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At least 19 recordsLinked to original sources
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↗
PubMed1978

Clearance of edema fluid into cerebrospinal fluid. A mechanism for resolution of vasogenic brain edema.

The authors present the results of an investigation studying the resolution of vasogenic brain edema using cold injury in cats. The appearance of RISA-I131 and sucrose-C14 lebeled edema fluid in the ventricular cerebrospinal fluid (CSF) was assessed by means of ventriculocisternal perfusion. The effect of low- or high-pressure perfusion on edema spread was determined by measuring the water, sodium, RISA-I131, and sucrose-C14 content of serial tissue blocks taken from the injured cortex through the white matter to the ventricular ependyma. The findings indicate that increasing the hydrostatic pressure gradient between edematous brain and CSF enhances the clearance of edema fluid into the ventricular CSF. This was conclusively demonstrated with low-pressure ventricular perfusion which markedly diminished the amount of edema close to the ventricles compared to the controls. The concentration of albumin, sodium, and potassium to the fluid removed from the tissue during low-pressure perfusion indicates that bulk flow was the primary method of edema movement through the extracellular space. With high-pressure perfusion the concentration profiles suggested alternative mechanisms of edema resolution, such as diffusion and reabsorption into capillaries.

Animals↗
PubMed1979

Dynamics of cerebral edema. The role of an intact vascular bed in the production and propagation of vasogenic brain edema.

Brain edema was produced in cats by a standardized cortical freezing lesion. With a careful microsurgical tehnique, the injured cortex was removed as a single piece, either immediately after induction or at 2, 4, or 8 hours after lesion production. The injured brain was either discarded or replaced in its bed. Brain edema and the defect in the blood-brain barrier were assessed by determining percent dry weight, increase in volume of white matter, and spread of Evans' blue by planimetry. The results indicate that 1) if the lesion is removed immediately after production, formation of the expected vasogenic brain edema is completely abolished; 2) replacement of the frozen brain is unable to induce significant increase in permeability of the surrounding blood-brain barrier or a significant amount of brain edema; and 3) if the lesion is removed at 2, 4, or 8 hours with or without replacement, advancement of the edema front and increase in the amount of edema is stopped. It appears that an intact vascular bed is necessary for the extracellular fluid component of brain edema, and that no edemagenic factors exist within the injured brain in this model that influence either the production or propagation of the increased extracellular fluid volume.

Animals↗
PubMed1976

Blood pressure, edema and proteinuria in pregnancy. 7. Edema-plus-proteinuria relationships.

1. A total of 488 pregnancies had the combination of two-plus or more proteinuria and edema of the hands and face. Of these, 208 were white and 280 were black gravidas. In the white gravidas, 8 fetal and neonatal deaths occurred with a perinatal mortality of 38.5 per 1,000. There were 13 perinatal deaths in the black subgroup with a perinatal mortality rate of 46.4 per 1,000. The overall perinatal mortality rate was 43.0 per 1,000, which could be compared to the overall perinatal mortality rate of 32.8 per 1,000 for the segment of the study population without edema or proteinuria. This underscored the implication of increased hazard to fetal outcome of these clinical signs in combination. 2. The analysis of the matrix data showed scattered rates throughout gestation in white median-age nulliparas. Their black counterparts had comparable increased mortality rates. In the white multiparas of ages 20 to 34 years, the highest rates were found at relatively low blood pressure levels. The black median-age multiparas had rates associated with higher pressure readings, especially at or above 125/75. In teenage mulliparas with edema and proteinuria, perinatal mortality rates were similar for both subgroups and were found in somewhat lower blood pressures. 3. The incremental analysis was remarkable in that rates were scattered widely in the white subgroups, but tightly clustered in the black subgroups. The black median-age nulliparas had perinatal mortality concentrated about 115 to 134 mm. Hg systolic and 65 to 84 mm. Hg diastolic. The overall mortality rates of this subgroup were the highest of the subgroups studied. The black 20 to 34 year old multiparas had highest coassociated deaths in the 134-154 mm. Hg systolic levels throughout pregnancy. The clustering effect was most pronounced in black teenage nulliparas in both systolic and diastolic blood pressure groups at much lower levels. 4. The use of a critical cut-off blood pressure level of 125 mm. Hg systolic and 75 mm. Hg diastolic emphasized the combination factor effect, especially by the increased perinatal mortality rates in the black median-age subgroups of both nulliparas and multiparas. In the white median-age subgroups the rates were not uniformly affected. The teenage nulliparas as a group showed increased mortality rates with lower pressure levels in general. This was seen when the diastolic level was above 75 mm. Hg. 5. Perinatal mortality rates of nulliparas were increased by proteinuria and edema. This increase was great in the case of the 20 to 34 year old black nulliparas, particularly in association with increased blood pressure. Trends are not so apparent for the white median-age nulliparas. Nulliparas of 19 years of age or less have higher perinatal loss with edema and proteinuria, but this is not necessarily augmented with blood pressure elevation. This is notably so in teenage black nulliparas in the early periods of gestation and at term.

Adolescent↗
PubMed1979

The effect of intracerebral ouabain administration on the composition of edema fluid isolated from cats with cold-induced brain edema.

Brain edema fluid was collected from cats with a freezing lesion in the left parietal cortex by the insertion into the brain of needles containing nylon wicks and connected to polyethylene tubes. The edema fluid samples which accumulated in the polyethylene tubes were regularly analyzed for Na+ and K+ content, colloid osmotic pressure, lactate dehydrogenase and creatine phosphokinase activity, and 99mTc-albumin radioactivity; the albumin tracer being introduced intravenously at the time of cold-injury. One series of cats received an intracerebral injection of ouabain solution, the control series an intracerebral injection of saline, at 100 min after the cold-injury. The ouabain injection was followed by an increase of K+ content, LDH and CPK activities but a decrease of Na+ concentration in the edema fluid, attributable to a concentration of solutes in the edema fluid as presumably water and Na+ were shifted into the cells and hence the extracellular space was reduced.

Animals↗
PubMed1979

Composition of isolated edema fluid in cold-induced brain edema.

Edema fluid isolated from cats with cold-induced brain edema was subjected to analysis of electrolyte content, enzyme activities, colloid osmotic pressure and the radioactivity of intravenously injected 99mTc-labeled albumin. The findings corroborate the essential features of vasogenic edema, such as its origin from the blood plasma, its rapid propagation into the white matter of the brain as contrasted with the delayed spread into gray matter, and its contribution to composition of cerebrospinal fluid. Moreover, the elevated activities of cellular enzymes and K+ content of edema fluid point to the admixture with cellular contents due to the freezing damage.

Albumins↗
PubMed1979

Influence of hypoxia on the composition of isolated edema fluid in cold-induced brain edema.

The isolation of edema fluid from cats with cold-induced cerebral edema allowed the study of changes of Na+ and K+ content, lactate dehydrogenase and creatine phosphokinase activity, colloid osmotic pressure and the level of intravenously administered 99mTc-albumin in the edema fluid during a period of hypoxia. The changes consisted of an increase of all mentioned parameters, except Na+; and could be interpreted as a concentration of solutes (but for Na+) in the extracellular edema fluid, concomitant to a reduction of the extracellular space, as the oxygen deficiency caused improper functioning of the cellular Na+-K+ pump, with a resulting shift of fluid (including Na+) into the cellular elements.

Albumins↗