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.

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: The Key to the Evolution of Air Breathing

Physiology ◽  
2003 ◽  
Vol 18 (4) ◽  
pp. 151-157 ◽  
Author(s):  
Christopher B. Daniels ◽  
Sandra Orgeig
Keyword(s):  
Surface Tension ◽  
Lipid Composition ◽  
Pulmonary Surfactant ◽  
Liquid Interface ◽  
Evolutionary Origin ◽  
Selection Pressures ◽  
Air Breathing ◽  
Evolutionary Selection ◽  
Air Liquid Interface

Pulmonary surfactant controls the surface tension at the air-liquid interface within the lung. This system had a single evolutionary origin that predates the evolution of the vertebrates and lungs. The lipid composition of surfactant has been subjected to evolutionary selection pressures, particularly temperature, throughout the evolution of the vertebrates.

Tracing surfactant transformation from cellular release to insertion into an air-liquid interface

2004 ◽  
Vol 286 (5) ◽  
pp. L1009-L1015 ◽  
Author(s):  
T. Haller ◽  
P. Dietl ◽  
H. Stockner ◽  
M. Frick ◽  
N. Mair ◽  
...  
Keyword(s):  
Surface Tension ◽  
Cultured Cells ◽  
High Surface ◽  
Lamellar Body ◽  
Liquid Interface ◽  
Alveolar Type ◽  
Tensile Forces ◽  
Modify Surface ◽  
Fluorescence Imaging Microscopy ◽  
Air Liquid Interface

Pulmonary surfactant is secreted by alveolar type II cells as lipid-rich, densely packed lamellar body-like particles (LBPs). The particulate nature of released LBPs might be the result of structural and/or thermodynamic forces. Thus mechanisms must exist that promote their transformation into functional units. To further define these mechanisms, we developed methods to follow LBPs from their release by cultured cells to insertion in an air-liquid interface. When released, LBPs underwent structural transformation, but did not disperse, and typically preserved a spherical appearance for days. Nevertheless, they were able to modify surface tension and exhibited high surface activity when measured with a capillary surfactometer. When LBPs inserted in an air-liquid interface were analyzed by fluorescence imaging microscopy, they showed remarkable structural transformations. These events were instantaneous but came to a halt when the interface was already occupied by previously transformed material or when surface tension was already low. These results suggest that the driving force for LBP transformation is determined by cohesive and tensile forces acting on these particles. They further suggest that transformation of LBPs is a self-regulated interfacial process that most likely does not require structural intermediates or enzymatic activation.

The Pulmonary Surfactant: Control of Fluidity at the Air-Liquid Interface

1980 ◽  
pp. 57-67
Author(s):  
Fred Possmayer ◽  
I. LeRoy Metcalfe ◽  
Goran Enhorning
Keyword(s):  
Pulmonary Surfactant ◽  
Liquid Interface ◽  
Air Liquid Interface

Effects of surface tension and intraluminal fluid on mechanics of small airways

1997 ◽  
Vol 82 (1) ◽  
pp. 233-239 ◽  
Author(s):  
Mark J. Hill ◽  
Theodore A. Wilson ◽  
Rodney K. Lambert
Keyword(s):  
Surface Tension ◽  
Bending Stiffness ◽  
Liquid Interface ◽  
Cross Sectional Area ◽  
Pressure Curve ◽  
Small Airways ◽  
Sectional Area ◽  
Cross Sectional ◽  
Inner Surface ◽  
Air Liquid Interface

Hill, Mark J., Theodore A. Wilson, and Rodney K. Lambert.Effects of surface tension and intraluminal fluid on the mechanics of small airways. J. Appl. Physiol.82(1): 233–239, 1997.—Airway constriction is accompanied by folding of the mucosa to form ridges that run axially along the inner surface of the airways. The muscosa has been modeled (R. K. Lambert. J. Appl. Physiol. 71: 666–673, 1991) as a thin elastic layer with a finite bending stiffness, and the contribution of its bending stiffness to airway elastance has been computed. In this study, we extend that work by including surface tension and intraluminal fluid in the model. With surface tension, the pressure on the inner surface of the elastic mucosa is modified by the pressure difference across the air-liquid interface. As folds form in the mucosa, intraluminal fluid collects in pools in the depressions formed by the folds, and the curvature of the air-liquid interface becomes nonuniform. If the amount of intraluminal fluid is small, <2% of luminal volume, the pools of intraluminal fluid are small, the air-liquid interface nearly coincides with the surface of the mucosa, and the area of the air-liquid interface remains constant as airway cross-sectional area decreases. In that case, surface energy is independent of airway area, and surface tension has no effect on airway mechanics. If the amount of intraluminal fluid is >2%, the area of the air-liquid interface decreases as airway cross-sectional area decreases, and surface tension contributes to airway compression. The model predicts that surface tension plus intraluminal fluid can cause an instability in the area-pressure curve of small airways. This instability provides a mechanism for abrupt airway closure and abrupt reopening at a higher opening pressure.

scholarly journals The Interaction of Chondroitin Sulfate with a Lipid Monolayer Observed by Using Nonlinear Vibrational Spectroscopy

2021 ◽  
Author(s):  
Gergo Peter Szekeres ◽  
Szilvia Krekic ◽  
Rebecca L. Miller ◽  
Mark Mero ◽  
Kevin Pagel ◽  
...  
Keyword(s):  
Secondary Structure ◽  
Spectroscopic Study ◽  
Chondroitin Sulfate ◽  
Vibrational Spectroscopy ◽  
Sum Frequency Generation ◽  
Liquid Interface ◽  
Lipid Monolayer ◽  
Dipalmitoyl Phosphatidylcholine ◽  
Sum Frequency ◽  
Air Liquid Interface

<p>We present the first vibrational sum-frequency generation spectroscopic study of chondroitin sulfate (CS) interacting with dipalmitoyl phosphatidylcholine (DPPC) at the air-liquid interface. In the presence of Ca<sup>2+</sup> and CS, the DPPC headgroups reoriented, while the tail orientations remained mostly unchanged. The results further suggest a chiral secondary structure for CS.</p>

A Mathematical Description of Pressures in Alveolar Pores of Kohn

1991 ◽  
Vol 113 (1) ◽  
pp. 104-107 ◽  
Author(s):  
De-fu Lu ◽  
Charles Stanley ◽  
German Nunez ◽  
David Frazer
Keyword(s):  
Surface Tension ◽  
Mathematical Models ◽  
Pore Size ◽  
Lung Tissue ◽  
Mathematical Description ◽  
Disease Process ◽  
Liquid Interface ◽  
Tissue Destruction ◽  
Air Liquid Interface ◽  
Pore Enlargement

Small interalveolar holes within the lung are called pores of Kohn. Some researchers have correlated enlarged pore size with diseases, e.g. emphysema, that are characterized by tissue destruction. Mathematical models of the pressures generated in closed, fluid-filled and open, fluid-lined pores demonstrate that pressures capable of rupturing lung tissue can be developed in a pore due to the surface tension and shape of the air-liquid interface. Pore enlargement accompanied by tissue destruction is presented as a possible mechanism for the disease process observed during aging and the development of emphysema in the lung.

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