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At least 19 recordsLinked to original sources
PubMed1983

[Experimental studies of brain edema by infusion edema model-- biophysical changes of edema fluid in white matter of the brain].

The important changes in the area of brain edema are the accumulation and the spreading of edema fluid through the extracellular space in white matter of the brain. In this study, we described the changes of tissue resistance and compliance as the increment of accumulated volume of fluid produced by the slow infusion of normal saline or plasma into white matter of the cat brain. Adult cats (22) were tracheotomized, paralyzed with Galamine (2 mg/kg) and maintained normocapnic, normotensive under nitrous oxide anesthesia. Normal saline or plasma of their own was infused slowly through 25 gauge needle implanted into left frontal white matter by stereotaxic technique. A low compliance pressure gauge transducer was connected to the line for the measurement of inflow pressure. Tissue resistance and compliance for the movement of infused fluid into white matter were delivered from the changes of inflow pressure by adding the 3 microlitter per minutes on top of the resting steady state pressure. Values of tissue resistance in normal white matter, determined at the accumulated volume of 0.05 ml was very high (normal saline infusion: 6.42 +/- 0.61 X 10(3) mmHg/ml/min, plasma infusion: 5.47 +/- 1.43 X 10(3) mmHg/ml/min). But it decreased rapidly followed by more gradual decrease of tissue resistance became more edematous, reaching a plateau of one sixth of initial value at an infused volume of 0.5 ml. Tissue compliance changed by an opposite pattern of rapid increase and plateau to the changes of tissue resistance.

Animals↗
PubMed2003

MD simulations of anthrax edema factor: calmodulin complexes with mutations in the edema factor "switch a" region and docking of 3'-deoxy ATP into the adenylyl cyclase active site of wild-type and mutant edema factor variants.

Bacillus anthracis, a spore-forming infectious bacterium, produces an exotoxin, called the edema factor (EF), that functions in part by disrupting internal signalling pathways. When complexed with human host cell calmodulin (CaM), EF becomes an active adenylyl cyclase, producing the internal signal substance cyclic-AMP in an uncontrolled fashion. Recently, the crystal structures for uncomplexed EF and EF:CaM complexes in the presence and absence of a substrate analog (3'-deoxy-ATP), were reported. EF mutational studies have implicated a number of residues important in CaM binding and/or in the generation of the adenylyl cyclase active site, formed by the movements of the EF switch A, B and C regions upon CaM binding. Here we report on the results of molecular dynamics (MD) simulations on two EF:CaM complexes, one containing wild-type EF and the other containing EF in which a cluster of residues in the switch A region (L523, K525, Q526 and V529) have been mutated to alanine. The switch A mutations cause a large increase in the flexibility of the switch C region, the rupture of a number of EF-CaM interactions, an expansion of the carboxyl-terminal domain of CaM, and a change in the Ca(2+) ion binding abilities of the CaM that is in complex with EF. The results indicate the importance of the mutated switch A residues in maintaining a compact EF:CaM complex that appears to be a prerequisite for the generation of a fully-functional adenylyl cyclase active site. The effects of mutating key residues (K346, K353, H577, E588, D590 and N639) in the active site region of EF (to alanine) on the ability of EF to bind the 3'-deoxy-ATP substrate analog were also examined. Active-site residue substitutions at positions 583 (N583A) and 577 (H577A) were found to be particularly disruptive for the placement of the adenine ring moiety into the position found in the x-ray crystal structure of the ligand-protein complex.

Adenylyl Cyclases↗
PubMed1981

The spectrum of pulmonary edema: differentiation of cardiogenic, intermediate, and noncardiogenic forms of pulmonary edema.

Pulmonary edema fluid and serum samples were obtained from 20 patients with cardiac and noncardiac pulmonary edema, and total protein, albumin, and globulin concentrations were measured. The mean edema fluid to serum protein ratio in patients with pure cardiogenic pulmonary edema was 0.37 +/- 0.09. In contrast, the patients with pure noncardiogenic pulmonary edema had protein ratios of 0.84 +/- 0.12 (p less than 0.001). Another group of patients with both cardiac and noncardiac causes for edema demonstrated edema fluid to serum protein ratios that were significantly higher than those found in the cardiogenic patients and lower than the protein ratios in the noncardiogenic patients (0.60 +/- 0.07) (p less than 0.01) A cardiac or noncardiac causes of pulmonary edema could be determined in all patients, using edema fluid to serum total protein ratios in conjunction with globulin ratios. Cardiogenic and noncardiogenic pulmonary edema represent the extremes in the spectrum of pulmonary edema. A combination of increased permeability and hydrostatic pressure may account for an intermediate form of pulmonary edema.

Adult↗
PubMed1994

Peritumoral brain edema associated with pediatric brain tumors: characteristics of peritumoral edema in developing brain.

The incidence and clinical significance of peritumoral brain edema in pediatric patients is not well understood. The purpose of this study is to clarify the clinical significance of peritumoral brain edema in pediatric patients. Seventy seven pediatric patients (under 15 year old) with brain tumor were studied by MRI. The volume of peritumoral edema and brain tumor were measured by integration of the cross-sectional area on serial MRI. The severity of brain edema was expressed by the ratio of edema volume to tumor volume. The results were compared with that of 408 adult patients with brain tumor. Incidence of the brain edema associated with supratentorial tumors is lower in pediatric group than in adult. Severity of brain edema is also less extent in the pediatric group. Forty two percent of supratentorial gliomas in pediatric group showed peritumoral edema. On the other hand, 63% of adult group showed peritumoral brain edema. In general, pediatric brain tumors rarely associated with marked peritumoral brain edema which observed in the adult group. However, intraventricular or paraventricular tumors with obstructed hydrocephalus showed remarkable brain edema in pediatric group. Low incidence and less severity of peritumoral edema are caused not only by histological bias of tumors, but also by the biological nature of developing brain.

Adolescent↗
PubMed1998

[Edema tester. Assessment of edema of the legs].

BACKGROUND: The aim of this study was the clinical evaluation of an original device produced to evaluate edema in a semi-quantitative way, the ACI Medical, Edema Tester (ET). ET1, is a soft plastic plate characterised by two parallel conic pyramidal protrusions. One side of the protrusion is rounded while the other side has an angular edge. The two protrusions are placed on the plate in inverse decreasing height. ET2 is characterised by two lines of 7 holes placed in the plate. The ET is applied at the internal perimalleolar region with the conic pyramidal protrusions in contact with the skin. A standard sphygmomanometer cuff is applied over the area and pressure is maintained at 50 mmHg for a period between 1 an 3 minutes. The cuff is then removed. ET1: skin marks are usually just visible in normal subjects without edema and disappear in a few minutes. When edema is moderate some half of each protrusion is visible as a skin mark. In limbs with severe edema the whole length of the protrusion is clearly visible. ET2: skin marks are usually just visible in normal limbs without edema and disappear in a few minutes. In limbs with edema the number of holes visible on the skin is increased and in severe edema all holes are visible. METHODS: To evaluate semi-quantitatively the level of edema the length of the two skin marks can be measured and for the ET2 the numbers of visible holes can be counted, as they are generally proportional to the degree of edema. The ET testers were evaluated in 22 normal subjects, 19 limbs with varicose veins, 22 patients with CVI and lipodermatosclerosis, 5 patients with initial primary lymphedema and in 8 subjects with severe, chronic, lymphedema and skin alterations. RESULTS: The results showed a significant difference between normal limbs an patients. CONCLUSIONS: In conclusion, the method of evaluating edema with ET can be used to supplement the clinical and noninvasive evaluation. In general practice the presence of edema measurable with ET indicate the need for treatment. The several degrees of skin marks visibility and disappearance time may be used as a general guideline to indicate the need for different types and length of treatment.

Adult↗
PubMedDate not supplied

Prevention of edema, flight microangiopathy and venous thrombosis in long flights with elastic stockings. A randomized trial: The LONFLIT 4 Concorde Edema-SSL Study.

UNLABELLED: The LONFLIT1/2 studies have established that in high-risk subjects after long (> 10 hours) flights the incidence of deep venous thrombosis (DVT) is between 4% and 6%. The LONFLIT4 study has been planned to evaluate the control of edema and DVT in low-medium-risk subjects. The aim of this study was to evaluate edema and its control with specific flight stockings, in long-haul flights. In the first part of the study 400 subjects at low-medium risk for DVT were contacted; 28 were excluded for several nonmedical problems; 372 were randomized into 2 groups to evaluate prophylaxis with stockings in 7-8-hour flights; the control group had no prophylaxis. Below-knee, Scholl, Flight Socks, producing 14-17 mm Hg of pressure at the ankle, were used in the treatment group. The occurrence of DVT was evaluated with high-resolution ultrasound scanning (femoral, popliteal, and tibial veins). Edema was assessed with a composite score based on parametric and nonparametric measurements. Part II: In this part of the study 285 subjects at low-medium risk for DVT were included and randomized into 2 groups to evaluate edema prophylaxis in 11-12-hour flights; the controls had no prophylaxis while the prevention group had below-knee, Scholl, Flight Socks (comparable to part I). RESULTS: Part 1: DVT evaluation. Of the 184 included subjects in the stockings group and 188 in the control group, 358 (96.2%) completed the study. Dropouts were due to compliance or connection problems. Age/sex distributions were comparable in the groups. Stockings Group: of 179 subjects (mean age 49; SD 7; M:F = 101:78), none had DVT or superficial thromboses. CONTROL GROUP: of 179 subjects (mean age 48.4; SD 7.3; M:F = 98:81), 4 (2.2%) had a DVT. There were also 2 superficial thromboses. In total, 3.35% (6) subjects had a thrombotic event. The difference (p<0.002) is significant. Intention-to-treat analysis detects 15 failures in the control group (9 lost + 6 thromboses) out of 188 subjects (7.9%) versus 5 subjects (2.7%) in the stockings group (p <0.05). All thrombotic events were observed in passengers sitting in nonaisle seats. The tolerability of the stockings was very good and there were no complaints or side effects. Thrombotic events were asymptomatic. No difference was observed in the distribution of events between men and women. The 3 women who had a thrombotic event were taking low-dose, oral contraceptives. Edema evaluation: The level of edema at inclusion was comparable in the 2 groups. After the flight there was a score of 6.7 (3.1) in controls; in the stockings group the score was 2.9 times lower (p<0.05). The control of edema with stockings was clear considering both parametric (circumference, volume) and nonparametric (analogue scale lines) data. Part II: DVT evaluation. Of the 285 included subjects, 271 (95%) completed the study. Dropouts were due to low compliance or connection problems. Age/sex distributions were comparable in the groups. Stockings Group: of 142 subjects (mean age 48; SD 8; M:F = 89:53), none had DVT or superficial thromboses. CONTROL GROUP: of 143 subjects (mean age 47; SD 8; M:F = 87:56), 3 had a popliteal DVT and 3 a superficial thrombosis. In total, 4.2% (6) subjects had a thrombotic event. The difference (p<0.02) between groups is significant. Intention-to-treat analysis detects 14 failures in the control group (8 lost + 6 thromboses = 9.7%) versus 6 (all lost = 4.2% in the stockings group) (p<0.05). Four of 6 events (3 DVT + 1 SVT) were observed in non-aisle seats. The tolerability of the stockings was very good. No difference was observed in the distribution of events between men and women. Edema evaluation: The level of edema at inclusion was comparable in the 2 groups. After the flight there was a score of 8.08 (2.9) in controls while in the stockings group the score was 2.56 (1.5) (p < 0.005). In conclusion. Scholl Flight Socks are very effective in controlling edema. Also this type of compression is effective in significantly reducing the incidence of DVT and thrombotic events in low-medium-risk subjects, in long-haul flights. CONCLUSIONS: Considering these observations, Flight Socks are effective in controlling edema and in reducing the incidence of DVT in low-medium-risk subjects, in long-haul flights (7-11 hours).

Aerospace Medicine↗
PubMed1991

Sequential changes of perivascular edema cuffs in models of permeability and hemodynamic pulmonary edema.

The areas of perivascular edema cuffs surrounding pulmonary arteries and veins were sequentially measured as an index of the fluid transport unit in lung interstitium (FTULI) in epinephrine-induced and oleic acid-induced pulmonary edema in rats. The former edema represents a model of hemodynamic edema and the latter, permeability pulmonary edema, respectively. In epinephrine-induced pulmonary edema, both the ratio of edema cuff area to cross-sectional area of the pulmonary artery (Rr) and the ratio of lung weight to body weight (L/B) were increased in parallel, reached maximum levels at 0.5 h after the treatment, and returned to the control levels after 3 h. In oleic acid-induced pulmonary edema, the changes in Rr and L/B were not parallel, and the maximum levels were reached at different times, Rr at 3 h and L/B at 1.5 h. Rr returned close to the control level in 24 h but L/B remained elevated so that rate of recovery was delayed. The cuffs around the veins appeared similar to those around the arteries, but were very slight in both models. The difference in the time course of Rr and L/B in the two models may suggest that the recruitment of FTULI is insufficient in oleic acid-induced pulmonary edema; this limitation seems to be an important factor which makes the permeability edema refractory to treatment, together with the damage to the blood gas barrier.

Animals↗
PubMed1992

[Postoperative cerebral edema. Physiopathology of the edema and medical therapy].

Cerebral edema complicates many neurosurgical conditions, such as head injuries, neoplasms and infections, and is the direct result of operative trauma. The recognition and the treatment of brain edema are of great practical importance, particularly in those conditions leading to brain herniations and/or intracranial hypertension. Brain edema can be distinguished into two major categories, based on the integrity of the blood brain-barrier (BBB). With intact BBB edema, the crucial pathogenic event is related to disturbances of cellular metabolism and ionic transport. All the cellular elements of brain may undergo swelling, with a concomitant reduction of the extracellular-fluid space of the brain. Open BBB edema, the most common form of brain edema, is characterized by increased permeability of the brain endothelial cells. Brain edema results from the oncotic forces generated from a serum protein influx into the nervous tissue, and edema fluid accumulates primarily in the extracellular space. The non-operative management of brain edema requires attention to the causes that have induced brain edema. Specific pharmacologic therapy with corticosteroids, hyperosmolar agents and furosemide or acetazolamide depend upon accurate assessment of BBB integrity.

Blood-Brain Barrier↗
PubMed1979

The value of edema fluid protein measurement in patients with pulmonary edema.

Alveolar fluid and plasma proteins were analyzed in 24 patients with florid pulmonary edema, in 21 of whom pulmonary capillary wedge pressure (Pcw) was also measured. In all patients with Pcw less than 20 mm Hg, the edema fluid to plasma protein ratio exceeded 0.6; the mean edema fluid to plasma protein ratio in the four patients with cardiogenic edema (increased Pcw) was 0.46. In the 21 patients in whom full data were available, the net intravascular filtration force (Pcw - plasma colloid osmotic pressure) was less than -4 mm Hg, the value at which (according to others) pulmonary edema should occur, in only 10. When the interstitial colloid osmotic pressure, approximated by the osmotic pressure of edema fluid protein, was added, the net filtration force became positive in 17 of 21 patients. Comparison of the protein concentrations of edema fluid and plasma aids in the diagnostic separation of increased permeability from high hydrostatic pressure edema and adds to our understanding of the relative osmotic and hydrostatic forces that contribute to pulmonary edema when the alveolar-capillary membrane is damaged.

Adolescent↗
PubMed1981

Edema fluid and coagulation changes during fulminant pulmonary edema.

Edema fluid and a coagulation profile were obtained in 45 patients (17 to 87 years) during fulminant pulmonary edema. Left ventricular failure and/or volume overload accounted for edema in 18 patients. In another 27 patients, edema developed in association with other features that typify the adult respiratory distress syndrome (ARDS). In the ARDS group, multiple disorders were implicated in the genesis of edema, including shock, bacteremia, drug overdose, and aspiration. Assessment of edema fluid and coagulation measurements is useful to classify and to determine the severity of the edema process. ARDS is characterized by permeability pulmonary edema that usually stems from a combination of multisystemic disorders. Permeability pulmonary edema and coagulation changes appear to be interrelated. However, it is not clear the extent to which the coagulation disturbances are a cause or a result of the alterations in the alveolar-capillary membrane.

Adolescent↗