Dipalmitoyl lecithin: studies on surface properties

1965 ◽  
Vol 20 (4) ◽  
pp. 779-781 ◽  
Author(s):  
Marian C. Kuenzig ◽  
Robert W. Hamilton ◽  
Leonard F. Peltier
Keyword(s):  
Surface Tension ◽  
Pulmonary Surfactant ◽  
Surface Film ◽  
Ethanol Solution ◽  
Original Surface ◽  
Dipalmitoyl Lecithin ◽  
Minimum Surface Tension ◽  
Humidified Air ◽  
Surface Balance ◽  
Normal Lungs

A preparation of synthetic dipalmitoyl lecithin has been devised whose activity on a Wilhelmy surface balance is similar to that of extracts from normal lungs. An ethanol solution of lecithin is precipitated with albumin, and a drop of the suspension containing approximately 0.04 mg lecithin is spread on the surface of 0.9% NaCl in the trough of the balance. This preparation appears to be insensitive to oxidation and when run under humidified air gives reproducible results. It has a low minimum surface tension (5—10 dynes/cm) when compressed to 20% of the original surface area and exhibits considerable hysteresis on re-expansion. Addition of certain lipids to the surface film produces changes similar to those caused by addition of these lipids to cat lung extracts. surface tension; surface activity; pulmonary surfactant Submitted on September 8, 1964

Surfactant convertase action is not essential for surfactant film formation

1997 ◽  
Vol 273 (5) ◽  
pp. L907-L912 ◽  
Author(s):  
N. J. Gross ◽  
R. Veldhuizen ◽  
F. Possmayer ◽  
R. Dhand
Keyword(s):  
Surface Tension ◽  
Film Formation ◽  
Surface Film ◽  
Lower Surface ◽  
Diisopropyl Fluorophosphate ◽  
Surfactant Film ◽  
Surface Active ◽  
Lower Surface Tension ◽  
Surface Balance

A serine-active enzyme, “surfactant convertase,” is required for the conversion of surfactant from the tubular myelin (TM) form to the small vesicular (SV) form. This transformation involves at least two steps, the conversion of TM to a surface-active film at the air-fluid interface and the reorientation of the film into the surface-inactive SV form; we asked if convertase was required for the first of these steps. Rat and mouse TMs were pretreated with diisopropyl fluorophosphate (DFP) to inactivate endogenous convertase activity or with vehicle and then were analyzed for their ability to lower surface tension in vitro as an index of the conversion of TM to a surface film. DFP pretreatment did not alter the ability of TM preparations to lower surface tension, as assessed by pulsating bubble, and it did not affect the behavior of TM in a surface balance. In an experiment designed to test the ability of TM to feed a surface film to exhaustion, TMs that had been pretreated with DFP or vehicle performed similarly. These experiments show that convertase activity is not required for the conversion of TM to a monolayer and suggest, instead, that convertase acts at a post surface film stage.

Effects of fixatives on function of pulmonary surfactant

2002 ◽  
Vol 93 (3) ◽  
pp. 911-916 ◽  
Author(s):  
H. Bachofen ◽  
U. Gerber ◽  
S. Schürch
Keyword(s):  
Surface Tension ◽  
Pulmonary Surfactant ◽  
Osmium Tetroxide ◽  
Uranyl Acetate ◽  
Film Stability ◽  
Minimum Surface ◽  
Natural Surfactant ◽  
Equilibrium Surface Tension ◽  
Minimum Surface Tension ◽  
Surface Active

The structure of pulmonary surfactant films remains ill defined. Although plausible film fragments have been imaged by electron microscopy, questions about the significance of the findings and even about the true fixability of surfactant films by the usual fixatives glutaraldehyde (GA), osmium tetroxide (OsO4), and uranyl acetate (UA) have not been settled. We exposed functioning natural surfactant films to fixatives within a captive bubble surfactometer and analyzed the effect of fixatives on surfactant function. The capacity of surfactant to reach near-zero minimum surface tension on film compression was barely impaired after exposure to GA or OsO4. Although neither GA nor OsO4 prevented the surfactant from forming a surface active film, GA increased the equilibrium surface tension to above 30 mN/m, and both GA and OsO4 decreased film stability as seen in the slowly rising minimum surface tension from 1 to ∼5 mN/m in 10 min. In contrast, the effect of UA seriously impaired surface activity in that both adsorption and minimum surface tension were substantially increased. In conclusion, the fixatives tested in this study are not suitable to fix, i.e., to solidify, surfactant films. Evidently, however, OsO4 and UA may serve as staining agents.

Effect of oxygen breathing at atmospheric pressure on pulmonary surfactant

1965 ◽  
Vol 20 (5) ◽  
pp. 855-858 ◽  
Author(s):  
Samuel T. Giammona ◽  
Donald Kerner ◽  
Stuart Bondurant
Keyword(s):  
Surface Tension ◽  
Atmospheric Pressure ◽  
Pulmonary Surfactant ◽  
Species Difference ◽  
Foam Fractionation ◽  
Minimum Surface ◽  
Oxygen Breathing ◽  
Minimum Surface Tension ◽  
Effect Of Oxygen

To evaluate the effects of oxygen breathing at atmospheric pressure on pulmonary surfactant, cats, rabbits, and rats were continuously kept in 98% oxygen until death occurred. Pulmonary surfactant was extracted by mincing of the lung and by foam fractionation of the lung. Surface tension of the extracts was measured on a Wilhelmy balance. Lung extracts prepared by both methods from the cats and rabbits kept in oxygen had greater surface tension than lung extracts from control animals. Surface tension of extracts prepared by foam fractionation of lungs of rats kept in oxygen did not differ from that of extracts of lungs of control rats, whereas surface tension of extracts prepared by mincing lungs of rats kept in oxygen had minimum surface tension greater than that of lung extracts of control rats. This species difference in the effects of oxygen breathing on pulmonary surfactant may reflect a difference in the pathogenesis of oxygen intoxication. oxygen intoxication; surface tension Submitted on October 19, 1964

Inhibition of pulmonary surfactant function by phospholipases

1991 ◽  
Vol 71 (1) ◽  
pp. 317-321 ◽  
Author(s):  
B. A. Holm ◽  
L. Keicher ◽  
M. Y. Liu ◽  
J. Sokolowski ◽  
G. Enhorning
Keyword(s):  
Surface Tension ◽  
Lung Injury ◽  
Pulmonary Surfactant ◽  
Detrimental Effect ◽  
Surface Film ◽  
Intratracheal Administration ◽  
Low Concentrations ◽  
Surfactant Activity ◽  
Inhibitory Agents ◽  
Biophysical Activity

Previous studies have shown that respiratory failure associated with disorders such as acute pancreatitis correlates well with increased levels of phospholipase A2 (PLA2) in lung lavages and that intratracheal administration of PLA2 generates an acute lung injury. In addition, bacteria such as Pseudomonas have been shown to secrete phospholipase C (PLC). We studied the effects of these phospholipases on pulmonary surfactant activity using a pulsating bubble surfactometer. Concentrations greater than or equal to 0.1 unit/ml PLA2 destroyed surfactant biophysical activity, increasing surface tension at minimum bubble size from less than 1 to 15 mN/m. This surfactant inactivation was predominantly related to the effect of lysophosphatidylcholine on the surface film, although the fatty acids released with higher PLA2 concentrations also had a detrimental effect on surfactant function. Similarly, as little as 0.1 unit PLC increased the surface tension at minimal size of an oscillating bubble from less than 1 to 15 mN/m, an effect that could be mimicked by the addition of dipalmitin to surfactant in the absence of PLC. Moreover, lower, noninhibitory concentrations (0.01 unit/ml) of PLA2 and PLC increased the sensitivity of surfactant to other inhibitory agents, such as albumin. Thus, relatively low concentrations of PLC and PLA2 can cause severe breakdown of surfactant function and may contribute significantly to some forms of lung injury.

Surfactant inactivation by hyperventilation: conservation by end-expiratory pressure

1975 ◽  
Vol 38 (3) ◽  
pp. 461-466 ◽  
Author(s):  
I. Wyszogrodski ◽  
K. Kyei-Aboagye ◽  
H. W. Taeusch ◽  
M. E. Avery
Keyword(s):  
Surface Tension ◽  
Specific Activity ◽  
Surface Film ◽  
Active Material ◽  
Positive End Expiratory Pressure ◽  
Elastic Recoil ◽  
Minimum Surface Tension ◽  
Surface Active ◽  
Film Balance ◽  
Surface Active Material

Hyperventilation, defined as repeated hyperinflations, for three hours in open-chested anesthetized cats increased elastic recoil and elevated minimum surface tension of lung extracts as measured on a surface film balance. Equivalent hyperventilation from an elevated lung volume did not alter the pressure-volume relationships. When a mixture of [3H]glycerol and [14C]palmitate had been injected 17 h before the three hour period of phyerventilation, an increase in the ratio of specific activity in wash to tissue lecithin occurred in the hyperventilated cats compared to controls. These findings suggest that hyperventilation promotes release of surface active material from tissue to alveolus, but the released material is inactivated. The application of 2.5 cmH2O positive end-expiratory pressure prevented the adverse effects of hyperventilation. The same increase in wash to tissue lecithin occurred during this study; since the material was appropriately surface active, we conclude that the positive end-expiratory pressure prevented its inactivation.

Disparity between tidal and static volumes of immature lungs treated with reconstituted surfactants

1996 ◽  
Vol 80 (1) ◽  
pp. 62-68 ◽  
Author(s):  
T. Kobayashi ◽  
W. Z. Li ◽  
K. Tashiro ◽  
R. Takahashi ◽  
Y. Waseda ◽  
...  
Keyword(s):  
Surface Tension ◽  
Pulmonary Surfactant ◽  
Static Pressure ◽  
Surfactant Adsorption ◽  
Minimum Surface ◽  
Natural Surfactant ◽  
Minimum Surface Tension ◽  
Volume Measurements ◽  
Porcine Lungs

We biologically assessed functions of several reconstituted surfactants with the same minimum surface tension (2-3 mN/m) as “complete” porcine pulmonary surfactant (natural surfactant) but with longer surface adsorption times. Administration of natural surfactant (adsorption time 0.29 s) into the lungs of surfactant-deficient immature rabbits brought a tidal volume of 16.1 +/- 4.4 (SD) ml/kg during mechanical ventilation with 40 breaths/min and 20 cmH2O insufflation pressure. In static pressure-volume recordings, these animals showed a lung volume of 62.4 +/- 9.7 ml/kg at 30 cmH2O airway pressure and maintained 55% of this volume when the pressure decreased to 5 cmH2O. With two reconstituted surfactants consisting of synthetic lipids or isolated lipids from porcine lungs plus surfactant-associated hydrophobic proteins (adsorption times 0.57 and 0.78 s, respectively), tidal volumes were < 38% of that with natural surfactant (P < 0.05), but static pressure-volume recordings were not different. Care is therefore needed in estimating the in vivo function of surfactant preparations from minimum surface tension or static pressure-volume measurements.

scholarly journals Changes in respiratory elastance after deep inspirations reflect surface film functionality in mice with acute lung injury

2015 ◽  
Vol 119 (3) ◽  
pp. 258-265 ◽  
Author(s):  
Ayuko Takahashi ◽  
Erzsébet Bartolák-Suki ◽  
Arnab Majumdar ◽  
Béla Suki
Keyword(s):  
Surface Tension ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Pulmonary Surfactant ◽  
Surface Film ◽  
Lavage Fluid ◽  
Strong Negative Correlation ◽  
Alveolar Collapse ◽  
Rate Of Increase ◽  
Organ Level

Pulmonary surfactant reduces surface tension in the lung and prevents alveolar collapse. Following a deep inspiration (DI), respiratory elastance first drops then gradually increases due to surface film and tissue viscoelasticity. In acute lung injury (ALI), this increase is faster and governed by alveolar collapse due to increased surface tension. We hypothesized that the rate of increase in elastance reflects the deficiency of surfactant in the lung. To test this, mice were ventilated before (baseline) and after saline lavage obtained by injecting 0.8 ml and withdrawing 0.7 ml fluid (severe ALI) or injecting 0.1 ml (mild ALI). After two DIs, elastance was tracked for 10 min followed by a full lavage to assess surfactant proteins B (SP-B) and C (SP-C) content. Following 2 DIs, the increases in elastance during 10 min ventilation (Δ H) were 3.60 ± 0.61, 5.35 ± 1.04, and 8.33 ± 0.84 cmH2O/ml in baseline mice and mice with mild and severe ALI, respectively ( P < 0.0001). SP-B and SP-C in the lavage fluid dropped by 32.4% and 24.9% in the mild and 50.4% and 39.6% in the severe ALI, respectively. Furthermore, Δ H showed a strong negative correlation with both SP-B ( r2 = 0.801) and SP-C ( r2 = 0.810) content. The Δ H was, however, much smaller when the lavage fluid also contained exogeneous SP-B and SP-C. Thus Δ H can be interpreted as an organ level measure of surface film functionality in lavage-induced ALI in mice. This method could prove useful in clinical situations such as diagnosing surfactant problems, monitoring recovery from lung injury or the effectiveness of surfactant therapy.

Interactions between plasma proteins and pulmonary surfactant: surface balance studies

1988 ◽  
Vol 66 (9) ◽  
pp. 1166-1173 ◽  
Author(s):  
Kevin M. W. Keough ◽  
Caroline S. Parsons ◽  
P. Terence Phang ◽  
Martin G. Tweeddale
Keyword(s):  
Surface Tension ◽  
Plasma Proteins ◽  
Pulmonary Surfactant ◽  
Dynamic Compression ◽  
Rate Of Change ◽  
Surfactant Monolayers ◽  
Human Fibrinogen ◽  
Compression And Expansion ◽  
Minimum Surface Tension ◽  
Surfactant Lipid

The influence of human fibrinogen, α-globulin, and albumin on the properties of monolayers of pulmonary surfactant under dynamic compression and expansion has been studied at 37 °C. Each of the proteins altered some of the properties of the normal compression and expansion isotherms of surfactant such that characteristics deemed desirable for proper lung function were impaired. The order of potency of these effects was fibrinogen>globulin>albumin. The proteins (a) decreased the maximum surface pressure (equivalent to the minimum surface tension) which the surfactant monolayers attained on compression, (b) decreased the areas occupied per mole of lipid phosphorus when the monolayers were at surface tensions of 20 and 12 mN∙m−1, (c) reduced the areas of the hysteresis between compression and expansion isotherms, and (d) decreased the rate of change of surface tension with area at the point of initial expansion of the monolayers. The proteins might compete with surfactant lipid for available space at the interface, especially at low film compression. They might also enhance the desorption of lipid from the monolayer. The findings are consistent with the loss of pulmonary function and presence of edema that occur in adult respiratory distress syndrome being contributed to by plasma proteins interfering with surfactant function.

LUNG PHOSPHOLIPIDS AND SURFACE TENSION CORRELATIONS IN INFANTS WITH AND WITHOUT HYALINE MEMBRANE DISEASE AND IN ADULTS

PEDIATRICS ◽  
1967 ◽  
Vol 40 (1) ◽  
pp. 13-19
Author(s):  
George W. Brumley ◽  
W. Alan Hodson ◽  
Mary Ellen Avery
Keyword(s):  
Fatty Acids ◽  
Surface Tension ◽  
Pulmonary Surfactant ◽  
Saturated Fatty Acids ◽  
Hyaline Membrane Disease ◽  
Low Concentrations ◽  
Hyaline Membrane ◽  
Minimum Surface Tension ◽  
Wet Weight ◽  
High Concentrations

Infants who have died with hyaline membrane disease have low concentrations of pulmonary phospholipids and reduced concentrations of saturated fatty acids at the alpha position of lung phosphatidyl choline. There is a highly significant correlation (p&lt; .001) between levels below 12.6 mg of pulmonary phospholipid per gram wet weight lung and high minimum surface tension values of lung saline extracts. Infants without hyaline membrane disease have high concentrations of pulmonary phospholipids (22.3 mg per gram wet weight). Infants who recovered from HMD and died of other causes show values intermediate to those of HMD and non-HMD infants. The excess above the critical minimum noted here suggests a reservoir of pulmonary surfactant.

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
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