scholarly journals Tracheal acid or surfactant instillation raises alveolar surface tension

2018 ◽  
Vol 125 (5) ◽  
pp. 1357-1367 ◽  
Author(s):  
Tam L. Nguyen ◽  
Carrie E. Perlman
Keyword(s):  
Surface Tension ◽  
Distress Syndrome ◽  
Exogenous Surfactant ◽  
Acid Aspiration ◽  
Isolated Lungs ◽  
Lavage Solution ◽  
Alveolar Surface ◽  
Normal Lungs ◽  
Alveolar Liquid

Whether alveolar liquid surface tension, T, is elevated in the acute respiratory distress syndrome (ARDS) has not been demonstrated in situ in the lungs. Neither is it known how exogenous surfactant, which has failed to treat ARDS, affects in situ T. We aim to determine T in an acid-aspiration ARDS model before and after exogenous surfactant administration. In isolated rat lungs, we combine servo-nulling pressure measurement and confocal microscopy to determine alveolar liquid T according to the Laplace relation. Administering 0.01 N (pH 1.9) HCl solution by alveolar injection or tracheal instillation, to model gastric liquid aspiration, raises T. Subsequent surfactant administration fails to normalize T. Furthermore, in normal lungs, tracheal instillation of control saline or exogenous surfactant raises T. Lavaging the trachea with saline and injecting the lavage solution into the alveolus raises T, suggesting that tracheal instillation may wash T-raising airway contents to the alveolus. Adding 0.01 N HCl or 5 mM CaCl2—either of which aggregates mucins—to tracheal lavage solution reduces or eliminates the effect of lavage solution on alveolar T. Following tracheal saline instillation, liquid suctioned directly out of alveoli through a micropipette contains mucins. Additionally, alveolar injection of gastric mucin solution raises T. We conclude that 1) tracheal liquid instillation likely washes T-raising mucins to the alveolus and 2) even exogenous surfactant that could be delivered mucin-free to the alveolus might not normalize T in acid-aspiration ARDS. NEW & NOTEWORTHY We demonstrate in situ in isolated lungs that surface tension is elevated in an acid-aspiration acute respiratory distress syndrome (ARDS) model. Following tracheal liquid instillation, also in isolated lungs, we directly sample alveolar liquid. We find that liquid instillation into normal lungs washes mucins to the alveolus, thereby raising alveolar surface tension. Furthermore, even if exogenous surfactant could be delivered mucin-free to the alveolus, exogenous surfactant might fail to normalize alveolar surface tension in acid-aspiration ARDS.

scholarly journals Sulforhodamine B and exogenous surfactant effects on alveolar surface tension under acute respiratory distress syndrome conditions

2020 ◽  
Vol 129 (6) ◽  
pp. 1505-1513 ◽  
Author(s):  
Tam L. Nguyen ◽  
Carrie E. Perlman
Keyword(s):  
Surface Tension ◽  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Exogenous Surfactant ◽  
Sulforhodamine B ◽  
Isolated Lungs ◽  
Surfactant Effects ◽  
Alveolar Surface

In the acute respiratory distress syndrome (ARDS), lowering surface tension, T, should reduce ventilation injury, yet exogenous surfactant has not reduced mortality. We show with direct T determination in isolated lungs that substances suggested to elevate T in ARDS indeed raise T, and exogenous surfactant reduces T. Further, we extend our previous finding that sulforhodamine B (SRB) reduces T below normal in healthy lungs and show that SRB, too, reduces T under ARDS conditions.

scholarly journals Sulforhodamine B and exogenous surfactant effects on alveolar surface tension under acute respiratory distress syndrome conditions

2020 ◽  
Author(s):  
Tam L. Nguyen ◽  
Carrie E. Perlman
Keyword(s):  
Surface Tension ◽  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Exogenous Surfactant ◽  
Sulforhodamine B ◽  
Surfactant Activity ◽  
Isolated Lungs ◽  
Alveolar Surface

AbstractIn the acute respiratory distress syndrome (ARDS), alveolar surface tension, T, may be elevated. Elevated T should increase ventilation-induced lung injury. Exogenous surfactant therapy, intended to lower T, has not reduced mortality. Sulforhodamine B (SRB) might, alternatively, be employed to lower T. We test whether substances suspected of elevating T in ARDS raise T in the lungs and test the abilities of exogenous surfactant and SRB to reduce T. In isolated rat lungs, we micropuncture a surface alveolus and instill a solution of a purported T-raising substance: control saline, cell debris, secretory phospholipase A2 (sPLA2), acid or mucins. We test each substance alone; with albumin, to model proteinaceous edema liquid; with albumin and exogenous surfactant; or with albumin and SRB. We determine T in situ in the lungs by combining servo-nulling pressure measurement with confocal microscopy, and applying the Laplace relation. With control saline, albumin does not alter T, additional surfactant raises T and additional SRB lowers T. The experimental substances, without or with albumin, raise T. Excepting under aspiration conditions, addition of surfactant or SRB lowers T. Exogenous surfactant activity is concentration and ventilation dependent. Sulforhodamine B, which could be delivered intravascularly, holds promise as an alternative therapeutic.New and NoteworthyIn the acute respiratory distress syndrome (ARDS), lowering surface tension, T, should reduce ventilation injury yet exogenous surfactant has not reduced mortality. We show with direct T-determination in isolated lungs that substances suggested to elevate T in ARDS indeed raise T, and exogenous surfactant reduces T. Further, we extend our previous finding that sulforhodamine B (SRB) reduces T below normal in healthy lungs and show that SRB, too, reduces T under ARDS conditions.

scholarly journals Surface tension in situ in flooded alveolus unaltered by albumin

2014 ◽  
Vol 117 (5) ◽  
pp. 440-451 ◽  
Author(s):  
Angana Banerjee Kharge ◽  
You Wu ◽  
Carrie E. Perlman
Keyword(s):  
Surface Tension ◽  
Plasma Proteins ◽  
Lung Surfactant ◽  
Exogenous Surfactant ◽  
Surfactant Activity ◽  
Interfacial Surfactant ◽  
Isolated Rat Lung ◽  
Alveolar Liquid

In the acute respiratory distress syndrome, plasma proteins in alveolar edema liquid are thought to inactivate lung surfactant and raise surface tension, T. However, plasma protein-surfactant interaction has been assessed only in vitro, during unphysiologically large surface area compression (%Δ A). Here, we investigate whether plasma proteins raise T in situ in the isolated rat lung under physiologic conditions. We flood alveoli with liquid that omits/includes plasma proteins. We ventilate the lung between transpulmonary pressures of 5 and 15 cmH2O to apply a near-maximal physiologic %Δ A, comparable to that of severe mechanical ventilation, or between 1 and 30 cmH2O, to apply a supraphysiologic %Δ A. We pause ventilation for 20 min and determine T at the meniscus that is present at the flooded alveolar mouth. We determine alveolar air pressure at the trachea, alveolar liquid phase pressure by servo-nulling pressure measurement, and meniscus radius by confocal microscopy, and we calculate T according to the Laplace relation. Over 60 ventilation cycles, application of maximal physiologic %Δ A to alveoli flooded with 4.6% albumin solution does not alter T; supraphysiologic %Δ A raise T, transiently, by 51 ± 4%. In separate experiments, we find that addition of exogenous surfactant to the alveolar liquid can, with two cycles of maximal physiologic %Δ A, reduce T by 29 ± 11% despite the presence of albumin. We interpret that supraphysiologic %Δ A likely collapses the interfacial surfactant monolayer, allowing albumin to raise T. With maximal physiologic %Δ A, the monolayer likely remains intact such that albumin, blocked from the interface, cannot interfere with native or exogenous surfactant activity.

scholarly journals Respiratory and Systemic Effects of LASSBio596 Plus Surfactant in Experimental Acute Respiratory Distress Syndrome

2016 ◽  
Vol 38 (2) ◽  
pp. 821-835 ◽  
Author(s):  
Johnatas Dutra Silva ◽  
Gisele Pena de Oliveira ◽  
Cynthia dos Santos Samary ◽  
Carla Cristina Araujo ◽  
Gisele de Araujo Padilha ◽  
...  
Keyword(s):  
Surface Tension ◽  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Cecal Ligation ◽  
Exogenous Surfactant ◽  
Experimental Sepsis ◽  
Apoptosis Protein ◽  
Anti Inflammatory

Background/Aims: Exogenous surfactant has been proposed as adjunctive therapy for acute respiratory distress syndrome (ARDS), but it is inactivated by different factors present in the alveolar space. We hypothesized that co-administration of LASSBio596, a molecule with significant anti-inflammatory properties, and exogenous surfactant could reduce lung inflammation, thus enabling the surfactant to reduce edema and improve lung function, in experimental ARDS. Methods: ARDS was induced by cecal ligation and puncture surgery in BALB/c mice. A sham-operated group was used as control (CTRL). After surgery (6 hours), CTRL and ARDS animals were assigned to receive: (1) sterile saline solution; (2) LASSBio596; (3) exogenous surfactant or (4) LASSBio596 plus exogenous surfactant (n = 22/group). Results: Regardless of exogenous surfactant administration, LASSBio596 improved survival rate and reduced collagen fiber content, total number of cells and neutrophils in PLF and blood, cell apoptosis, protein content in BALF, and urea and creatinine levels. LASSBio596 plus surfactant yielded all of the aforementioned beneficial effects, as well as increased BALF lipid content and reduced surface tension. Conclusion: LASSBio596 exhibited major anti-inflammatory and anti-fibrogenic effects in experimental sepsis-induced ARDS. Its association with surfactant may provide further advantages, potentially by reducing surface tension.

Surfactant replacement increases compliance in premature lamb lungs during partial liquid ventilation in situ

1998 ◽  
Vol 84 (4) ◽  
pp. 1316-1322 ◽  
Author(s):  
Peter Tarczy-Hornoch ◽  
Jack Hildebrandt ◽  
Thomas A. Standaert ◽  
J. Craig Jackson
Keyword(s):  
Force Balance ◽  
Exogenous Surfactant ◽  
Partial Liquid Ventilation ◽  
Liquid Ventilation ◽  
Lung Inflation ◽  
Surfactant Replacement ◽  
Improve Compliance ◽  
Alveolar Surface ◽  
Force Balance Equation

Treatments available to improve compliance in surfactant-deficient states include exogenous surfactant (ES) and either partial (PLV) or total liquid ventilation (TLV) with perfluorochemical (PFC). Because of the additional air-lung and air-PFC interfaces introduced during PLV compared with TLV, we hypothesized that compliance would be worse during PLV than during TLV. Because surfactant is able to reduce interfacial tension between air and lung as well as between PFC and lung, we further hypothesized that compliance would improve with surfactant treatment before PLV. In excised preterm lamb lungs, we used Survanta for surfactant replacement and perflubron as the PFC. Compliance during PLV was intermediate between TLV and gas inflation, both with and without surfactant. Surfactant improved compliance during PLV, compared with PLV alone. Because of the force-balance equation governing the behavior of immiscible droplets on liquid surfaces, we predict that PFC droplets spread during PLV to cover the alveolar surface in surfactant-deficient lungs during most of lung inflation and deflation but that the PFC would retract into droplets in surfactant-sufficient lungs, except at end inspiration.

scholarly journals Edematous alveolar surface tension in situ in the lung

2011 ◽  
Vol 25 (S1) ◽  
Author(s):  
Carrie E. Perlman ◽  
Angana Banerjee Kharge
Keyword(s):  
Surface Tension ◽  
Alveolar Surface

Urea permeability of alveolar membrane; hemodynamic effects of liquid in the alveolar spaces

1960 ◽  
Vol 198 (5) ◽  
pp. 1029-1031 ◽  
Author(s):  
Cecil E. Cross ◽  
P. Andre Rieben ◽  
Peter F. Salisbury
Keyword(s):  
Urea Concentration ◽  
Hemodynamic Parameters ◽  
Hemodynamic Effects ◽  
Endotracheal Tubes ◽  
Closed Chest ◽  
Lobar Bronchus ◽  
Flow Through ◽  
Isolated Lungs ◽  
Lavage Solution

The blood flow through isolated lungs, excised or in situ, was measured while air or isotonic lavage solution was injected into and withdrawn from the lobar bronchus under variable pressures. Lavage of isolated lobes, intubated via the lobar bronchus with cuffed endotracheal tubes, was also performed in closed-chest experiments while certain hemodynamic parameters were recorded. Urea equilibration between the blood and the alveolar fluid could be expressed as an asymptotic line; the urea concentration of the alveolar fluid reached 30% and 55% of the blood urea concentration when the lavage solution remained in the alveoli for 5 and 15 minutes, respectively. Regardless of the presence or absence of liquid in the alveoli, vascular resistance in the isolated lobe was determined by airway pressure. In closed-chest experiments the hemodynamic effects of pulmonary lavage were minimal as long as low positive and negative pressures were used to inject and withdraw the lavage solution.

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