentrations in the pulmonary edema fluid from patients with acute lung injury, and to determine if the presence of TGF-alpha is specific for acute lung injury by including control patients with hydrostatic edema. Using an enzyme-linked immunosorbent assay, plasma and pulmonary edema fluid TGF-alpha levels were measured in 43 patients (34 with increased permeability edema, nine with hydrostatic edema). TGF-alpha was detected in 24 of 34 patients (71%) with increased permeability pulmonary edema (range, 0.035 to 2.57 ng/mL) compared with only two of nine patients with hydrostatic edema (p < 0.05). TGF-alpha was not detected in any plasma samples. These concentrations of TGF-alpha in pulmonary edema fluid have potent in vivo and in vitro effects on alveolar epithelial sodium transport and alveolar epithelial cell motility. In conclusion, biologically relevant concentrations of soluble TGF-alpha are present in the pulmonary edema fluid on day 1 of patients with acute lung injury, a remarkable finding with important implications for the repair and resolution of acute lung injury, particularly since TGF-alpha was detected so early in the course of acute lung injury.

Adult↗
PubMed2005

Edema and malignancy in meningiomas.

PURPOSE: In recent years there have been many attempts to define a subset of aggressive malignant meningiomas based on histopathology and imaging technologies. The purpose of this study was to evaluate the level of peritumoral edema and its volume using the imaging technologies, computer tomography and magnetic resonance imaging, and correlate these results with the histological WHO classification. Reported causes of tumoral edema and its relationships to the histological characteristics were also reviewed. METHODS: The cases of 55 patients with meningiomas who underwent surgery at the Hospital das Clinicas (Fac Med Univ Sao Paulo) between September 1993 and September 1997 were reviewed. The level of edema according to the classification of Ide et al. (1995) was compared to the histological WHO classification. RESULTS: Classification of the degree of edema was: level 0 edema--28 cases ; level I edema--19 cases; level II edema--8 cases. Histological classification was: benign meningioma--43 cases; atypical meningiomas--11 cases; malignant meningioma--1 case. There was a significant (P=.0089) correlation between the degree of tumoral edema and the histological characteristics. CONCLUSIONS: These results suggest that the degree of edema as revealed by computer tomography and magnetic resonance imaging can be an important clinical predictive factor for the histological grade of the meningioma.

Adolescent↗
PubMed2000

Treatable chondral injuries in the knee: frequency of associated focal subchondral edema.

OBJECTIVE: In the knee, chondral flaps and fractures are radiographically occult articular cartilage injuries that can mimic meniscal tears clinically; once correctly diagnosed, these injuries can be treated surgically. We investigated an associated MR imaging finding--focal subchondral bone edema--in a series of surgically proven lesions. MATERIALS AND METHODS: Two musculoskeletal radiologists retrospectively reviewed the MR studies of 18 knees with arthroscopically proven treatable cartilage infractions, noting articular surface defects and associated subchondral bone edema; subchondral edema was defined as focal regions of high signal intensity in the bone immediately underlying an articular surface defect on a T2-weighted or short inversion time inversion recovery (STIR) image. RESULTS: The first observer saw focal subchondral edema deep relative to a cartilage surface defect in 15 (83%) of the 18 cases; in two additional cases a surface defect was seen without underlying edema. The second observer identified 13 knees (72%) with surface defects and associated subchondral edema and three with chondral surface defects and no associated edema. Subchondral edema was seen more frequently on fat-suppressed images and on STIR images than non-fat-suppressed images. CONCLUSION: Focal subchondral edema is commonly visible on MR images of treatable, traumatic cartilage defects in the knee; this MR finding may prove to be an important clue to assist in the detection of these traumatic chondral lesions.

Adolescent↗
PubMed1989

Release of glutamate and of free fatty acids in vasogenic brain edema.

The pathophysiological potential of mediator substances in manifestations of secondary brain damage is attracting increased attention. This is particularly true of the excitatory transmitters glutamate and arachidonic acid. Noxious properties of these compounds in central nervous tissue have been demonstrated. The current study was performed to determine whether glutamate and arachidonate are released in brain tissue secondary to focal trauma. For this purpose, a cold injury of exposed cerebral cortex was induced in cats. Marked accumulation of glutamate was observed in interstitially drained edema fluid, reaching 10 to 15 times the level that was assessed in normal cerebrospinal fluid (CSF) prior to trauma. The extracellular release of glutamate was further dramatically enhanced by a critical decrease of the cerebral perfusion pressure due to a malignant increase of intracranial pressure. Under these conditions, glutamate concentrations 1000 to 1500 times normal levels accumulated in vasogenic edema fluid, demonstrating a relationship between the extent of the release of glutamate in damaged brain and the severity of the insult. Although under normal conditions glutamate concentrations in plasma were considerably higher than in the interstitial fluid, the pronounced increase of glutamate in this compartment due to trauma cannot be explained by transport of the compound together with the plasma-like edema from the intravascular space. Corresponding findings were obtained for free fatty acid concentrations in edema fluid. Almost all fatty acids that were studied had a significantly higher concentration in edema fluid than in normal CSF obtained as a control prior to trauma. However, contrary to the findings for glutamate, fatty acid concentrations in edema fluid were lower than in plasma. Accumulation of fatty acids in vasogenic edema fluid might, therefore, have resulted from uptake of the material together with edema fluid through the breached blood-brain barrier. Arachidonic acid was an exception. Its concentrations were significantly higher in edema fluid than in plasma, suggesting that it was released from cerebral parenchyma as the underlying mechanism of its extracellular accumulation. The current observations provide further support for a mediator function of glutamate and arachidonic acid in acute traumatic lesions of the brain. Quantitative assessment of the release of highly active mediator substances in brain tissue may facilitate analysis of the therapeutic efficiency of specific treatment aimed at interfering with the release or pathological function of mediators of secondary brain damage.

Animals↗
PubMed1993

Effect of neonatal capsaicin treatment on neurogenic pulmonary edema from fluid-percussion brain injury in the adult rat.

The frequent occurrence of acute death from pulmonary failure in experimental head injury studies on Sprague-Dawley rats prompted an investigation into the manner in which acute neurogenic pulmonary edema develops in these animals as a result of an applied fluid pressure pulse to the cerebral hemispheres. Studies were performed in adult animals using histamine H1 and H2 blocking agents, or in adult animals treated as neonates with capsaicin to destroy unmyelinated C-fibers. Recordings were made of either the pulmonary arterial or the right ventricular pressure, and the left atrial and femoral arterial pressures before, during, and after injury to provide a record of the hemodynamic response throughout the development of neurogenic pulmonary edema. Head injury triggered the almost immediate development of pressure transients with and without neurogenic pulmonary edema. All rats, regardless of treatment, reacted with nearly identical systemic arterial pressure responses; however, the pulmonary responses followed a time course that was independent of systemic arterial pressure changes. Acute neurogenic pulmonary edema was always associated with a substantial increase in pulmonary arterial and left atrial pressures; conversely, pressure increases of similar magnitude were not always associated with edema. Histamine H1 and H2 blockers significantly reduced the pulmonary pressure surges only in rats free of neurogenic pulmonary edema. All capsaicin-treated rats showed suppressed pulmonary pressure responses, normal lung water content, elevated lung surface tension, and significantly reduced levels of immunoreactive substance P in the spinal cord and vagus nerve. While the pressures cannot clarify how edema influences the observed hemodynamics, they do not support the view that edema is the direct consequence of pulmonary hypertension. It is proposed that neurogenic pulmonary edema is a functional disturbance provoked by adverse stimuli from outside the lungs and that in the rat the primary afferent fiber is essential to the production of this entity.

Animals↗
PubMed1997

Contribution of vasogenic and cellular edema to traumatic brain swelling measured by diffusion-weighted imaging.

The contribution of brain edema to brain swelling in cases of traumatic brain injury remains a critical problem. The authors believe that cellular edema, the result of complex neurotoxic events, is the major contributor to brain swelling and that vasogenic edema, secondary to blood-brain barrier compromise, may be overemphasized. The objective of this study, therefore, was to quantify temporal water content changes and document the type of edema that forms during the acute and late stages of edema development following closed head injury (CHI). The measurement of brain water content was based on magnetic resonance imaging-determined values of tissue longitudinal relaxation time (T1-weighted imaging) and their subsequent conversion to percentage of water, whereas the differentiation of edema formation (cellular vs. vasogenic) was based on the measurement of the apparent diffusion coefficient (ADC) by diffusion-weighted imaging. A new impact-acceleration model was used to induce CHI. Thirty-six adult Sprague-Dawley rats were separated into two groups: Group I, control (six animals); and Group II, trauma (30 animals). Fast ADC measurements (localized, single-voxel) were obtained sequentially (every minute) up to 1 hour postinjury. The T1-weighted images, used for water content determination, and the diffusion-weighted images (ADC measurement with conventional diffusion-weighted imaging) were obtained at the end of the 1st hour postinjury and on Days 1, 3, 7, 14, 28, and 42 in animals from the trauma and control groups. In the animals subjected to trauma, the authors found a significant increase in ADC (10 +/- 5%) and brain water content (1.3 +/- 0.9%) during the first 60 minutes postinjury. This is consistent with an increase in the volume of extracellular fluid and vasogenic edema formation as a result of blood-brain barrier compromise. This transient increase, however, was followed by a continuing decrease in ADC that began 40 to 60 minutes postinjury and reached a minimum value on Days 7 to 14 (10 +/- 3% reduction). Because the water content of the brain continued to increase during the first 24 hours postinjury (1.9 +/- 0.9%), it is suggested that the decreased ADC indicated cellular edema formation, which started to develop soon after injury and became dominant between 1 and 2 weeks postinjury. The study provides supportive evidence that cellular edema is the major contributor to posttraumatic swelling in diffuse CHI and defines the onset and duration of the increase in cellular volume.

Acceleration↗
PubMed1998

Erythrocytes and delayed brain edema formation following intracerebral hemorrhage in rats.

OBJECT: The mechanisms of brain edema formation following spontaneous intracerebral hemorrhage (ICH) are not well understood. In previous studies, no significant edema formation has been found 24 hours after infusion of packed red blood cells (RBCs) into the brain of a rat or pig; however, there is evidence that hemoglobin can be neurotoxic. In this study, the authors reexamined the role of RBCs and hemoglobin in edema formation after ICH. METHODS: The experiments involved infusion of whole blood, packed RBCs, lysed RBCs, rat hemoglobin, or thrombin into the right basal ganglia of Sprague-Dawley rats. The animals were killed at different time points and brain water and ion contents were measured. The results showed that lysed autologous erythrocytes, but not packed erythrocytes, produced marked brain edema 24 hours after infusion and that this edema formation could be mimicked by hemoglobin infusion. Although infusion of packed RBCs did not produce dramatic brain edema during the first 2 days, it did induce a marked increase in brain water content 3 days postinfusion. Edema formation following thrombin infusion peaked at 24 to 48 hours. This is earlier than the peak in edema formation that follows ICH, suggesting that there is a delayed, nonthrombin-mediated, edemogenic component of ICH. CONCLUSIONS: These results demonstrate that RBCs play a potentially important role in delayed edema development after ICH and that RBC lysis and hemoglobin toxicity may be useful targets for therapeutic intervention.

Animals↗
PubMed2000

Role of hydrodynamic processes in the pathogenesis of peritumoral brain edema in meningiomas.

OBJECT: In a prospective study, 28 patients with 32 intracranial meningiomas were examined to determine the role of hydrodynamic interaction between tumor and surrounding brain tissue in the pathogenesis of peritumoral brain edema. METHODS: Gadolinium-diethylenetriamine pentaacetic acid (Gd-DPTA), an extracellular contrast agent used for routine clinical imaging, remains strictly extracellular without crossing an intact blood-brain barrier. Therefore, it is well suited for investigations of hydrodynamic extracellular mechanisms in the development of brain edema. Spin-echo T1-weighted magnetic resonance images were acquired before and after intravenous administration of 0.2 mmol/kg Gd-DPTA. Additional T1-weighted imaging was performed 0.6, 3.5, and 6.5 hours later. No significant Gd-DPTA diffused from tumor into peritumoral brain tissue in 12 meningiomas without surrounding brain edema. In contrast, in 17 of 20 meningiomas with surrounding edema, contrast agent in peritumoral brain tissue was detectable after 3.5 hours and 6.5 hours. In three of 20 meningiomas with minimum surrounding edema (<5 cm3), contrast agent effusion was absent. After 3.5 hours and 6.5 hours strong correlations of edema volume and the maximum distance of contrast spread from the tumor margin into adjacent brain parenchyma (r = 0.84 and r = 0.87, respectively, p < 0.0001) indicated faster effusion in larger areas of edema. CONCLUSIONS: The results of this study show that significant contrast agent effusion from the extracellular space of the tumor into the interstitium of the peritumoral brain tissue is only found in meningiomas with surrounding edema. This supports the hypothesis that hydrodynamic processes play an essential role in the pathogenesis of peritumoral brain edema in meningiomas.

Adult↗
PubMed1976

Blood pressure, edema and proteinuria in pregnancy. 3. Study design, population and data characteristics.

1. The mean blood pressure runs a curvilinear pattern during the course of pregnancy, with the lowest reading between 20 and 27 weeks of gestation, a continuous rise from 28 to 36 weeks, followed by a plateau. 2. the mean blood pressure in pregnancies without edema and proteinuria are lowest throughout pregnancy. However, the mean blood pressures in pregnancies complicated by edema, proteinuria, or both, are less than 5 mm. Hg higher after 28 weeks of gestation. 3. The mean blood pressures are lower in black gravidas than in white gravidas throughout pregnancy, independent of the presence or absence of edema, proteinuria, or their combinations. 4. The mean blood pressure is related to age and parity. Median-age gravidas (20-34 years) of parity 1-5 have the lowest mean blood pressures overall at any time during gestation. The mean blood pressure of nulliparas, independent of age, is elevated over the mean blood pressure of comparable multiparas. Independent of parity, maternal age systematically affects the mean blood pressure. 5. The standard deviations for the mean diastolic and systolic blood pressures are approximately 9 and 11 mm. Hg, respectively, independent of the weeks of gestation. They are affected very little by the absence or presence of edema or proteinuria, or both. 6. Edema of hands and/or face occurs more often in black gravidas. 7. The overall perinatal mortality rates in pregnancies complicated by edema are not higher than in pregnancies without edema. Perinatal mortality rates in pregnancies with proteinuria, or edema and proteinuria, on the other hand, are approximately double the rates for pregnancies without edema and proteinuria.

Adolescent↗
PubMed1999

[Relationship between brain edema induced by freezing injury and concentration of Evan blues and cytosolic free calcium in brain tissues].

The authors studied the changes of Evan blues(EB) of brain tissues and concentration of cytosolic free calcium ([Ca2+]i), and relationship between them and water content of brain tissues following freezing brain edema in rats, to elucidate mechanism and type of brain edema induced by freezing injury. The results indicated that there were close positive relationship between water content and EB of brain tissues, and between [Ca2+]i and water content. We found that not only cytotoxic brain edema(intracellular edema) occurred but also occurred vasogenic brain edema(extracellular edema) followed by blood brain barrier breakdown after brain edema. Freezing brain edema is mixed brain edema.

Animals↗
PubMed2002

Surgical improvement of brain edema related to hypertensive intracerebral hemorrhage.

BACKGROUND: Patients with hypertensive intracerebral hemorrhage (ICH) are at risk for delayed neurological deterioration, especially during the second week after onset. Mass effect due to vasogenic edema caused by ICH has been shown to cause later deterioration. Control of brain edema and increased intracranial pressure (ICP) are related events that determine outcome. In this study, we compared the effects of three different treatments on brain edema caused by ICH. METHODS: Thirty-nine patients with ICH were involved in this study. Of these patients, 11 had medical therapy (group A), 15 were treated with stereotactic aspiration plus local administration of urokinase (group B), and 13 underwent conventional craniotomy and hematoma removal (group C). The intracerebral hematoma volume on admission was measured on the the brain computed tomographs (CTs), and the cerebral edema volumes surrounding the hematoma were assessed with CT scans every 5 to 7 days after symptom onset. RESULTS: The median intracerebral hematoma volumes were 23, 50 and 51 ml in groups A, B and C, respectively. Peak edema volume surrounding the hematoma was observed 5 to 15 days after symptom onset. A significant correlation (p < 0.05) was noted between peak edema and hematoma volumes in all groups. The ratio of median peak edema volume to median hematoma volume was 3.280 in group A, which was significantly higher than those in group B (0.745) and group C (0.863) (p < 0.05). CONCLUSIONS: The study revealed that brain edema induced by hypertensive ICH could be significantly ameliorated by surgical management. Stereotactic aspiration with local administration of urokinase was as effective as conventional craniotomy in reduction of brain edema volume caused by ICH and was characterized by its minimal invasiveness, easy performance, and safety.

Adult↗
PubMed2002

[Internal limiting membrane peeling in vitreous surgery for diabetic macular edema].

PURPOSE: To evaluate the effect of internal limiting membrane (ILM) peeling in vitreous surgery for diabetic macular edema. METHODS: This study was done on 135 eyes of 103 patients who all underwent diabetic macular edema surgery under the same surgeon. The subjects were 74 eyes of 55 males and 61 eyes of 48 females, aged 35-81 years, with an average of 62 years. The postoperative follow-up period ranged from 12 to 39 months, with an average of 20 months. The ILM peeling was performed in 74 eyes. The subjects were divided in two types of macular edema from the presence (type II, 81 eyes) or absence (type I, 54 eyes) of hard exudates in the macular region. We evaluated the effects of the ILM peeling on the absorption rate of macular edema, the period required for absorption of macular edema, and the postoperative visual acuity. RESULTS: The absorption rate of macular edema was more than 90% with or without the ILM peeling. The period required for absorption of macular edema in eyes with ILM peeling was shorter in type II. There was no difference in the postoperative visual acuity with or without ILM peeling. ILM peeling was not an important factor for the postoperative visual acuity. RESULTS: ILM peeling accelerates the absorption of edema in more severe diabetic macular edema, but we could not find any improvement of visual acuity.

Adult↗
PubMed1991

[Mechanisms of development of brain edema in neurosurgical pathology].

As many as 120 neurosurgical patients were examined after the excision of hemispheric gliomas, basal and subtentorial tumors. Based on an the computer-aided analysis biochemical and clinical data, attempts have been made to unify the mechanisms responsible for brain edema development in patients with neurosurgical pathology. In the early postoperative period, brain edema occurs in 95% of neurosurgical patients. Edema development, spreading and intensity depend on the site and nature of the primary pathological focus as well as on traumatism of surgical interventions. It is proved that edema is an original, biologically expedient brain response to its injury. This response manifests in hyperhydration of all tissues, with the maximum intensity being concentrated in the focus of injury. Specific (neurogenic neurohumoral) and nonspecific (biochemical, autoimmune, mechanical, and so forth) factors of brain edema development may be distinguished. The differences in the neurogenic and neurohumoral mechanisms by which brain edema develops may be accounted for by the topography of the focus of injury. The closer the pathological focus is to the stem and diencephalic structures, the more remarkable the action of neurogenous and neurohumoral factors and the more distinct the tendency toward edema generalization are. At the diencephalic level of injury, damaged are the structures responsible for central regulation of metabolism and trophicity of nerve cells. The neurogenously precipitated diffuse impairment of permeability of the cells entails their hyperhydration, which marks cellular (cytotoxic) edema. The subtentorial process that affects the vasomotor centre of the stem triggers the neurogenic diffuse alterations in the vascular tone, manifesting in an increase of permeability for water and plasma proteins which is characteristic of vasogenic edema.(ABSTRACT TRUNCATED AT 250 WORDS)

Body Water↗
PubMedDate not supplied

Delayed insulin absorption due to subcutaneous edema.

A prospective study to determine if subcutaneous edema interferes with insulin absorption was performed. Forty-six patients entered the study. Three groups were formed. Twenty patients with generalized edema (Group 1), ten of them with non-insulin dependent diabetes mellitus (NIDDM). Twenty patients without edema (Group II). 10 of them with NIDDM; and six patients with mild edema (Group III). The disappearance of I125-insulin was measured throughout 360 minutes. The rate of absorption in group I was significantly lower and delayed than in group II. The amount of insulin absorbed at 360 minutes was 3 to 4 fold lower in group I than in group II (p 0.001). Group III had intermediate values. The peak of plasma I125-insulin level was 3 to 4 fold lower in group I than group II. The impairment of insulin absorption in subjects with edema was more evident in those with NIDDM. In conclusion, this study demonstrates that subcutaneous edema impairs insulin absorption. Insulin absorption from subcutaneous tissue varies due to several conditions, resulting in a difficult glycemic control. Previous studies have shown that insulin absorption is affected by several factors as the site of injection, room and skin temperature, physical exercise, the thickness of adipose tissue, local massage, and local degradation of insulin. Edema due to chronic complications such as nephropathy and cardiopathy often occurs in long-standing diabetic subjects. However, the effects of edema of the skin and subcutaneous tissue on insulin absorption has not been previously examined. The aim of this study was to assess if edema affects the absorption of insulin.

Abdomen↗
PubMed1990

[Changes in epidural pulse pressure in brain edema following experimental focal ischemia].

It is well known that epidural pulse pressure (PP) increases with rising intracranial pressure (ICP). However, PP at the same ICP is not always identical in various intracranial pathologies. Many authors have investigated PP at increased states of ICP, but few studies related to brain edema have been done. This study was carried out in order to clarify the changes of PP in brain edema following focal ischemia. ICP and PP were measured in two groups of anesthetized dogs; 1) increased volume of CSF by cisternal saline injection (control, n = 5), 2) brain edema caused by focal ischemia (edema, n = 11). Ischemia was induced by electro-coagulation of the right anterior cerebral artery and by clipping the right middle cerebral artery and right internal carotid artery transorbitaly. The brain was recirculated for 6 hours after 2 hours of ischemia. The ischemic areas were identified by Evans blue, triphenyl tetrazolium chloride (TTC) or histological examination. Water content of the brain was measured by the wet-dry weight method. The canine focal ischemic model showed consistent ischemic damage in the caudate nucleus and produced brain edema successfully. PP increased linearly with rising ICP to 35 mmHg, and PP in the edema group was significantly smaller than that in the control group at the same ICP value. The slopes of the regression equation of ICP and PP were significantly different between the edema and control group (edema: 0.061 +/- 0.030, control: 0.107 +/- 0.015, mean +/- SD, p less than 0.01). These results suggest that PP is easily affected by ischemic brain edema.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

[The influence of gestational edema on maternal and perinatal outcome].

In order to detect the influence of edema on maternal and perinatal outcome, 1,326 records of pregnant women without vascular nor renal diseases who were delivered of single infants were reviewed. The results were as follows. 1. Edema was observed in 214 of 1,326 subjects (16%). 2. In subjects with edema, 86% in primipara and 97% in multipara had no additional signs of preeclampsia subsequently during pregnancy and postpartum. 3. In thirteen subjects with edema before 28 weeks of gestation, five subjects (38.5%) had additional signs of preeclampsia subsequently and four developed severe preeclampsia. In 201 subjects with edema after 28 weeks of gestation, fourteen subjects (7%) had additional signs of preeclampsia subsequently and only one woman developed severe preeclampsia. 4. Mean birth weights in subjects with edema were significantly higher than that in subjects without edema in primipara. But, among the other parameters, no significant difference was found. These results indicate that edema by itself does not affect the maternal and perinatal outcome. However, the onset of edema before 28 weeks of gestation may be a useful sign to predict the onset of hypertension and proteinuria.

Edema↗
PubMed1974

Experimental edema disease of swine (E. coli enterotoxemia). I. Dectection and preparation of an active principle.

Freeze-thaw lysates prepared from strains of Escherichia coli belonging to serogroups O138, O139, and O141 contained a principle (edema disease principle) which induced edema disease in swine. All freeze-thaw lysates contained endotoxic activity that tended to obscure the edema disease syndrome and methods were developed to reduce such activity. Freeze-thaw lysates prepared from E. coli O139 induced the most characteristic edema disease syndrome. Partially purified edema disease principle prepared from O139 freeze-thaw lysates by sequential precipitation with ammonium sulphate and streptomycin sulphate had increased specific activity with markedly reduced endotoxic activity. This material was insoluble at acidic pH but readily soluble at alkaline pH. The effective molecular weight of edema disease principle, based on retention and filtration properties of diaflo membranes, appeared to be greater than 50,000 and less than 100,000. The biological activity of edema disease principle was thermolabile. Sodium deoxycholate treatment of edema disease principle further reduced endotoxic activity. A thermolabile, ammonium sulphate precipitable material was prepared from E. coli O139 that induced a predictable syndrome which resembled edema disease clinically and pathologically following intravenous inoculation in pigs.

Ammonium Sulfate↗
PubMed1996

[Sequential observations of brain edema with proton magnetic resonance imaging and spectroscopy].

The purpose of this study was to assess the relationship between morphological and metabolic changes in brain edema using proton magnetic resonance systems. The serial changes during the first 24 hours in the cold-injury trauma rat brain model were investigated by proton magnetic resonance imaging (1H MRI) and high-resolution proton MR spectroscopy (1H MRS). We also analyzed the efficacy of AVS 1,2-bis (nicotinamide)-propane which can scavenge free radicals to the edema in this experiment. The edema was developing extensively via the corpus callosum in ipsi- and contralateral hemispheres as shown by gradually increased signal intensity on 1H MRI. 1H MRS initially showed accumulation of acetate and lactate, and transient increasing of glutamine. After 24 hours, the increased glutamine decreased below the control, alanine increased, and N-acetyl asparatate decreased with the edema development. AVS-treatment significantly suppressed edema development, increases of lactate and alanine and decreases of N-acetyl asparatate. We suggest that the cold-induced lesion contains anaerobic glycolysis deterioration and results in severe brain tissue breakdown. AVS is proved valuable for the treatment of this edema lesion. Clinical 1H MRS showed prolonged lactate elevation and significant decreases of other metabolites in human ischemic stroke edema. In peritumoral edema, decreased N-acetyl asparatate gradually improved, and slightly elevated lactate disappeared after tumor removal. 1H MRS feasibly characterizes the ischemic and peritumoral edema and makes a quantitative analysis in human brain metabolism. We believe the combined 1H MRI and MRS study is a practical method to monitor the brain conditions and will make it easy and possible to find new therapeutic agents to some brain disorders.

Aged↗