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PubMed1996

Renal natriuretic effects of atrial natriuretic peptide in dogs with alloxan-induced acute pulmonary edema.

OBJECTIVE: To test the effect of atrial natriuretic peptide (ANF) in dogs with acute pulmonary edema in the absence of urinary sodium retention. ANF is normally a potent natriuretic agent, although this effect is attenuated in generalized edema or acute renal failure. DESIGN: Animal study. SUBJECTS: Twenty-nine dogs. INTERVENTION: Induction of acute pulmonary edema with intravenously administered alloxan and administration of ANF according to five protocols. OUTCOME MEASURES: Natriuretic effect of ANF before and after the induction of pulmonary edema during the protocols. RESULTS: In six control animals, induction of pulmonary edema was associated with diuresis (mean 0.38, standard error of the mean [SEM] 0.003 mL/min before alloxan administration v. mean 0.75, SEM 0.11 mL/min after); natriuresis (mean 60, SEM 8 mumol/min before v. mean 103, SEM 12 mumol/min after); and a decline in blood pressure (mean 114, SEM 7 mm Hg before v. mean 93, SEM 9 mm Hg after) and in the glomerular filtration rate (mean 52, SEM 3.3 mL/min before v. mean 36, SEM 3.7 mL/min after). When isoncotic dextran solution was infused in dogs with pulmonary edema, blood pressure was maintained but the glomerular filtration rate still declined by 42% and there was natriuresis. When the renal arteries were clamped for 5 minutes during the infusion of alloxan, diuresis and natriuresis were prevented, but the glomerular filtration rate still declined, although blood pressure was maintained. ANF administered intravenously during pulmonary edema induced a further significant natriuresis in all experimental protocols. Catalase, administered intravenously as a bolus just before the alloxan infusion, prevented pulmonary edema and the associated renal changes. CONCLUSIONS: Although alloxan appears to be directly nephrotoxic, renal damage caused by this compound does not impair the natriuretic effect of ANF in acute pulmonary edema.

Acute Disease↗

PubMed1996

[The relationship between peripheral edema and right heart function in COPD induced cor pulmonale].

OBJECTIVE: To estimate the role of right heart function in the development of edema in COPD induced cor pulmonale. METHOD: 44 cases in exacerbation stage with hypoxia and hypercapnia were studied. Pulmonary hemodynamic parameters were measured by Swan-Ganz catheter and compared with the presence and extent of peripheral edema. RESULTS: Peripheral edema was noted in 40 cases and right arterial pressure < or = 1.33 kPa in 23 cases (23/40 = 57.5%), 17 cases showed edema, with right artrial pressure > 1.33 kPa. There was no significant difference in peripheral edema between that two groups. CONCLUSION: A high proportion of COPD patients with edema do not show right heart failure. The development of edema in COPD may be related to a complex mechanism, including hypoxia and hypercapnia induced natrium and water retention, Right heart failure is not a prerequisite for edema. The significance of edema in COPD induced cor pulmonale should be interpreted correctly in clinical practice.

Aged↗

PubMed1998

Edema along the optic tract: a useful MR finding for the diagnosis of craniopharyngiomas.

BACKGROUND AND PURPOSE: The pattern of edema caused by craniopharyngiomas and other common suprasellar masses could be useful for determining the differential diagnosis of lesions in this region. The purpose of this study was to ascertain whether the pattern of edema spread on MR images can be used in the diagnosis of craniopharyngiomas. METHODS: The preoperative MR images in eight consecutive patients with craniopharyngiomas, 15 patients with large pituitary adenomas compressing the optic chiasm, and six patients with tuberculum sellae meningiomas were evaluated. All the patients were treated surgically at our hospital and a pathologic diagnosis was obtained. We analyzed the spread of edema surrounding the tumor on the coronal dual-echo fast spin-echo images and compared this finding with tumor location and size as seen on contrast-enhanced T1-weighted images. RESULTS: Not only peritumoral edema but also edema spreading along the optic tracts was observed in five patients with craniopharyngiomas, one of whom also had edema within one optic nerve. The location of edema in the visual pathway was not always associated with the degree of visual disturbance. None of the patients with large pituitary adenomas or with tuberculum sellae meningiomas had such edema along the visual pathway. CONCLUSION: Edema caused by craniopharyngiomas tends to spread along the optic tracts. It is a useful MR finding for distinguishing craniopharyngiomas from other common parasellar tumors.

Adult↗

PubMed1992

Edema and tumor perfusion: characterization by quantitative 1H MR imaging.

Tumor perfusion is of central importance to the clinical oncologist because it has a direct effect on the success of cancer therapy. Yet determining whether a tumor is well or poorly perfused is difficult without the use of invasive techniques, because the variables that affect tumor perfusion are poorly understood. Quantitative MR imaging of tumor edema may provide a means of characterizing tumor perfusion, of studying heterogeneity of perfusion within the tumor mass, or of monitoring changes in tumor perfusion after therapy. A combination of factors often results in production of a large amount of edema within cranial or extracranial tumors. Any tumor that is encapsulated, whether by a fibrous tumor capsule or by a structure such as the cranium, will have an elevation in interstitial fluid pressure because dissipation of fluid is hindered. Elevated pressure of interstitial fluid acts to occlude tumor capillaries, so edema can cause a striking reduction of tumor perfusion. Because MR imaging can potentially be used for quantitative imaging of tumor edema, it may provide a means of indirectly measuring tumor perfusion. A review of the literature suggests that diffusion-weighted MR imaging may be better than T1- or T2-weighted MR imaging for quantitative imaging of tumor edema. I do not propose that diffusion-weighted imaging can measure perfusion directly; rather I hypothesize that a diffusion-weighted image can be correlated with tumor edema. Because edema indirectly regulates perfusion through the mechanism of interstitial fluid pressure, I propose an indirect correlation between the diffusion-weighted image and regional tissue perfusion. If the relationship between tumor perfusion and the pharmacokinetics of chemotherapeutic agents is better understood, MR imaging of tumor edema may even aid in predicting the delivery of drugs to a tumor.

Brain Edema↗

PubMed1997

Edema in childhood.

There are two types of edema: localized edema and generalized edema. The causes of generalized edema in childhood are diverse. Formation of generalized edema involves retention of sodium and water in the kidney. The treatment of generalized edema depends on the primary etiology. Supportive nutritional and medical therapies are needed to prevent further edema. These and related features of edema in childhood are discussed in this review.

Child↗

PubMed1978

Correlation of epinephrine use and macular edema in aphakic glaucomatous eyes.

One hundred twenty-eight consecutive aphakic glaucomatous eyes of 91 patients were examined by fluorescein angiography. Macular edema was present in 16 (28%) of 56 eyes currently being treated with epinephrine and 9 (13%) of 72 eyes not currently being treated with epinephrine. This difference is statistically significant at the 95% confidence level. Epinephrine therapy was discontinued in seven eyes with macular edema. A follow-up of these patients for six months to one year with serial anglograms showed resolution of edema in six of seven eyes. In one eye without macular edema, administration of epinephrine was associated with appearance of edema. Discontinuing epinephrine therapy was associated with resolution of edema. No significant correlation was found between use of other antiglaucomatous medications and macular edema. It is evident from this study that there is statistical support for the concept of an epinephrine-induced macular edema.

Adult↗

PubMed1993

Rebound of macular edema with continued use of methazolamide in patients with retinitis pigmentosa.

PURPOSE: To assess the effect of methazolamide on chronic macular edema in patients with retinitis pigmentosa in a double-masked, placebo-controlled, crossover study. Three subjects who had an initial improvement in their macular edema as demonstrated on fluorescein angiography received a continued course of methazolamide to assess its effect on macular edema. METHODS: Seventeen subjects were enrolled in the initial study. On angiography, nine subjects demonstrated improvement in their macular edema with the use of methazolamide for 3 weeks; three of these continued receiving the drug at a dosage of 50 mg twice daily for either an additional 6 (one subject) or 12 (two subjects) weeks. All subjects were assessed at each visit with fluorescein angiography and on best corrected visual acuity, both undilated and dilated; a subjective impression was also documented. RESULTS: After 6 and 12 weeks of treatment, all three subjects experienced a rebound of angiographic macular edema to some extent. The visual acuity varied only slightly (up to 7 letters) from both the baseline and most recent examinations after 6 and 12 weeks of treatment. CONCLUSION: Results from these few subjects suggest that at least a partial rebound of macular edema seen angiographically may occur with the continued use of methazolamide in patients with retinitis pigmentosa and chronic macular edema. Further study is required to determine if this rebound effect also occurs in treatment of other ocular disorders with chronic macular edema.

Adult↗

PubMed2003

Hydrostatic brain edema: basic mechanisms and clinical aspect.

The term hydrostatic brain edema results from unfavorable hydrtostatic pressure gradiernts between blood vessels and brain tissue. Arterial hypertension combined with decompressive craniectomy produces extensive brain edema in the arterial boundary zone of the decompressive area. The increased hydrostatic pressure gradient enhances tissue damage and causes the biphasic opening of the blood-brain barrier (BBB). The hydrostatic pressure alone is capable of causing the initial BBB opening and this induced edema results in derangement of cerebral microcirculation and metabolism. With morphological opening and metabolic damage of the vascular wall, the second BBB opening is elicited by the amplified hydrostatic pressure gradient, which is similar to that in vasogenic edema. In the clinical aspect, the beneficial effect of decompressive craniectomy in the treatment of uncontrollable ICP and brain edema remains controversial. External decompression may have adverse effects on severe brain edema and swelling. In this regards, control of driving force for the formation of brain edema could be the treatment of choice as an initial step. In addition, recent reports provided by MR imaging indicated new information on the pathophysiological features of the patients with acute hypertension. In the patients with hypertension due to reversible posterior leucoencephalopathy (RPL) syndrome, MR images show reversible signal abnormalities in the bilateral occipital lobes, suggesting hydrostatic brain edema.

Animals↗

PubMed2003

Edema fluid accumulation within necrotic brain tissue as a cause of the mass effect of cerebral contusion in head trauma patients.

The early massive edema caused by severe cerebral contusion results in progressive intracranial pressure (ICP) elevation and clinical deterioration within 24-72 hours post-trauma. Surgical excision of the necrotic brain tissue represents the only therapy, which can provide satisfactory control of the elevated ICP and clinical deterioration. In order to elucidate the mechanisms underlying the early massive edema, we have carried out a series of detailed clinical studies. Diffusion magnetic resonance (MR) imaging and apparent diffusion co-efficient (ADC) mapping suggest that cells in the central area of contusion undergo shrinkage, disintegration and homogenization, whereas cellular swelling is predominant in the peripheral area during the period of 24-72 hours post-trauma. The ADC values in the central and peripheral areas are maximally dissociated during this period. A large amount of edema fluid accumulates within the necrotic brain tissue of the central area beginning at approximately 24 hours post-trauma. We have found that fluid-blood interface formation within the central area does not represent an uncommon finding in various neuroimaging examinations of cerebral contusions, indicating layering of red blood cells within the necrotic brain tissue accumulating voluminous edema fluid. Intravenous slow infusion of gadolinium-DTPA and delayed MR imaging revealed that the central area of contusion can be enhanced at 24-48 hours post-trauma. implying that water supply from the blood vessels is not completely interrupted. Necrotic brain tissue sampled from the central area of contusion during surgery demonstrates a very high osmolality. It appears that the capacitance for edema fluid accumulation increases in the central area, whereas cellular swelling in the peripheral area elevates the resistance for edema fluid propagation. Combination of these circumstances may facilitate edema fluid accumulation in the central area. We also suggest that the dissociation of ADC values and high osmolality within the necrotic brain tissue may generate an osmotic potential across the central and peripheral areas and contribute to the early massive edema caused by cerebral contusion.

Body Fluids↗

PubMed1994

A high-field magnetic resonance imaging study of experimental vasogenic brain edema and its response to AVS: 1,2-bis (nicotinamido)-propane.

We clearly represented brain structures of rats and permitted a rapid assessment of water gradient of the brain edema by cortical freezing utilizing a high-field (7T) proton magnetic resonance imaging (MRI). The typical time course of vasogenic edema and the efficacy of AVS; 1,2-bis (nicotinamide)-propane upon the edema were presented. Twelve rats with edema induced by cortical freezing were divided into two groups; one group of animals received 0.5 ml of physiological saline with 100 mg (/kg) AVS every eight hours intraperitoneally. The other group of untreated animals received only saline. One three, six, 12, and 24 hours after lesion production, the profiles of edema fluid spreading and the maximum signal intensity (MI) of some regions of interest (ROI) were assessed by T2 weighted images (TE = 70 ms, TR = 3500 ms). One hour after lesion production in the untreated group, a low heterogeneous intensity area was seen mainly in the primarily injured cortex. Two hours later, the margin of the lesion gradually increased in intensity and MI of ROIs around the lesion also gradually increased. Twenty-four h after lesion production edema extended contralaterally via corpus callosum. AVS reduced edema fluid spreading beginning from about six hours after lesion production. The MIs of the AVS treated group were significantly lower than in the untreated group (p < 0.01). We conclude that sequential observation of edema using MRI is a quite practical technique for evaluation of the efficacy of any therapeutic agent.

Animals↗

PubMed1994

A study on peritumoral brain edema around meningiomas by MRI and contrast CT.

In the present study upon 9 meningiomas, the volume of peritumoral brain edema was calculated by integration of the cross-sectional edematous areas on serial MRI slices. It was zero in 3 cases and ranged from 11 to 176.4 ml in the other cases. There was disruption of the cortex in all cases, ranging from slight to severe. T1 and T2 measurements were made at the level of maximum edema extension (at 1.5 T), using a mixed sequence. From the T2 values tissue water content in % was calculated using equations, which had been obtained by correlating water content with relaxation rates. These had been measured on human brain autopsy specimens subjected to hydration or dehydration. Assuming that spread of contrast agent marks the advancement of the front of edema produced by the tumor, calculation of the excess of edema production per unit tumor volume Veff/VN was performed on the basis of CT-studies made before, and at 1.5, 3 and 6 hr after contrast infusion. Of 6 tumors with edema (mean water content of peritumoral white matter of 91% and mean edema volume of 69.2 ml) the Veff/VN was 0.18-1.08 ml/h/cm3 tumor volume, whereas 3 tumors without associated edema had a Veff/VN of 0.03-0.12 ml/h/cm3. In meningiomas cortex penetration seemed to be a separate factor determining the spread of edema.

Blood-Brain Barrier↗

PubMed1992

Classification of the cerebral edemas with reference to hydrocephalus and pseudotumor cerebri.

Cerebral edema is a common clinical disorder that results from an abnormal increase in water content within the extracellular (EC) compartment of the brain. It is distinguished from two other types of brain bulk enlargement: (1) vascular swelling, caused by arterial dilatation or venous obstruction; and (2) cellular swelling, caused by cytotoxic injuries or metabolic storage. Under normal conditions, the EC compartment has two fluids, the interstitial fluid (ISF) and the cerebrospinal fluid (CSF), and extends from the blood brain barrier (BBB) through a series of 100 to 150-A-wide intercellular spaces that are anatomically continuous with the CSF spaces. There are four primary types of EC edema: (1) vasogenic edema, which results from an increase in brain capillary permeability, the most common type, in which leakage of plasma constituents into the brain follows the pathways of ISF bulk flow and is governed by the interaction of systemic arterial pressure and tissue resistance; (2) osmotic edema, which results from an unfavorable osmotic gradient between the plasma and ISF across an intact BBB; (3) compressive edema, which results from obstruction of ISF bulk flow pathways; and (4) hydrocephalic edema, which results from obstruction of CSF bulk flow pathways. In this latter type of edema, distension of the collecting channels proximal to the block leads to retrograde flooding of the EC compartment with the formation of periventricular edema. The syndrome of pseudotumor cerebri includes several different types of brain bulk enlargement.

Animals↗

PubMed1996

Effect of dexamethasone, barbiturate and hypothermy on edema induced by CO2 laser brain lesion in the dog: light and electron microscopic study.

Experiments were carried out to compare the effectiveness of dexamethasone, a barbiturate, and hypothermy on experimental cerebral edema caused by CO2 laser in dogs. Experimental brain lesions were created over the right frontal cortex of the dogs through the intact dura mater with CO2 laser energy (40 W impact, 0.5 second duration, for a total time of 4 seconds on a 12.5 mm surface). Animals were divided into four groups and treated with dexamethasone, a barbiturate, hypothermy, and a crystalloid (control group). The brains were examined 48 hours after injury. Histologically all brain lesions showed three distinct layers with a vaporized center bordered by a zone of coagulation necrosis surrounded by edema. The main finding in the surrounding coagulation and edematous layers was dilatation of the vessels. Hemorrhage was sometimes observed mainly in the edematous layer. The effect of these therapies on the laser lesion and the effectiveness of these therapies on surrounding cerebral edema were evaluated by both light and electron microscopy. The control group showed significantly greater edema than the dexamethasone group. There was only a minimal difference between the control group and the barbiturate group, and there was no significant difference in amount of edema between control group and the hypothermy group. There was less edema in the dexamethasone group than in the other ones. These data suggest that dexamethasone inhibits edema in CO2 laser lesions with the same efficacy as shown in the treatment of vasogenic edema.

Animals↗

PubMed1979

Effect of furosemide (lasix) on acute severe experimental cerebral edema.

The effect of furosemide (Lasix) therapy on a standardized experimental cerebral edema, induced in rats by applying a cooling stamp to the right side of the skull over the right coronal suture by means of a stereotactic instrument, was examined. The hemispherically separated water and electrolyte contents of the brain were analyzed after 24 h. Following furosemide therapy, the behavior of these edema parameters was compared statistically with dexamethasone, glycerol and albumin. An increase of the water and sodium content, and a decrease of potassium was observed 24 h after the trauma, especially in the right hemisphere. Furosemide did not improve either the water content or the electrolyte balance. By contrast, the administration of dexamethasone, glycerol and albumin was followed by a significant improvement of the edema. In experiments with cats, the course of the edema and the effect of furosemide on the cold brain injury of the right hemisphere were observed by measuring the intracranial pressure (ICP) values, and by continuous monitoring of the EEG. The ventricular CSF pressure and epidural pressures were also recorded. The electrical brain activity was continuously compared with the course of the ICP by means of computer analysis. In addition, the blood osmolality and diuresis were monitored. The ICP increased rapidly after the trauma, establishing considerable pressure gradients, and the EEG power intensities decreased markedly on the right side. Histologically, there was an extended edema of the white matter of both hemispheres. The ICP was not lowered by single injections or high dose infusions of furosemide, and the EEG power intensities also did not improve. Infusions of large volumes of furosemide even resulted in an increase of ICP, but infusion of 40% sorbitol effected a rapid decrease of ICP and EEG recovery over the left hemisphere. Sorbitol infusion also caused a marked rise in the blood osmolality, whereas furosemide had no such effect. The results raise considerable doubts as to the propriety of the exclusive use of furosemide for cases of acute cerebral edema with raised ICP. The diuretic effect is insufficient to establish an osmotic gradient, and its general dehydrating effect does not acutely influence the ICP. The absence of effect on the experimental tissue edema would not appear to commend furosemide as basic therapy for cases of traumatic cerebral edema.

Albumins↗

PubMed1996

The role of the coagulation cascade in brain edema formation after intracerebral hemorrhage.

The coagulation cascade has a potential role in brain edema formation due to intracerebral hemorrhage. In this study blood and other solutions were injected stereotactically into the right basal ganglia in rats. Twenty-four hours following injection, brain water and ion contents were measured to determine the amount of brain edema. Intracerebral blood resulted in an increase in brain water content. The amount of brain edema surrounding the intracerebral hematoma was reduced by a thrombin inhibitor N alpha-(2-Naphthalenesulfonylglycyl)-4-amidino-DL-phenylalaninep iperidide, (alpha-NAPAP) infused into the hematoma after the clot had been allowed to solidify. The inhibitor did not alter the actual size of the clot mass. An artificial clot composed of fibrinogen, thrombin, and styrene microspheres also produced brain edema. A fibrin clot led to edema formation even in the absence of mass effect provided by the microspheres. The single component responsible for production of brain edema in all these models was thrombin. The edema was formed in response to a fibrinogen-independent pathway. These results indicate that the coagulation cascade is involved in brain edema that develops adjacent to an intracerebral hematoma.

Animals↗

PubMed1985

Modulation of mouse ear edema by cyclooxygenase and lipoxygenase inhibitors and other pharmacologic agents.

Inhibitors of arachidonic acid (AA) metabolism and other pharmacologic agents were evaluated against ear edema produced in mice by tetradecanoylphorbol acetate (TPA) or AA. Drugs were administered orally and topically either 30 min prior to AA or 30 min after TPA, except for steroids which were administered 2.5-3 hr prior to AA. Several cyclooxygenase (CO) inhibitors including indomethacin, aspirin, piroxicam and timegadine were without effect when administered orally against either irritant; the same drugs inhibited TPA edema when they were administered topically. Mixed CO/lipoxygenase (LO) inhibitors, phenidone and BW755C, were active orally against AA edema (ED50S of 84 and 65 mg/kg, respectively) and against TPA edema (ED50S of 235 and 88 mg/kg, respectively). Phenidone was more active topically against AA edema (ED50, 0.1 mg/ear) than BW755C (ED50, 2.8 mg/ear); however, BW755C was more active topically against TPA edema (ED50, 0.2 mg/ear) than phenidone (ED50, 0.6 mg/ear). Methylprednisolone was very effective in the AA (oral ED50, 17 mg/kg; topical ED50, greater than 1 mg/ear) and TPA models (oral ED50, 4.3 mg/kg; topical ED50, 0.03 mg/ear. MK-447 was topically and orally effective only in the TPA model. Not surprisingly, drugs were more effective topically than orally in both mouse ear edema assays. The models were somewhat selective for CO and CO/LO inhibitors; however, dapsone was orally effective in the ear models, and a number of mediator antagonists and CNS drugs, especially anti-psychotics, were topically active primarily against TPA edema. These models may be useful for the detection of in vivo activity of CO/LO or 5-LO inhibitors.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗

PubMed1989

Pharmacologic modulation of D-49 phospholipase A2-induced paw edema in the mouse.

Paw edema was produced in CD-1 mice by the injection of 0.3 micrograms of snake venom PLA2 (A.p. piscivorus D-49) into the hind paw. Edema peaked at 10 min, remained elevated until 60 min, and then declined slowly. The PLA2 inhibitors, luffariellolide and aristolochic acid, reduced the edema but only when coinjected with the PLA2. The histamine/serotonin antagonists were the most effective drug class against PLA2-induced paw edema. The PAF antagonists, CV-6202 (iv) and kadsurenone (coinjected) reduced the PLA2-induced edema, whereas high doses of the corticosteroids, dexamethasone and hydrocortisone, were also effective. NSAIDs only partially inhibited the paw edema. The LO/CO inhibitors yielded varying activities, with only BW755C and NDGA inhibiting the edema. These results suggest that PLA2 induces paw edema in the mouse via the action of several classes of inflammatory mediators.

Animals↗

PubMed1993

Rat paw edema and leukocyte immigration induced by plant lectins.

Lectins from Dioclea grandiflora (DG) and Canavalia brasiliensis (CB) were compared with Concanavalin A (ConA) for their ability to induce paw edema and peritoneal cell immigration in rats. ConA caused a slight edema with a peak at 1 h after injection, while DG or CB induced a pronounced and long-lasting edema that reached a maximum at about 6 h. Different antiinflammatory drugs partially inhibited the edema. alpha-D-glucose (GLU) partially blocked the edema caused by ConA and markedly inhibited that due to CB, but had no effect on the edema induced by DG. alpha-Methyl mannoside (alpha-MM) blocked the edema caused by DG and ConA, but did not affect that caused by CB. At doses much lower than those used to induce paw edema, the lectins promoted an intense accumulation of neutrophil and mononuclear cells in the rat peritoneal cavity. CB and DG were more potent than ConA, which also presented a different profile of cell immigration. GLU significantly inhibited leukocyte accumulation caused by all lectins. alpha-MM impaired ConA- and DG-induced cell immigration, but only partially inhibited CB. Thus, despite their physicochemical similarities with ConA, DG and CB have more powerful pro-inflammatory effects. This difference seems to be related to their sugar-binding properties. However, while ConA- and DG-induced effects were inhibited more by alpha-MM than by GLU, CB-induced effects were inhibited more by glucose.

Animals↗