Plasmalogens effectively reduce the surface tension of surfactant-like phospholipid mixtures

1998 ◽  
Vol 274 (1) ◽  
pp. L143-L148 ◽  
Author(s):  
M. Rüdiger ◽  
I. Kolleck ◽  
G. Putz ◽  
R. R. Wauer ◽  
P. Stevens ◽  
...  
Keyword(s):  
Surface Tension ◽  
Phase Behavior ◽  
Minimal Surface ◽  
Pulmonary Surfactant ◽  
Minor Components ◽  
Dipalmitoyl Phosphatidylcholine ◽  
Morphological Studies ◽  
Alveolar Surfactant ◽  
Plasmalogen Content ◽  
Ethanolamine Plasmalogens

The alkenyl-acyl subclass of phosphatidylethanolamine (PtdEtn) and phosphatidylcholine (plasmalogens) are minor components of alveolar surfactant. Plasmalogens promote and stabilize hexagonal structures of phospholipids. In another study (W. R. Perkins, R. B. Dause, R. A. Parente, S. R. Michey, K. C. Neuman, S. M. Gruner, T. F. Taraschi, and A. S. Janoff. Science 273: 330–332, 1996), it was shown that polymorphic phase behavior may have an important role in the effective functioning of pulmonary surfactant. Therefore, we hypothesized that surface properties of phospholipid mixtures that contain plasmalogens are superior to plasmalogen-free mixtures. The effect of plasmalogens on surface tension of surfactant-like phospholipid mixtures (70 mol% dipalmitoyl phosphatidylcholine, 10 mol% phosphatidylglycerol, and 20 mol% PtdEtn) was measured. Using the pulsating bubble surfactometer, we show that an increasing amount of ethanolamine plasmalogens [plasmenylethanolamine (PlsEtn)] results in reduction of surface tension (0 mol% PlsEtn 44.7 ± 1.7, 2 mol% 33.5 ± 1.7, 4 mol% 36 ± 3.1, 6 mol% 26.2 ± 2.9, and 8 mol% 22.2 ± 0.3 mN/m). By means of the captive bubble surfactometer, minimal surface tension reached with 8 mol% PlsEtn was even lower (3.8 ± 0.7 mN/m). With regard to morphological studies (B. Fringes, K. Gorgas, and A. Reith. Eur. J. Cell Biol. 46: 136–143, 1988), clofibrate treatment of rats might increase the plasmalogen content of alveolar surfactant. However, in the present study, we could not show that synthesis and secretion of plasmalogens are affected by clofibrate treatment.

Pulmonary surfactant

1982 ◽  
Vol 53 (1) ◽  
pp. 1-8 ◽  
Author(s):  
R. J. King
Keyword(s):  
Surface Tension ◽  
Pulmonary Surfactant ◽  
Mechanical Stability ◽  
Hormonal Control ◽  
Type Ii Cells ◽  
Type Ii ◽  
Dipalmitoyl Phosphatidylcholine ◽  
Alveolar Epithelial ◽  
Lipoprotein Complex ◽  
Air Liquid Interface

Pulmonary surfactant reduces the surface tension of the alveolar air-liquid interface, thereby providing mechanical stability and preventing alveolar atelectasis. More than 50% of surfactant is dipalmitoyl phosphatidylcholine, a material that is capable of reducing the surface tension of the alveolar interface to uniquely low values. The functions of the remaining 25% unsaturated phosphatidylcholines, 5–10% phosphatidylglycerol, 5% cholesterol, and 8–10% protein are unknown. Surfactant is synthesized by alveolar epithelial type II cells and is probably secreted as a lipoprotein complex. Lamellar bodies, which distinguish type II cells, are likely to be intracellular sites of transport of processing. The catabolism of surfactant after it is secreted into the alveolar lumen is complicated and involves different turnover times for the phosphatidylcholines, phosphatidylglycerol, and the proteins. The metabolic events are under hormonal control and may involve an interplay between beta-adrenergic agonists cAMP, and prostaglandins. In disease, such as the neonatal and adult respiratory distress syndromes, derangements in the metabolic processes may produce surfactant that is abnormal with respect to its chemical and physical properties.

Pulmonary surfactant

1984 ◽  
Vol 62 (11) ◽  
pp. 1121-1133 ◽  
Author(s):  
Fred Possmayer ◽  
Shou-Hwa Yu ◽  
J. Marnie Weber ◽  
Paul G. R. Harding
Keyword(s):  
Surface Tension ◽  
Pulmonary Surfactant ◽  
Liquid Interface ◽  
Biological Assays ◽  
Dipalmitoyl Phosphatidylcholine ◽  
Essential Properties ◽  
Surfactant Activity ◽  
Mammalian Lung ◽  
Reduce Surface Tension ◽  
Air Liquid Interface

The mammalian lung is stabilized by a specialized material, the pulmonary surfactant, which acts by reversibly reducing the surface tension at the air–liquid interface of the lung during breathing. Pulmonary surfactant contains approximately 90% lipid and 10% proteins. Dipalmitoyl phosphatidylcholine, the major lipid component, appears to be primarily responsible for the ability to reduce surface tension to near 0 dyn/cm (1 dyn = 10 μN). The other components of pulmonary surfactant promote the adsorption and spreading of this disaturated lecithin at the air–liquid interface. Surfactant activity can be accessed by physical and biological assays. Apparent discrepancies between the results obtained with the Wilhelmy plate surface balance and the pulsating bubble surfactometer have led to the suggestion that separate "protein-facilitated" (catalytic type) and "protein-mediated" (chemical type) processes may be involved in adsorption and (or) spreading at the different surfactant concentrations used with these two techniques. Artificial surfactants, which mimic the essential properties of the natural product with the pulsating bubble surfactometer, can be produced with synthetic lipids. Treatment of prematurely delivered infants suffering from the neonatal respiratory distress syndrome with lipid extracts of pulmonary surfactant leads to a marked improvement in gaseous exchange.

Interactions between plasma proteins and pulmonary surfactant: pulsating bubble studies

1989 ◽  
Vol 67 (6) ◽  
pp. 663-668 ◽  
Author(s):  
Kevin M. W. Keough ◽  
Caroline S. Parsons ◽  
Martin G. Tweeddale
Keyword(s):  
Surface Tension ◽  
Plasma Proteins ◽  
Pulmonary Surfactant ◽  
Distress Syndrome ◽  
Adsorption Process ◽  
Human Albumin ◽  
Water Interface ◽  
Dipalmitoyl Phosphatidylcholine ◽  
Air Water Interface ◽  
Surfactant Inhibition

The influence of human albumin, α-globulin, and fibrinogen on the actions of porcine pulmonary surfactant in a pulsating bubble surfactometer has been investigated. All three proteins detracted from the ability of the surfactant to adsorb to the air–water interface. The proteins also reduced the ability of surfactant to lower the opening pressures of bubbles cycling between different sizes in suspensions of surfactant. This was equivalent to restricting the ability of the surfactant to achieve low surface tension during compression of the surface. Of the three proteins, globulin competed most effectively with surfactant during the adsorption process, and albumin competed the least effectively. The proteins also may have interfered with the processes of surface refinement, which usually yields a monolayer enriched enough in dipalmitoyl phosphatidylcholine to achieve very low surface tension (very low opening pressures in the bubbles). Of the three proteins tested, albumin was least deleterious to surface refining whereas globulin and fibrinogen appeared to be about equally detrimental to the process.Key words: pulmonary surfactant, surface tension, adsorption, adult respiratory distress syndrome, surfactant inhibition.

Inhibition of pulmonary surfactant by oleic acid: mechanisms and characteristics

1992 ◽  
Vol 72 (5) ◽  
pp. 1708-1716 ◽  
Author(s):  
S. B. Hall ◽  
R. Z. Lu ◽  
A. R. Venkitaraman ◽  
R. W. Hyde ◽  
R. H. Notter
Keyword(s):  
Surface Tension ◽  
Oleic Acid ◽  
Pulmonary Surfactant ◽  
Dynamic Compression ◽  
Molar Ratio ◽  
Surface Films ◽  
Dipalmitoyl Phosphatidylcholine ◽  
Rat Lungs ◽  
Tissue Compliance ◽  
Volume Characteristics

The inhibitory effects of oleic acid (OA) on the surface activity of pulmonary surfactant were characterized by use of the oscillating bubble surfactometer, the Wilhelmy balance, and excised rat lungs. Oscillating bubble studies showed that OA prevented lavaged calf surfactant [0.5 mM phospholipid (PL)] from lowering surface tension below 15 mN/m at or above a molar ratio of OA/PL = 0.5. In contrast to inhibition of surfactant by plasma proteins, increasing the surfactant concentration did not eliminate inhibition by oleic acid, which occurred at OA/PL greater than 0.67 on the oscillating bubble even at surfactant concentrations of 1.5 and 12 mM PL. Studies of surfactant adsorption showed that preformed films of OA had little effect on the adsorption of pulmonary surfactant. Wilhelmy balance studies showed that OA did interfere with the ability of spread films of surfactant to reach low surface tensions during dynamic compression. Further balance experiments with binary films of OA and dipalmitoyl phosphatidylcholine showed that these compounds were miscible in surface films. Together these findings suggested that OA inhibited pulmonary surfactant activity by disrupting the rigid interfacial film responsible for the generation of very low surface tension during dynamic compression. Mechanical studies in excised rat lungs showed that instillation of OA gave altered deflation pressure-volume characteristics with decreased quasi-static compliance, indicating disruption of pulmonary surfactant function in situ. This alteration of mechanics occurred without major changes in the composition of lavaged PLs or in the tissue compliance of the lungs defined by mechanical measurements during inflation-deflation with saline.(ABSTRACT TRUNCATED AT 250 WORDS)

Alterations in pulmonary surfactant after rapid arousal from torpor in the marsupial Sminthopsis crassicaudata

1999 ◽  
Vol 86 (6) ◽  
pp. 1959-1970 ◽  
Author(s):  
Olga V. Lopatko ◽  
Sandra Orgeig ◽  
David Palmer ◽  
Samuel Schürch ◽  
Christopher B. Daniels
Keyword(s):  
Surface Tension ◽  
Minimal Surface ◽  
Surface Activity ◽  
Lipid Composition ◽  
Pulmonary Surfactant ◽  
Total Phospholipid ◽  
Sminthopsis Crassicaudata ◽  
Rapid Changes ◽  
Surfactant Lipid ◽  
Surfactant Composition

Torpor in the dunnart, Sminthopsis crassicaudata, alters surfactant lipid composition and surface activity. Here we investigated changes in surfactant composition and surface activity over 1 h after rapid arousal from torpor (15–30°C at 1°C/min). We measured total phospholipid (PL), disaturated PL (DSP), and cholesterol (Chol) content of surfactant lavage and surface activity (measured at both 15 and 37°C in the captive bubble surfactometer). Immediately after arousal, Chol decreased (from 4.1 ± 0.05 to 2.8 ± 0.3 mg/g dry lung) and reached warm-active levels by 60 min after arousal. The Chol/DSP and Chol/PL ratios both decreased to warm-active levels 5 min after arousal because PL, DSP, and the DSP/PL ratio remained elevated over the 60 min after arousal. Minimal surface tension and film compressibility at 17 mN/m at 37°C both decreased 5 min after arousal, correlating with rapid changes in surfactant Chol. Therefore, changes in lipids matched changes in surface activity during the postarousal period.

scholarly journals Revisiting Kelvin equation and Peng–Robinson equation of state for accurate modeling of hydrocarbon phase behavior in nano capillaries

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ilyas Al-Kindi ◽  
Tayfun Babadagli
Keyword(s):  
Experimental Data ◽  
Surface Tension ◽  
Equation Of State ◽  
Phase Behavior ◽  
Pore Radius ◽  
Microfluidic Chips ◽  
Tight Sandstone ◽  
Kelvin Equation ◽  
Rock Samples ◽  
Robinson Equation

AbstractThe thermodynamics of fluids in confined (capillary) media is different from the bulk conditions due to the effects of the surface tension, wettability, and pore radius as described by the classical Kelvin equation. This study provides experimental data showing the deviation of propane vapour pressures in capillary media from the bulk conditions. Comparisons were also made with the vapour pressures calculated by the Peng–Robinson equation-of-state (PR-EOS). While the propane vapour pressures measured using synthetic capillary medium models (Hele–Shaw cells and microfluidic chips) were comparable with those measured at bulk conditions, the measured vapour pressures in the rock samples (sandstone, limestone, tight sandstone, and shale) were 15% (on average) less than those modelled by PR-EOS.

Pulmonary surfactant: phase behavior and function

2002 ◽  
Vol 12 (4) ◽  
pp. 487-494 ◽  
Author(s):  
Barbora Piknova ◽  
Vincent Schram ◽  
StephenB Hall
Keyword(s):  
Phase Behavior ◽  
Pulmonary Surfactant ◽  
Surfactant Phase ◽  
And Function

Effect of Fluorocarbon Liquid on Surface Tension Properties of Pulmonary Surfactant

CHEST Journal ◽  
1970 ◽  
Vol 57 (3) ◽  
pp. 263-265 ◽  
Author(s):  
Jerome H. Modell ◽  
Frank Gollan ◽  
Samuel T. Giammona ◽  
Donald Parker
Keyword(s):  
Surface Tension ◽  
Pulmonary Surfactant ◽  
Tension Properties

ACCELERATED PULMONARY SURFACTANT AFTER INTRAUTERINE INFECTION IN THE FETAL RABBIT

PEDIATRICS ◽  
1973 ◽  
Vol 51 (4) ◽  
pp. 655-659
Author(s):  
Robert V. Kotas
Keyword(s):  
Staphylococcus Aureus ◽  
Surface Tension ◽  
Pulmonary Surfactant ◽  
Intrauterine Infection ◽  
Low Pressure ◽  
Secondary Effect ◽  
Lung Maturation ◽  
Air Breathing ◽  
Rabbit Fetuses ◽  
Pressure Stability

Intrauterine inoculation of Staphylococcus aureus into 24-day rabbit fetuses resulted in changes in lung maturation at 27 days comparable to those seen after glucocorticoid injection. The lungs of infected litters had increased low pressure stability and distensibility with decreased surface tension upon compression, and resembled 29- to 30-day control lungs. Although intrauterine infection is found to be harmful to the fetus, it may have a secondary effect of preparing a fetus for premature air breathing.

Surface tension and pulmonary compliance in premature rabbits

1989 ◽  
Vol 66 (5) ◽  
pp. 2039-2044 ◽  
Author(s):  
M. R. Mercurio ◽  
J. M. Fiascone ◽  
D. M. Lima ◽  
H. C. Jacobs
Keyword(s):  
Surface Tension ◽  
Surface Properties ◽  
Pulmonary Surfactant ◽  
Dynamic Compliance ◽  
Ringer Solution ◽  
Tween 20 ◽  
Adult Rabbit ◽  
Equilibrium Surface ◽  
Equilibrium Surface Tension ◽  
Pulmonary Compliance

In vitro surface properties of pulmonary surfactant thought to be essential to its ability to increase pulmonary compliance include minimum surface tension less than 10 dyn/cm and large surface tension variability and hysteresis. We tested four surface-active agents (Tween 20, a detergent; and FC-100, FC-430, and FC-431, industrial fluorocarbons), all lacking these properties, for their ability to increase pulmonary compliance in surfactant-deficient premature rabbits. Fetal rabbits were delivered by cesarean section at 27 days (full term = 31 days) and injected via tracheostomy with 50% lactated Ringer solution, adult rabbit surfactant, or one of the four experimental agents. Dynamic compliance was measured using 1 h of mechanical ventilation followed by alveolar lavage. Each experimental agent produced a dynamic compliance significantly higher than 50% lactated Ringer solution and statistically equal to or greater than natural surfactant. Equilibrium surface tension of the agents and minimum and equilibrium surface tension of the alveolar washes each correlated with compliance (P less than 0.05). This suggests that some surface properties of pulmonary surfactant believed to be essential are not, although surface tension does seem to play a role in pulmonary compliance.

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