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PubMed1997

Biphasic pathophysiological response of vasogenic and cellular edema in traumatic brain swelling.

The objective of this study was to quantify the temporal water content changes and document the type of edema (cellular versus vasogenic) that is occurring during both the acute and the late stages of edema development following closed head injury. Adult Sprague rats (n = 50) were separated into two groups: Group I: Sham (n = 8), Group II: Trauma (n = 42). The measurement of brain water content (BWC) was based on T1, whereas the differentiation of edema on the measurement of the random, translational motion of water protons (apparent diffusion coefficients-ADC) by MRI. In trauma animals, we found a significant increase in ADC (105%) as well as in BWC (0.7 +/- 0.3%) during the first 60 minutes post injury indicating vasogenic edema formation. This transient increase; however, was followed by a continuing decrease in ADC beginning at 45 minutes post injury and reaching a minimum at days 7-14 (-103%). Since the BWC continued to increase during the next day (10.3%), it is suggested cellular edema formation started to develop soon after injury and became dominant between 1-2 weeks post injury. In conclusion we may consider, that there is a predominantly vasogenic edema formation immediately after injury and later a more widespread and slower edema formation due to a predominantly cellular swelling.

Animals↗
PubMed1997

A new model of spinal cord edema.

Edema of the spinal cord has not been well understood. Brain edema produced by Marmarou's infusion method is essentially similar to vasogenic edema. This infusion method for producing edema was applied to a cat spinal cord. After laminectomy, a 30-gauge needle was inserted into the intumescentia cervicalis. A total amount of 10 microliters of 2% Evans' blue or autoserum were infused using an infusion pump at a rate of 5 microliters/hr. Macroscopally, Evans' blue was observed in the vicinity of infused site at the same level of the needle insertion and was seen spreading mainly longitudinally in the lateral column for a certain distance. The extracellular space was markedly distended in the in fused white mater and filled with electron-dense materials which were thought to be proteins in the electron microscopic study. The fine structural features were similar to the findings which were seen in Marmarou's infusion type of brain edema. Using this model, it seems to be feasible to produce reproducible spinal cord edema at any location in order to investigate not only the morphological aspect but also physiological aspect of the edema.

Animals↗
PubMed1994

Chronological changes in brain edema induced by experimental intracerebral hematoma in cats.

To investigate the temporary profile of changing perifocal brain edema around an intracerebral hematoma (ICH), we developed an experimental ICH model using cats. The developing perifocal edema in the white matter around the hematoma was measured by means of a gravimetric technique. Edema was more severe near the ICH, and declined with increasing distance. Edema was mild 2 hours after the onset of the ICH, and was most severe in all the regions examined 3 days later. Edema decreased but still existed in all regions 7 days after the onset of the ICH. The results suggest that the mechanism of the development of edema associated with ICH seems to differ from that associated with a cold injury. This experimental ICH model proved to be useful for the study of formation, expansion, and resolution of edema associated with ICH.

Animals↗
PubMed1994

Subcortical U-fibers layer preservation in brain edema.

The mechanism involved in the relative preservation of the subcortical U-fibers in the arcuate zone was studied in a post infarct edema after sagittal superior sinus occlusion. Superior sagittal sinus (SSS) of 36 mongrel cats were occluded by polymer injection. Immediately before the occlusion Evans-blue (EB) was administered intravenously. The cats were killed 1, 2, 3, 6, 12, 24, 72 and 120 hours after sinus occlusion. In 20 cats in which cortical veins were occluded, in addition to the SSS, EB was extravasated. In 9 of these cats, which had moderate edema, EB-staining was present only in the cortex. In 11 cats with severe edema, massive EB extravasation was observed also in the white matter. The U-fiber layer was free of EB, suggesting that the extension of edema was blocked by this zone. Our findings demonstrated that the U-fibers act not only as a resistance against extension of edema from white to gray matter, but also in a reverse direction. The characteristics of the spread of brain edema is not yet completely understood; both anatomical and biochemical peculiarities from its basis. Different morphological patterns in the astrocytic reaction as well as the U-fibers sector vascularization are important. To evaluate the role of each one of these factors in the preservation of subcortical U-fiber layer in brain edema further investigations should be done.

Animals↗
PubMed1996

Magnetic resonance relaxation times in acute hydrostatic pulmonary edema induced by noradrenaline in rats.

Models of pulmonary edema have been used to study the nuclear magnetic resonance (NMR) characteristics of lung water. Several investigators have measured changes in the relaxation times in the permeability type of pulmonary edema, but relatively few have measured relaxation times in the hydrostatic type of pulmonary edema. In this study we determined the characteristics of NMR relaxation times T1, T2 (Hahn spin-echo decay) and water content in acute hydrostatic pulmonary edema induced by noradrenaline administration in rats. Changes in T1 and T2 showed a significant prolongation in hydrostatic pulmonary edema. T2 decay curves for peripheral lung tissues were multiexponential and fit two components [T2 fast (T2f) and T2 slow (T2s)]. With two-component T2 analysis, T2s showed greater prolongation than did T2f. The increase in T2s was significantly correlated with an increase in water content, but the increase in the T2f value was not correlated with water content or with a change in T2s. The T2s component, which likely reflected changes in interstitial water, was more closely related than the T2f component to an increase in water content in hydrostatic pulmonary edema. Results suggested that regional changes in hydrostatic pulmonary edema may be evaluated by multicomponent T2 analysis.

Animals↗
PubMedDate not supplied

Interureteric ridge edema: incidence and etiology.

BACKGROUND: Interureteric ridge edema may be seen at intravenous urography (IVU) and is related to acute lower ureteral obstruction, trauma, or calculi. The purpose of this study was to explore the relationship between interureteric ridge edema and acute distal ureteral obstruction caused by ureteral calculi. METHODS: A total of 338 patients who had IVU for various indications during a 6-month period were reviewed for the presence of interureteric ridge edema. RESULTS: Interureteric ridge edema was seen in 12 (4%) of 338 patients, all with acute lower ureteral obstruction from stones. Interureteric ridge edema was best demonstrated with the partially filled bladder film or post-void bladder film in all cases. CONCLUSION: Interureteric ridge edema is most commonly caused by stone-induced distal ureteral obstruction and is less commonly seen with recent passage of a stone or other etiologies. Interureteric ridge edema was present in 26% of patients with acute lower ureteral obstruction.

Adult↗
PubMed1988

Blood-brain barrier disruption and exacerbation of ischemic brain edema after restoration of blood flow in experimental focal cerebral ischemia.

The mechanism of exacerbation of ischemic brain edema after blood flow restoration was studied in 20 cats under ketamine and alpha-chloralose anesthesia. Regional cerebral blood flow was measured by the hydrogen clearance method, and the left middle cerebral artery (MCA) was occluded for 6 h in group A, and for 3 h with subsequent 3 h recirculation in group B. Severity of brain edema was assessed by specific gravity measurement of tissue samples taken from coronal brain sections at the MCA area, while severity of blood-brain barrier (BBB) disruption was determined by measuring the amount of extravasated serum albumin by using [125I]albumin and tissue-uptake method in the same samples as those used for gravimetry. Structural and ultrastructural change was correlated with the severity of ischemic brain edema and BBB disruption. The results obtained showed that: (i) ischemic brain edema observed in group A was not associated with BBB opening to serum proteins; (ii) ischemic edema in group B was exacerbated significantly after recirculation in correlation with serum protein extravasation in most of the post-ischemic area; (iii) in the severely edematous area, serum protein extravasation reached a plateau and morphological examination at this type of area revealed cell membrane disruption especially of astrocytes, with leakage of intracellular substances. Our study indicated that the increase of extracellular osmotic pressure due to leakage of serum proteins via the disrupted BBB and of intracellular substances via the ischemically injured cell membrane into the extracellular space is the mechanism responsible for edema fluid accumulation in exacerbated ischemic brain edema.

Animals↗
PubMed1979

A specific immunofluorescence technique for the demonstration of vasogenic brain edema in paraffin embedded material.

Serum proteins as constituents of vasogenic brain edema were visualized both macroscopically and microscopically applying a double layer immunofluorescence technique to paraffin embedded material derived from three experimental series: peritumorous edema following xeno-transplantation of glioma cells, edema after cerebral embolization with micropheres, and edema after unilateral MCA occlusion. Exclusively cats were used as experimental animals. The staining procedures resulted in selective green fluorescence of vessel contents as well as edema protein, which was demonstrable even macroscopically at times, where edema formation reaches a maximum in each experimental series. Microscopically, serum protein could be traced up to the end of observation time ranging from 1 to 4 weeks, where the specific fluorescence was related to cellular structures. As compared to other techniques employed in brain edema localization, immunostaining mainly offers the following advantages: avoidance of in vivo tracing, better structural resolution in paraffin than in freeze sections, high specificity and sensitivity in antigen localization.

Animals↗
PubMed1986

Platelet involvement in rat paw edema induced by 2-methoxy-PAF.

PAF-acether (PAF) or 2-methoxy-PAF (2-MX) caused a dose-dependent paw edema showing a 1:25 ratio between their inflammatory activities. 2-MX caused a thrombocytopenia, whereas PAF did not alter the number of these cells. Both phospholipids induced reductions in total leukocyte count. Rat antiplatelet serum produced platelet depletion by PAF-induced paw edema was unaffected. The edema of 2-MX was significantly reduced by antiplatelet serum, under conditions where normal serum was inactive against the edema induced by PAF or 2-MX. Histopathological analysis of PAF and 2-MX-induced edema showed, in the first case, a small infiltrate of neutrophils, some lymphocytes, and several mastocytes around the vessels and, in the second, a neutrophilic infiltrate. These results suggest that PAF and 2-MX may produce edema through different mechanisms and that 2-MX causes edema in part through platelet activation.

Animals↗
PubMed1984

Elevated concentrations of leukotriene D4 in pulmonary edema fluid of patients with the adult respiratory distress syndrome.

The possible contribution of metabolites of arachidonic acid to the increased permeability of the alveolar-capillary barrier in the adult respiratory distress syndrome was examined by quantifying the pulmonary edema fluid concentrations of lipoxygenase and cyclooxygenase products. The concentration of leukotriene D4 in pulmonary edema fluid of 10 patients with the adult respiratory distress syndrome (18.5 +/- 6.8 pmol/ml; mean +/- SD), assessed by specific radioimmunoassay after isolation of the mediator, was significantly higher (P less than 0.001) than that of five patients with cardiogenic pulmonary edema (4.4 +/- 1.1 pmol/ml). The concentrations of leukotrienes B4 and C4, prostaglandin E2, and thromboxane B2 in edema fluid were not significantly different in the adult respiratory distress syndrome patients than in the other subjects with pulmonary edema. The edema fluid concentration of leukotriene D4 correlated with the ratio of edema fluid to plasma concentrations of albumin (r = 0.64). Leukotriene D4 thus may contribute to the permeability defect which allows an accumulation of protein-rich alveolar fluid in the adult respiratory distress syndrome.

Adolescent↗
PubMed1987

Role of early edema in the development of regional seizure-related brain damage.

Kainic acid-induced seizures produced early (2 hr) generalized edema and later (24 and 48 hr) necrotic edema in temporal cortex and hippocampus as measured by specific gravity changes. Mannitol given during the seizure partially protected against the early edema and prevented the necrotic edema indicating early edema may play a role in later brain damage. However, H2O intoxication, causing much greater generalized edema than the kainic acid-induced seizures, caused no necrotic edema in temporal cortex or hippocampus at 48 hr. Thus it appears that mannitol protection against kainic acid-induced brain damage may be by a mechanism in addition to dehydration.

Animals↗
PubMed1989

Edema and cell infiltration in the phorbol ester-treated mouse ear are temporally separate and can be differentially modulated by pharmacologic agents.

The temporal patterns of edema and accumulation of the PMN marker enzyme, myeloperoxidase (MPO), were examined following application of tetradecanoylphorbol acetate (TPA) to mouse ears. After application of 2.5 micrograms TPA, edema peaked at 6 hr, while MPO activity peaked at 24 hr. Pharmacological agents with defined mechanisms of action, delivered orally or topically, were assessed for effects on these responses. For oral administration, compounds were delivered 1 hr before and 6 hr after TPA and for topical administration compounds were delivered at 15 min and 6 hr after TPA. Topical and oral corticosteroids inhibited both edema and MPO accumulation. Cyclooxygenase and lipoxygenase inhibitors were very effective against MPO accumulation but were either inactive or moderately active vs edema. Anti-histamine/anti-serotonin agents had little effect on edema, but could inhibit or exacerbate MPO accumulation depending on dose and route of administration. Topically applied histamine itself did not effect TPA-induced edema, but markedly suppressed MPO accumulation. Acetone, the vehicle, when topically applied between 0.5 and 2 hr after TPA inhibited MPO accumulation by 60-80%, but had little effect on edema. Acetone applied before 0.5 hr or after 2 hr had no effect on either parameter. These results indicate that in the TPA-induced ear inflammation model the MPO response at 24 hr may be a useful additional indicator of drug activity.

Animals↗
PubMed1980

Pharmacological modulation of edema mediated by prostaglandin, serotonin and histamine.

Previous studies demonstrated that the formamidine pesticide chlordimeform (CDM) reversibly inhibited prostaglandin biosynthesis and prevented the late (PG-mediated) phase of carrageenin-induced hind paw edema. This study emphasizes antagonism by CDM of the early (5HT and histamine-mediated) phase of carrageenin edema. CDM and cyproheptadine both antagonized paw edema induced by albumin (5HT and histamine-mediated) and by the direct injection of 5HT and histamine, whereas aspirin and the PG antagonist, SC-19220, were ineffective. As expected, cyproheptadine selectively reduced the early phase, whereas aspirin and SC-19220 selectively reduced the late phase of carrageenin-induced edema. These results are thus consistent with earlier studies demonstrating PG mediation of the late phase of carrageenin edema, and 5HT and histamine mediation of albumin edema and the early phase of carrageenin edema. In addition, they indicate that CDM possesses multiple acute anti-inflammatory actions not exhibited by aspirin, by SC-19220 or by cyproheptadine alone.

Albumins↗
PubMed1978

Mechanism of the pulmonary edema induced by intravenous injection of scorpion toxin in the rat.

The intravenous injection of purified scorpion toxin (tityustoxin, TsTX) into unanesthetized rats induces a severe systemic hypertension followed by a hemorrhagic edema of the lungs. The edema is focal or diffuse, whereas the hemorrhage is always focal and less prominent than the edema. Anesthesia of the rats prevents the appearance of pulmonary edema. It seems likely that this protective action of the anesthesia is due, at least in part, to an interference with the hypertension induced by TsTX. The pulmonary edema is prevented by bilateral adrenalectomy, guanethidine or phenoxybenzamine. It is suggested that the edema depends on a sympathetic-adrenal discharge and that catecholamines released by TsTX act on alpha adrenergic receptors. The mean kininogen content of the rat plasma, 1 h after TsTX injection, is not significantly different from that found in the control animals. The possible role played by kinins and other mediators in the early phases of the pulmonary edema induced by TsTX is under investigation.

Adrenalectomy↗
PubMed1992

Effect of clonidine on experimental brain edema in the rat.

Several experimental brain edema models are currently available for drug evaluation. Brain edemas are essentially vasogenic and/or cytotoxic, and eicosanoids are involved in the development of these edemas. Thus, a new model developed in our laboratory, which was obtained by phospholipase A2 intracerebral injection was used to study the antiinflammatory effect of clonidine. The copper wire edema model was chosen as reference. Edemas were evaluated by determining the swelling and Na+ and K+ tissue concentrations of each hemisphere. Drugs were administered intraperitoneally. Dexamethasone was the only drug to inhibit copper wire-induced edema, whereas indomethacin and clonidine as well as dexamethasone exhibited marked antiedematous activity in our model. The effect of clonidine, which could be inhibited by prior administration of yohimbine, suggests that central alpha 2-adrenergic stimulation is involved in reducing experimental brain edema.

Animals↗
PubMed1998

[Chronic laryngeal edema as a late reaction to radiochemotherapy].

In addition to mucositis and myelotoxicity as well known early reactions after radiotherapy or radiochemotherapy in advanced head and neck tumors, late toxicity following treatment is an often underestimated problem. Between 1992 and 1995, 68 patients with advanced oro- and hypopharyngeal tumors were treated primarily with accelerated concomitant boost radiochemotherapy (total dose irradiations of 66 Gy and carboplatin as chemotherapy). Ninety-three per cent of the patients had stage IV disease according to the UICC-TNM classification. Monitoring of follow-up included late toxicity with special attention given to laryngeal edema. In 37 patients (54%) edema of the larynx as a late complication of radiochemotherapy was observed by clinical investigation and CT scan. The median onset of laryngeal edema was found 121 days after completion of therapy, with a median time of observation of 250 days. Observations in these patients demonstrated the chronic character of this edema. An increase in the laryngeal edema in 5 cases resulted in tracheostomy. Laryngeal edema in 10 patients was associated with recurrence of tumor. These results show that after xerostomia laryngeal edema is the main late toxicity in the head and neck after radiochemotherapy and should lead to further investigations to exclude possible recurrent tumor.

Adult↗
PubMed2006

[Distal clavicle edema].

PURPOSE: Distal clavicle marrow edema: frequency, MRI in the early stage and macroscopic correlation to the bone marrow distribution and to evaluate frequency and diagnostic criteria of a posttraumatic clavicula disorder with an edema pattern on MRI. An additional macroscopic study of the clavicle should elucidate anatomic peculiarities which could explain the reaction of the distal clavicle. MATERIAL AND METHODS: 285 MRI of traumatized patients were analyzed for edema pattern of the distal clavicle. Pattern A edema within the clavicle and the acromion was distinguished from pattern B edema within the clavicle only. Dissection in 20 cadavers should reveal vascular peculiarities and the bone marrow distribution within clavicle and acromion or vascular peculiarities. RESULTS: In 38 patients (13,3%) we found edema within the distal clavicle. Pattern A was found in 28 (9,8%) and pattern B in 10 patients (3,5%). Pattern A was usually associated with swelling of the AC joint (27 out of 28). Other injuries were not evident. 18 cadavers showed hematopoietic marrow within the distal clavicle and fatty marrow within the acromion. CONCLUSION: The distal clavicle can frequently react with edema pattern after trauma without evidence for another injury. Distinguish in cases with and cases without synovitis of the AC joint could have impact on therapy. A peculiar vascular supply of the distal clavicle could not be found.

Adolescent↗
PubMed2006

Prediction of cardiogenic pulmonary edema onset by monitoring right lung impedance.

OBJECTIVE: To evaluate the ability of internal thoracic impedance (ITI) monitors to predict cardiogenic pulmonary edema in patients at risk. DESIGN AND SETTING: Prospective, controlled multicenter study. PATIENTS: We examined 328 consecutive patients admitted for cardiac conditions. Of these 265 patients aged 27-83 years with no clinical signs of pulmonary edema, extracardiac respiratory failure or pacemakers comprised the study cohort. INTERVENTION: Monitoring of the lung's electrical impedance was used for predicting cardiogenic pulmonary edema since accumulation of blood and fluid decreases impedance values. MEASUREMENTS AND RESULTS: Impedance of the lung is the main feature of ITI measured by the RS-207 monitor: decreased ITI prior to the clinical signs of cardiogenic pulmonary edema was used as the prediction criterion. The clinical signs used for confirmation of its prediction were dyspnea, cyanosis, pulmonary rales, crepitations, arterial hypoxemia, and radiographic evidence of pulmonary congestion in chest radiographs. Clinicians were blinded to the results of ITI measurements and radiologists were blinded to both ITI and clinical data. Thirty-seven patients developed cardiogenic pulmonary edema while being monitored. ITI decreased by more than 12% of baseline in all of them; this occurred at 30 min or longer (26 patients) and at 60 min or longer (11 patients) before the appearance of clinical signs. ITI fell by less then 10.1% of baseline in all 228 patients who did not develop the edema. CONCLUSION: Monitoring ITI is suitable for early prediction of cardiogenic pulmonary edema, before the appearance of the clinical signs.

Adult↗