Protein composition of lung fluids in acute alloxan edema in dogs

1976 ◽  
Vol 230 (2) ◽  
pp. 376-379 ◽  
Author(s):  
CE Vreim ◽  
NC Staub
Keyword(s):  
Pulmonary Edema ◽  
Protein Concentration ◽  
Interstitial Fluid ◽  
Protein Composition ◽  
Total Protein Concentration ◽  
Alveolar Epithelial ◽  
Anesthetized Dogs ◽  
Free Interstitial ◽  
High Concentrations ◽  
Paired Analysis

In 11 anesthetized dogs with acute alloxan-induced pulmonary edema, we measured the protein composition of 1-mul samples of plasma, free interstitial fluid, alveolar fluid, and airway fluid. We obtained plasma and airway fluid at regular intervals as edema developed. We sampled alveolar fluid by pleural micropuncture in the unfrozen, excised lung and free interstitial fluid from perivascular cuffs in the frozen, excised lung. The average (+/- 1 SD) total protein concentration of plasma was 4.9 +/- 0.6, airway fluid 4.4 +/- 0.7, free interstitial fluid 4.9 +/- 0.7, and alveolar fluid 5.2 +/- 0.8 g/100 ml. The average fractions of albumin were 0.42 +/- 0.05, 0.50 +/- 0.05, 0.49 +/- 0.06, and 0.49 +/- 0.07, respectively. By paired analysis, the protein concentration of interstitial fluid was not significantly different from alveolar fluid. The protein concentration of airway fluid was significantly less than that in interstitial and alveolar fluid. The albumin fraction of the three lung fluids was identical but significantly different from plasma. We conclude that in alloxan-induced pulmonary edema the lung fluids contain high concentrations of protein and the alveolar epithelial membrane becomes freely permeable to protein molecules.

Lung lymph and free interstitial fluid protein composition in sheep with edema

1976 ◽  
Vol 230 (6) ◽  
pp. 1650-1653 ◽  
Author(s):  
CR Vreim ◽  
PD Snashall ◽  
RH Demling ◽  
NC Staub
Keyword(s):  
Plasma Protein ◽  
Protein Concentration ◽  
Interstitial Fluid ◽  
Protein Composition ◽  
Lymph Flow ◽  
Base Line ◽  
Interstitial Edema ◽  
Plasma Protein Concentration ◽  
Free Interstitial ◽  
Lung Lymph

In 10 anesthetized sheep with mild or moderate pulmonary edema we determined whether the protein composition of lung lymph is representative of free interstitial fluid. We measured protein concentration and albumin fraction in 1-mul samples of plasma, lung lymph, and free interstitial fluid. We also measured lung lymph flow. In five sheep with edema caused by increased pulmonary microvascular pressure, the average (+/- 1 SE) plasma protein concentration was 6.0 +/- 0.4 g/100 ml, lung lymph 3.4 +/- 0.2, and interstitial fluid 3.1 +/- 0.3. Lymph flow increased from an average base-line value of 9.4 ml/h to 43.4 ml/h during edema. Average albumin fractions in lymph and interstitial fluid were 0.56 +/- 0.02 and 0.50 +/- 0.01, respectively, compared with 0.44 +/- 0.01 for plasma. In five sheep with increased-permeability edema, average plasma protein concentration was 5.7 +/- 0.3 g/100 ml, lung lymph 4.1 +/- 0.4, and interstitial fluid 4.6 +/- 0.4. Base-line lymph flow was 11.0 ml/h and increased to 27.8 ml/h during edema. Average albumin fractions in lymph and interstitial fluid were 0.53 +/- 0.01 and 0.50 +/- 0.02, respectively, compared with 0.43 +/- 0.01 for plasma. We conclude in both high-pressure and altered-permeability edema, the protein composition of lung lymph collected from the major lung efferent lymphatic is representative of the free interstitial edema fluid.

Human parotid saliva protein composition: dependence on physiological factors

1982 ◽  
Vol 242 (3) ◽  
pp. G231-G236 ◽  
Author(s):  
S. G. Oberg ◽  
K. T. Izutsu ◽  
E. L. Truelove
Keyword(s):  
Protein Concentration ◽  
Composition Dependence ◽  
Polyacrylamide Gel Electrophoresis ◽  
Sodium Dodecyl ◽  
Protein Composition ◽  
Parotid Saliva ◽  
Total Protein Concentration ◽  
Physiological Factors ◽  
Feeding Effects ◽  
Human Parotid Saliva

The relative concentrations of the major proteins in human parotid saliva as measured by sodium dodecyl sulfate-polyacrylamide gel electrophoresis varied greatly between the six individuals included in this study but were remarkably constant for a given individual. Individual relative parotid protein concentrations differed in salivas collected under unstimulated and stimulated conditions but were at least partially independent from circadian and feeding effects. In addition, the relative concentrations of certain salivary proteins decreased with continued lemon-drop stimulation. A total of 29 different bands was composited from the six subjects. Five of the bands had mobilities corresponding with those of calibration proteins selected for their known occurrence in parotid saliva. Only those proteins comprising at least 0.75% of the total protein concentration were detected. Relative protein concentrations of parotid saliva samples collected 12 mo apart from given individuals were identical.

Microvascular membrane permeability in high surface tension pulmonary edema

1986 ◽  
Vol 60 (1) ◽  
pp. 253-259 ◽  
Author(s):  
C. E. Bredenberg ◽  
G. F. Nieman ◽  
A. M. Paskanik ◽  
A. K. Hart
Keyword(s):  
Surface Tension ◽  
Pulmonary Edema ◽  
Protein Concentration ◽  
High Surface ◽  
Base Line ◽  
Total Protein Concentration ◽  
Airway Edema ◽  
Major Increase ◽  
Dioctyl Sodium Sulfosuccinate ◽  
Alveolar Surface

Pulmonary edema was induced in dogs by an aerosol of detergent dioctyl sodium sulfosuccinate. The permeability of the pulmonary microvascular membrane was assessed by cannulating an afferent tracheobronchial lymphatic and comparing the lymph-to-plasma total protein concentration (CL/CP) during high lymph flows induced by increasing left atrial (LA) pressure after detergent aerosol. Base-line CL/CP of 0.69 +/- 0.02 fell to 0.55 +/- 0.03 with increased LA pressure alone. CL/CP fell to 0.47 +/- 0.02 when LA pressure was increased following detergent, 0.51 +/- 0.04 following an aerosol of the vehicle in which the detergent was dissolved, and 0.73 +/- 0.10 following intravenous alloxan. In additional animals protein concentration of the airway edema fluid was compared with that of plasma. The ration of protein concentration of airway fluid to plasma was 0.63 +/- 0.08 following detergent aerosol, 0.64 +/- 0.10 following increased LA pressure, and 0.94 +/- 0.09 following administration of alloxan. These data indicate no major increase in pulmonary microvascular permeability following detergent aerosol and support the concept that pulmonary edema is the consequence of reduced interstitial perimicrovascular hydrostatic pressure caused by increased alveolar surface tension.

Protein composition of the rabbit foetal fluids

1965 ◽  
Vol 163 (990) ◽  
pp. 90-115 ◽  
Keyword(s):  
Amniotic Fluid ◽  
Protein Concentration ◽  
Stomach Contents ◽  
Protein Composition ◽  
Maternal Serum ◽  
Starch Gel Electrophoresis ◽  
Total Protein Concentration ◽  
Uterine Fluid ◽  
Starch Gel

The total protein concentration of fluids in different compartments of the rabbit conceptus from 20 to 28 days of age was measured, and concentrates of these fluids analysed electrophoretically in order to determine their protein composition. For comparison, similar analyses of foetal sera, maternal sera and, where possible, uterine fluid were carried out. The allantoic fluid had a protein concentration less than that of the amniotic fluid, whilst the exocoelomic fluid had a protein concentration greater than that of the amniotic fluid. The total protein concentration of these fluids increased from about 23 days onwards. Compared to the other fluids, protein became much more concentrated in the foetal stomach contents. When analysed by fluid agar electrophoresis, the foetal exocoelomic, amniotic and allantoic fluids and stomach contents contained similar electrophoretic components (albumin, α -1- globulin, α -2-globulin, β -globulin and γ -globulin) and resembled each other in the proportion of the components. These proportions (as best exemplified in the amniotic fluid) changed during the period investigated, and at all times were different to those of the foetal and maternal sera. In certain respects these proportions more closely resembled those of the proteins in the uterine fluid. Analysis of the foetal fluids, both by starch gel electrophoresis and immunoelectrophoresis, revealed a paucity of lipoproteins and of α -1- and α -2-macroglobulins. Some samples of uterine fluid showed a similar paucity of these components. An α -2-globulin component, common to the foetal exocoelomic, amniotic and allantoic fluids, stomach contents and serum, but absent from the maternal serum, was detected (with a rat antiserum to the combined foetal amniotic fluid and stomach contents). Additional components were detected in the foetal stomach contents, both by the rat antiserum and by starch gel electrophoresis. Experiments on the permeability of the membranes in vitro were performed. No obvious increase in permeability of the amnion and yolk sac splanchnopleur with increasing gestational age could be found when maternal serum was dialysed across the isolated foetal membranes. The proportions of the protein components in the dialysates were similar, indicating that no alteration in permeability of the membranes had occurred. The paraplacental chorion, as compared to the yolk sac splanchnopleur, showed a greater permeability to protein in vitro . The role which the uterine fluid and foetal serum might play in governing the protein composition of the foetal fluids is discussed. It is suggested that the paraplacental chorion is the major site for the passage of proteins to the foetal fluids other than the blood.

Interstitial fluid volumes and albumin spaces in pulmonary oxygen toxicity

1984 ◽  
Vol 57 (6) ◽  
pp. 1767-1772 ◽  
Author(s):  
S. Matalon ◽  
E. A. Egan
Keyword(s):  
Skeletal Muscle ◽  
Pulmonary Edema ◽  
Interstitial Fluid ◽  
Oxygen Toxicity ◽  
Systemic Circulation ◽  
Base Line ◽  
Epithelial Permeability ◽  
Bovine Albumin ◽  
Alveolar Epithelial ◽  
Cellular Compartments

In rabbits exposed to 100% O2 at 1 ATA from 48 to 72 h, we measured the accumulation of intravenously injected 125I-bovine albumin, [57Co]cyanocobalamin, and 51Cr-erythrocytes in the intestine, skeletal muscle, heart, and lungs. From these data, we calculated the extravascular albumin and cyanocobalamin spaces (EVAS, EVECS) and the partition of water among vascular, interstitial, and cellular compartments in these organs. All variables remained at their base-line levels at 48 h in O2. At 64-66 h, the lung EVECS remained unchanged, but its EVAS increased by 210%. This change occurred after the previously documented increase of the alveolar epithelial permeability to solute and of the pulmonary conductance to water but before the appearance of pulmonary edema and arterial hypoxemia. The only change in the systemic circulation was a 17% increase of the heart EVAS. The increased heart and lung EVAS values, in the absence of any fluid volume shifts, are consistent with damage to the tissue polysaccharides of these organs by the toxic O2 species.

Effect of lysophosphatidylcholine on the filtration coefficient in intact dog lungs

1989 ◽  
Vol 257 (5) ◽  
pp. H1466-H1470
Author(s):  
B. D. Butler ◽  
I. Davies ◽  
R. E. Drake
Keyword(s):  
Weight Gain ◽  
Pulmonary Edema ◽  
Membrane Permeability ◽  
Microvascular Permeability ◽  
Filtration Coefficient ◽  
Fluid Filtration ◽  
Low Concentrations ◽  
Anesthetized Dogs ◽  
High Concentrations ◽  
The Relationship

Lysophosphatidylcholine (lyso-Pc) is a lysophospholipid normally found in low concentrations in the lung. At high concentrations lyso-Pc, instilled into the airways, causes pulmonary edema. We tested the hypothesis that the edema caused by lyso-Pc was due to an increase in pulmonary microvascular membrane permeability. In 11 anesthetized dogs we continuously weighed the left lower lobes (LLL) while instilling lyso-Pc (20 mM) into the LLL airways. After 30 min we determined the microvascular membrane fluid filtration coefficient (Kf) from the relationship between the rate of LLL weight gain and the pulmonary microvascular pressure. Kf was not significantly different between the lyso-Pc-treated lobes (0.048 +/- 0.018 ml.min-1.mmHg-1) vs. control lobes (0.067 +/- 0.031 ml.min-1.mmHg-1). Our data do not support the hypothesis that lyso-Pc, instilled into the airways, causes an increase in pulmonary microvascular permeability.

Protein composition of lung fluids in anesthetized dogs with acute cardiogenic edema

1976 ◽  
Vol 231 (5) ◽  
pp. 1466-1469 ◽  
Author(s):  
CE Vreim ◽  
PD Snashall ◽  
NC Staub
Keyword(s):  
Total Protein ◽  
Interstitial Fluid ◽  
Balloon Catheter ◽  
Alveolar Epithelium ◽  
Protein Composition ◽  
Capillary Endothelium ◽  
Cellulose Acetate Electrophoresis ◽  
Fluid Filtration ◽  
Lowry Method ◽  
Free Interstitial

We measured the protein composition of plasma and lung fluids from nine dogs with cardiogenic edema. To produce the edema, we increased left atrial pressure an average of 36 cmH2O by inflating a balloon catheter in the left atrium, infusing norepinephrine, and infusing large volumes of saline or saline-diluted blood. Blood samples were collected every 15 min, and airway fluid was collected from five dogs that developed severe edema. Terminally, the chest was opened and the lungs were removed. Samples of alveolar fluid were taken from the excised lung by direct pleural puncture with micropipettes. The lungs were frozen in liquid nitrogen and samples of free interstitial fluid were taken from the perivascular and peribronchial cuffs. Plasma and lung fluids were analyzed for total protein by the Lowry method and for albumin-globulin fractions by cellulose acetate electrophoresis. The average total protein concentrations (g/100 ml) were--plasma, 2.65; free interstitial fluid, 1.05; alveolar fluid, 1.23; and airway fluid, 1.29. The average albumin fraction of plasma was 0.40; of alveolar fluid, 0.43; and of airway fluid, 0.43. The protein concentrations in the three lung fluids were nearly identical to each other, but were less than half that of plasma. We conclude that in high-pressure pulmonary edema with alveolar flooding, the capillary endothelium retains the ability to restrict protein relative to fluid filtration, but the alveolar epithelium becomes freely permeable to protein.

Clearance of different-sized proteins from the alveolar space in humans and rabbits

1992 ◽  
Vol 73 (4) ◽  
pp. 1310-1316 ◽  
Author(s):  
R. H. Hastings ◽  
M. Grady ◽  
T. Sakuma ◽  
M. A. Matthay
Keyword(s):  
Total Protein ◽  
Protein Concentration ◽  
Experimental Studies ◽  
Lavage Fluid ◽  
Human Studies ◽  
Total Protein Concentration ◽  
Alveolar Epithelial ◽  
Protein Clearance ◽  
Human Proteins ◽  
Therapeutic Peptides

Investigation of the clearance of proteins from the air spaces is important for an understanding of the resolution of pulmonary edema and also because of current interest in delivery of therapeutic peptides via the distal air spaces. Few experimental studies have examined the size dependence for alveolar clearance of large macromolecules; there have been no human studies. In anesthetized rabbits, we measured clearance of cyanocobalamin and different-sized human proteins instilled into the air spaces. After 8 h, the amounts of instilled tracer recovered in the lungs were [57Co]cyanocobalamin, 19.4 +/- 3.0% (Stokes radius 0.65 nm); 125I-labeled insulin, 64.6 +/- 3.9% (1.2 nm); 131I-labeled albumin, 87.0 +/- 4.0% (3.5 nm); and 125I-labeled immunoglobulin G, 91.8 +/- 3.3% (5.5 nm) (P < 0.05). Sieving of different-sized proteins occurred across the alveolar epithelial barrier because tracer concentrations in air space lavage fluid after 8 h were decreased more for the smaller tracers than the larger ones. Size selectivity for alveolar protein clearance in humans with resolving alveolar edema was investigated by measuring the changes in albumin and total protein concentration. The fraction of total protein concentration made up of albumin was greater in the edema fluid than in the plasma initially. The albumin fraction decreased with time in 9 of 10 patients with resolving edema, from 0.62 +/- 0.2 to 0.58 +/- 0.10 (P < 0.05) after 10 +/- 5 h. Thus both rabbit studies and human studies provide evidence for size-dependent clearance of protein from the air spaces of the lung.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Higher mini-BAL total protein concentration in early ARDS predicts faster resolution of lung injury measured by more ventilator-free days

2017 ◽  
Vol 312 (5) ◽  
pp. L579-L585 ◽  
Author(s):  
Carolyn M. Hendrickson ◽  
Jason Abbott ◽  
Hanjing Zhuo ◽  
Kathleen D. Liu ◽  
Carolyn S. Calfee ◽  
...  
Keyword(s):  
Lung Injury ◽  
Clinical Outcomes ◽  
Total Protein ◽  
Protein Concentration ◽  
Colorimetric Assay ◽  
Acute Injury ◽  
P Value ◽  
Linear Regression Models ◽  
Total Protein Concentration ◽  
Alveolar Epithelial

The protein concentration of alveolar edema fluid in acute respiratory distress syndrome (ARDS) is dynamic. It reflects alveolar flooding during acute injury, as well as fluid and protein clearance over time. We hypothesized that among ARDS patients treated with low tidal volume ventilation, higher concentrations of protein in mini-bronchoalveolar lavage (mBAL) samples would predict slower resolution of lung injury and worse clinical outcomes. Total protein and IgM concentrations in day 0 mBAL samples from 79 subjects enrolled in the aerosolized albuterol (ALTA) ARDS Network Albuterol Trial were measured by colorimetric assay and ELISA, respectively. Linear regression models were used to test the association of mBAL proteins with clinical outcomes and measures of length of illness, including ventilator-free days (VFDs). Median mBAL total protein concentration was 1,740 μg/ml [interquartile range (IQR): 890–3,170]. Each 500 μg/ml increase in day 0 mBAL total protein was associated with an additional 0.8 VFDs [95% confidence interval (CI): 0.05–1.6, P value = 0.038]. Median mBAL IgM concentration was 410 ng/ml (IQR: 340–500). Each 50 ng/ml increase in mBAL IgM was associated with an additional 1.1 VFDs (95% CI 0.2–2.1, P value = 0.022). These associations remained significant and were not attenuated in multivariate models adjusted for age, serum protein concentration, and vasopressor use in the 24 h before enrollment. Thus, higher mBAL total protein and IgM concentrations at day 0 are associated with more VFDs in patients with ARDS and may identify patients with preserved alveolar epithelial mechanisms for net alveolar fluid clearance.

scholarly journals Dexmedetomidine alleviates pulmonary edema through the epithelial sodium channel (ENaC) via the PI3K/Akt/Nedd4-2 pathway in LPS-induced acute lung injury

2021 ◽  
Author(s):  
Yuanxu Jiang ◽  
Mingzhu Xia ◽  
Jing Xu ◽  
Qiang Huang ◽  
Zhongliang Dai ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Sodium Channel ◽  
Pulmonary Edema ◽  
Cell Injury ◽  
A549 Cells ◽  
Alveolar Epithelial ◽  
Phosphorylated Akt ◽  
Epithelial Sodium Channel Enac

AbstractDexmedetomidine (Dex), a highly selective α2-adrenergic receptor (α2AR) agonist, has an anti-inflammatory property and can alleviate pulmonary edema in lipopolysaccharide (LPS)-induced acute lung injury (ALI), but the mechanism is still unclear. In this study, we attempted to investigate the effect of Dex on alveolar epithelial sodium channel (ENaC) in the modulation of alveolar fluid clearance (AFC) and the underlying mechanism. Lipopolysaccharide (LPS) was used to induce acute lung injury (ALI) in rats and alveolar epithelial cell injury in A549 cells. In vivo, Dex markedly reduced pulmonary edema induced by LPS through promoting AFC, prevented LPS-induced downregulation of α-, β-, and γ-ENaC expression, attenuated inflammatory cell infiltration in lung tissue, reduced the concentrations of TNF-α, IL-1β, and IL-6, and increased concentrations of IL-10 in bronchoalveolar lavage fluid (BALF). In A549 cells stimulated with LPS, Dex attenuated LPS-mediated cell injury and the downregulation of α-, β-, and γ-ENaC expression. However, all of these effects were blocked by the PI3K inhibitor LY294002, suggesting that the protective role of Dex is PI3K-dependent. Additionally, Dex increased the expression of phosphorylated Akt and reduced the expression of Nedd4-2, while LY294002 reversed the effect of Dex in vivo and in vitro. Furthermore, insulin-like growth factor (IGF)-1, a PI3K agonists, promoted the expression of phosphorylated Akt and reduced the expression of Nedd4-2 in LPS-stimulated A549 cells, indicating that Dex worked through PI3K, and Akt and Nedd4-2 are downstream of PI3K. In conclusion, Dex alleviates pulmonary edema by suppressing inflammatory response in LPS-induced ALI, and the mechanism is partly related to the upregulation of ENaC expression via the PI3K/Akt/Nedd4-2 signaling pathway.

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