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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied the effects of crystalloid (75 ml/kg of Ringer's lactate) or colloid (6% dextran-70, 6% hydroxyethyl starch, or 25 ml/kg of 5% human serum albumin) fluid infusions or no treatment (control) on the calculated lung capillary (Pc)-plasma oncotic pressure (pi c) gradient and pulmonary edema. Two sets of mongrel dogs were studied: uninjured (n = 25; 14 to 22 kg) and pulmonary fibrin-microembolized (n = 25; 15 to 23 kg). In both sets of experiments, left atrial pressure was controlled (15 mm Hg) throughout the 4-h plus experimental period. In the uninjured set, the Pc-pi c gradient averaged +1.0 and -0.2 mm Hg in the hydroxyethyl starch and dextran groups, +0.7 and +2.3 mm Hg in the human serum albumin and control groups, and +6.2 mm Hg in the Ringer's lactate group. In the fibrin-microembolized group, this gradient averaged 2.6, 2.4, 3.0, 5.3, and 9.5, respectively. The extravascular lung water to bloodless dry lung wet weight ratios in the no-fluid treatment group of the uninjured and microembolism groups with increased pressure (3.8 +/- 0.3 to 4.1 +/- 0.4 [SEM]; NS) are consistent with interstitial or perivascular edema. There were, however, no significant differences noted between the respective control groups or any fluid treatment group in either set of experiments. These data support the view that infusion of either colloid or crystalloid solutions in normal or pulmonary fibrin-microembolized lungs does not produce sufficient change in the Pc-pi c gradient to elevate edemagenesis when pulmonary capillary pressure is limited to 22 mm Hg in dogs.
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PMID:Effects of colloid or crystalloid solutions on edemagenesis in normal and thrombomicroembolized lungs. 367 64

A quasi steady-state noninvasive, radioisotopic technique for measuring regional lung water distribution in man is described. The method depends upon the dilution principle. 123I labelled human serum albumin (HSA) and sodium iodide (NaI) were injected intravenously, allowed to mix completely within the body fluids and then counted externally over the chest. The size of each compartment to which the markers are confined was calculated from the external count rate and the isotopic concentration of the marker in plasma. 123I-HSA was used to estimate intravascular water and 123I-NaI extracellular water. Ratio analysis of the differential attenuation of the two photoenergies of 123Iodine (29 keV, 159 keV) by the lung and chest wall was used to estimate the absolute amount of isotope in the lung, independent of chest wall contribution, after validation by phantom studies. Regional pulmonary plasma (PPVr) and interstitial (PIVr) fluid volumes in normal subjects were 7.1 +/- 1.4 and 7.6 +/- 1.3 ml.100 cm-3 lung (mean +/- SD; n = 13) at mid-tidal volume, respectively. In patients with the adult respiratory distress syndrome, PPVr and PIVr were 7.0 +/- 2.9 and 15.9 +/- 4.6 ml.100 cm-3 lung (n = 18), respectively. The pulmonary artery wedge (Paw) pressure was normal (12.5 +/- 2.5 mmHg; n = 5). In patients with pulmonary oedema due to left heart disease, PPVr and PIVr were 7.2 +/- 2.7 and 12.1 +/- 3.7 ml.100 cm-3 lung (n = 8), respectively. The mean Paw pressure in this group was high (28.5 +/- 3.9 mmHg).
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PMID:Noninvasive measurement of regional lung water distribution in healthy man and in pulmonary oedema. 369 23

Similarities between oleic acid (OA)-induced pulmonary injury and clinical adult respiratory distress syndrome (ARDS) have resulted in extensive use of this model. Using technetium 99m (Tc-99m)-labeled human serum albumin (Tc-HSA) we examined the effect of indomethacin (a prostaglandin synthetase inhibitor) and dexamethasone (a corticosteroid) alone and in combination on OA-induced pulmonary protein leak. Computer-acquired dynamic gamma camera imaging before (15 min), during, and after (60 min) OA infusion were used to generate time-activity curves for lung and heart regions. A lung:heart activity ratio curve with a positive slope indicates pulmonary capillary protein leak of the labeled substance. Tc-99m labeling of red blood cells followed by OA injury showed no significant change in slope, indicating that lung hemorrhage was not being measured; however, Tc-HSA showed significant protein leakage following OA injury. Pretreatment with indomethacin or dexamethasone did not significantly alter either the preinsult or the postinsult slope. Combined pretreatment with indomethacin and dexamethasone significantly decreased, but did not eliminate, the pulmonary protein leak produced by OA injury. Our results indicate that multiple factors are involved in the production of the pulmonary capillary leak in OA-induced lung injury. In addition to the possible therapeutic efficacy of combined corticosteroids and nonsteroidal antiinflammatory drugs, our results demonstrate that these substances may be useful in defining the pathophysiology involved in permeability pulmonary edema.
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PMID:Indomethacin and dexamethasone decrease oleic acid-induced pulmonary protein leak in rabbits. 380 24

Perfluorocarbon (PFC) emulsions are promising oxygen-carrying blood supplements for the treatment of shock and in organ preservation for transplantation. We used the isolated, blood-perfused, canine right lower lung lobe (RLL) to determine the effect of a PFC emulsion, Oxypherol (FC-43), upon lung fluid balance and hemodynamics. Eighteen RLLs were divided into three equal groups, one of which was infused with a bovine serum albumin (BSA) solution to 10% of the total perfusate volume, and two of which were infused with Oxypherol to 10% and 20% of the final blood volume, respectively. At 145 min after infusion, there was no significant difference among the three groups in pH, blood gases, and lobar compliance. Arterial pressure and lobar vascular resistance were significantly (p less than .05) greater in the 20% Oxypherol group than in the BSA group. PFC-related changes in lobar permeability were determined by measuring the pulmonary filtration coefficient (Kf), which was not significantly different among groups. Thus, Oxypherol did not increase microvascular permeability (i.e., lung edema).
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PMID:Pulmonary fluid balance and hemodynamics after perfluorocarbon infusion in the dog lung. 393 10

Cardiac side effects from aspirin are uncommon; however, severe acid-base imbalance, pulmonary edema, ventricular ectopic activity and cardiopulmonary arrest have been reported in patients with toxic serum salicylate concentrations. We saw a patient with salicylate toxicity who developed a variety of sinus and atrioventricular nodal conduction disturbances and atrial arrhythmias with a relatively low toxic serum salicylate concentration. The cardiac rhythm returned to normal as the serum salicylate concentration decreased, and results of subsequent electrophysiologic testing and Holter monitoring were normal. A low serum albumin level may have resulted in altered salicylate binding in this patient, thereby increasing the availability of unbound (active) drug for toxic effects.
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PMID:Cardiac conduction abnormalities and atrial arrhythmias associated with salicylate toxicity. 395 6

Indicator-dilution curves can be interpreted and analysed by describing the system between injection- and sampling site with a physical model. Till now mainly compartmental and distributed models have been investigated. One feature of distributed models is the possibility to interpret skewness or asymmetry of the curve in terms of a parameter, proportional with the Peclet number, which is a measure of the relative contribution between convection and diffusion in indicator transport. In patients with and without pulmonary edema, we analyzed a number of curves obtained with an intravascular indicator (131I radioiodinated serum albumin, RISA) and a diffusing indicator (tritiated water, THO) over the pulmonary vascular bed. Edema was measured by indexed extravascular lung water and by critical pressure, defined as the difference between pulmonary capillary wedge pressure and plasma colloid osmotic pressure. The significant decrease of the symmetry of the RISA curves with increasing cardiac output we explained by an increasing labyrinth dispersion and increasing turbulence at higher flows. For normals we found all THO curves to be less skew than albumin curves. This difference diminished and even reversed when the degree of pulmonary edema increased. We suggest a hypothesis for this phenomenon by considering various mechanisms responsible for dispersion and capillary exchange of the indicator during transport from injection to sampling site. In normals the contribution of Taylor diffusion during laminar flow in parts of the circulatory system may be responsible for the greater symmetry of THO curves; with increasing pulmonary edema, transcapillary diffusion of THO causes THO curves to become more skew and even more asymmetric when compared with albumin curves.
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PMID:Physiological interpretation of the skewness of indicator-dilution curves; theoretical considerations and a practical application. 638 58

Computerized gamma scintigraphy revealed a significant (p less than 0.001) rising lung:heart radioactivity ratio, which has been called "slope of injury" or "slope index", with both 99mTechnetium-tagged human serum albumin (99mTc-HSA) and 99mTechnetium-tagged red blood cells (99Tc-RBC) after 0.05 or 0.2 ml/kg iv oleic acid administration to dogs. This slope index was significantly greater with 99mTc-HSA than 99mTc-RBC (p less than 0.001). These findings verify that the scintigraphic 99mTc-HSA slope of injury is a result of a pulmonary capillary protein leak and not oleic acid induced changes in pulmonary blood or air volume. The leak of red blood cells noted with scintigraphy was confirmed by light microscopy and examination of the tracheal edema fluid. The leak of albumin, however, was much greater than the leak of red blood cells by microscopy and tracheal fluid examination, confirming the scintigraphic data. This study provides further evidence that computerized gamma scintigraphy will be of value for the diagnosis of permeability pulmonary edema and its response to treatment.
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PMID:Comparative scintigraphy in oleic acid pulmonary microvascular injury. 645 10

Eleven patients with suspected adult respiratory distress syndrome (ARDS) and five control patients were studied using a computerized gamma imaging and analysis technique and 99mTc-labeled human serum albumin. The heart and right lung were imaged, lung:heart ratio was plotted vs. time, and a linear regression was fitted to the data points displayed. The slope of this fit was termed the "slope index." An index value of 2 standard deviations greater than the control mean was considered positive. Radiographs from the six positive studies revealed typical diffuse air-space disease. Radiographs from two of the five negative studies demonstrated air-space consolidation. Both of these patients had elevated pulmonary capillary wedge pressure, cardiomegaly, and clinical course consistent with cardiogenic pulmonary edema. These preliminary data demonstrated a good correlation between positive slope index and clinical ARDS.
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PMID:Computerized scintigraphic technique for the evaluation of adult respiratory distress syndrome: initial clinical trials. 646 Oct 25

Recent investigations of the role of large infusions of concentrated serum albumin on the acute pulmonary edema caused by hydrochloric acid (HCl) aspiration have produced contradictory results. We used the open thorax anesthetized dog with weighed lung lobe as well as completely isolated perfused weighed lobes. The results were the same with both preparations. Instillation of 0.1 N HCl (2 ml/kg) caused small increases in pulmonary artery pressure, and the rate of lung weight gain increased from 1.2 to 2.5 g/h to 22.2 to 30.2 g/h. Addition of 25% human serum albumin, either before or after acid instillation, had no significant effect on the rate of lobe weight gain. Additional experiments showed that after HCl the rate of lobe weight gain was exquisitely sensitive to pulmonary arterial pressure. Albumin therapy is without benefit in the prevention or treatment of the pulmonary edema caused by HCl aspiration.
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PMID:Concentrated albumin does not affect lung edema formation after acid instillation in the dog. 663 76

We infused hyperoncotic albumin (25 or 50 gm of a 50% solution) into patients with noncardiac pulmonary edema (adult respiratory distress syndrome [ARDS]) to evaluate its effect on the transmicrovascular flux from blood to pulmonary edema fluid of two radiotracers--111In-DTPA (mol wt 504) and 125I-human serum albumin (HSA) (mol wt 69,000). Two groups of patients were studied--one with a modest increase in permeability of the pulmonary alveolocapillary membrane to 125I-HSA (group 1) and another with a large increase in permeability to 125I-HSA (group 2). We used furosemide, when necessary, to minimize the effect of albumin infusion to increase the pulmonary microvascular hydrostatic pressure (Pmv), measured clinically as the pulmonary capillary wedge pressure (PCWP). Therapy significantly increased the mean colloid osmotic pressure (COP) in both groups, but not the mean PCWP or calculated Pmv. Albumin had no significant effect on the mean pulmonary transmicrovascular flux of the radiotracers in either group, despite the increase in COP. In individual patients, a change in the Pmv in response to albumin infusion was directly correlated with the change in flux of 111In-DTPA [group 1: delta In-DTPA (%) = 8.66 + 1.4 delta Pmv (%) r = 0.51, P less than 0.02; group 2: delta In-DTPA (%) = -3.43 + 1.6 delta Pmv (%) r = 0.67, P less than 0.01]. A change in the transmicrovascular flux of I-HSA also correlated with a change in the intravascular Starling forces in both groups. We conclude that albumin infusion in patients with ARDS will not augment the pulmonary transmicrovascular flux of low or high molecular-weight solutes when the effect of albumin to increase the Pmv is minimized; nor, however, does an increase in plasma COP significantly reduce the flux of such solutes.
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PMID:The short-term effects of increasing plasma colloid osmotic pressure in patients with noncardiac pulmonary edema. 684 68


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