Polyhexamethylene guanidine aerosol triggers pulmonary fibrosis concomitant with elevated surface tension via inhibiting pulmonary surfactant

2021 ◽  
pp. 126642
Author(s):  
Xin Li ◽  
Jianzhong Zhang ◽  
Chao Du ◽  
Yingying Jiang ◽  
Wanjun Zhang ◽  
...  
Keyword(s):  
Surface Tension ◽  
Pulmonary Fibrosis ◽  
Pulmonary Surfactant ◽  
Polyhexamethylene Guanidine ◽  
Elevated Surface

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.

Alterations in the surface properties of lung surfactant in the torpid marsupial Sminthopsis crassicaudata

1998 ◽  
Vol 84 (1) ◽  
pp. 146-156 ◽  
Author(s):  
Olga V. Lopatko ◽  
Sandra Orgeig ◽  
Christopher B. Daniels ◽  
David Palmer
Keyword(s):  
Surface Tension ◽  
Surface Properties ◽  
Surface Activity ◽  
Pulmonary Surfactant ◽  
Lung Surfactant ◽  
Lung Compliance ◽  
Equilibrium Surface Tension ◽  
Sminthopsis Crassicaudata

Lopatko, Olga V., Sandra Orgeig, Christopher B. Daniels, and David Palmer. Alterations in the surface properties of lung surfactant in the torpid marsupial Sminthopsis crassicaudata. J. Appl. Physiol. 84(1): 146–156, 1998.—Torpor changes the composition of pulmonary surfactant (PS) in the dunnart Sminthopsis crassicaudata [C. Langman, S. Orgeig, and C. B. Daniels. Am. J. Physiol. 271 ( Regulatory Integrative Comp. Physiol. 40): R437–R445, 1996]. Here we investigated the surface activity of PS in vitro. Five micrograms of phospholipid per centimeter squared surface area of whole lavage (from mice or from warm-active, 4-, or 8-h torpid dunnarts) were applied dropwise onto the subphase of a Wilhelmy-Langmuir balance at 20°C and stabilized for 20 min. After 4 h of torpor, the adsorption rate increased, and equilibrium surface tension (STeq), minimal surface tension (STmin), and the %area compression required to achieve STmin decreased, compared with the warm-active group. After 8 h of torpor, STmin decreased [from 5.2 ± 0.3 to 4.1 ± 0.3 (SE) mN/m]; %area compression required to achieve STmindecreased (from 43.4 ± 1.0 to 27.4 ± 0.8); the rate of adsorption decreased; and STeqincreased (from 26.3 ± 0.5 to 38.6 ± 1.3 mN/m). ST-area isotherms of warm-active dunnarts and mice at 20°C had a shoulder on compression and a plateau on expansion. These disappeared on the isotherms of torpid dunnarts. Samples of whole lavage (from warm-active and 8-h torpor groups) containing 100 μg phospholipid/ml were studied by using a captive-bubble surfactometer at 37°C. After 8 h of torpor, STmin increased (from 6.4 ± 0.3 to 9.1 ± 0.3 mN/m) and %area compression decreased in the 2nd (from 88.6 ± 1.7 to 82.1 ± 2.0) and 3rd (from 89.1 ± 0.8 to 84.9 ± 1.8) compression-expansion cycles, compared with warm-active dunnarts. ST-area isotherms of warm-active dunnarts at 37°C did not have a shoulder on compression. This shoulder appeared on the isotherms of torpid dunnarts. In conclusion, there is a strong correlation between in vitro changes in surface activity and in vivo changes in lipid composition of PS during torpor, although static lung compliance remained unchanged (see Langman et al. cited above). Surfactant from torpid animals is more active at 20°C and less active at 37°C than that of warm-active animals, which may represent a respiratory adaptation to low body temperatures of torpid dunnarts.

The late asthmatic response is linked with increased surface tension and reduced surfactant protein B in mice

2002 ◽  
Vol 283 (4) ◽  
pp. L755-L765 ◽  
Author(s):  
Angela Haczku ◽  
Elena N. Atochina ◽  
Yaniv Tomer ◽  
Yang Cao ◽  
Colleen Campbell ◽  
...  
Keyword(s):  
Surface Tension ◽  
Pulmonary Surfactant ◽  
Late Phase ◽  
Surfactant Protein ◽  
Intratracheal Administration ◽  
Asthmatic Response ◽  
Surfactant Protein B ◽  
Airway Response ◽  
Allergen Provocation ◽  
Surfactant Dysfunction

Pulmonary surfactant dysfunction may significantly contribute to small airway obstruction during the asthmatic response, but neither its exact role nor its regulation is clear. Surfactant function and composition was studied in an Aspergillus fumigatus ( Af)-induced late-phase allergic airway response in sensitized BALB/c mice. The peak of Af-induced airway hyperresponsiveness in sensitized and challenged mice 24 h after allergen provocation coincided with a significant fall in surface activity of the pulmonary surfactant. The underlying changes included time-dependent elaboration of eotaxin and IL-5 followed by eosinophil influx into the airways. The height of airway inflammation and hyperresponsiveness was preceded by release of IL-4 and marked reductions in surfactant protein (SP)-B, a hydrophobic surfactant protein responsible for maintaining low surface tension of the lining fluid of distal air spaces. Furthermore, intratracheal administration of IL-4 significantly inhibited SP-B, indicating a regulatory role of this cytokine in the surfactant biophysical changes. Thus surfactant dysfunction induced by an IL-4-driven SP-B deficiency after allergen provocation may be an important part of the late asthmatic airway response.

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

An estimation of mechanical stress on alveolar walls during repetitive alveolar reopening and closure

2015 ◽  
Vol 119 (3) ◽  
pp. 190-201 ◽  
Author(s):  
Zheng-long Chen ◽  
Yuan-lin Song ◽  
Zhao-yan Hu ◽  
Su Zhang ◽  
Ya-zhu Chen
Keyword(s):  
Surface Tension ◽  
Respiratory Rate ◽  
Inflation Rate ◽  
Mechanical Stresses ◽  
Normal Lung ◽  
Shear Stresses ◽  
Fluid Viscosity ◽  
Small Airways ◽  
Protective Ventilation Strategy ◽  
Elevated Surface

Alveolar overdistension and mechanical stresses generated by repetitive opening and closing of small airways and alveoli have been widely recognized as two primary mechanistic factors that may contribute to the development of ventilator-induced lung injury. A long-duration exposure of alveolar epithelial cells to even small, shear stresses could lead to the changes in cytoskeleton and the production of inflammatory mediators. In this paper, we have made an attempt to estimate in situ the magnitudes of mechanical stresses exerted on the alveolar walls during repetitive alveolar reopening by using a tape-peeling model of McEwan and Taylor (35). To this end, we first speculate the possible ranges of capillary number ( Ca) ≡ μU/ γ (a dimensionless combination of surface tension γ, fluid viscosity μ, and alveolar opening velocity U) during in vivo alveolar opening. Subsequent calculations show that increasing respiratory rate or inflation rate serves to increase the values of mechanical stresses. For a normal lung, the predicted maximum shear stresses are <15 dyn/cm2 at all respiratory rates, whereas for a lung with elevated surface tension or viscosity, the maximum shear stress will notably increase, even at a slow respiratory rate. Similarly, the increased pressure gradients in the case of elevated surface or viscosity may lead to a pressure drop >300 dyn/cm2 across a cell, possibly inducing epithelial hydraulic cracks. In addition, we have conceived of a geometrical model of alveolar opening to make a prediction of the positive end-expiratory pressure (PEEP) required to splint open a collapsed alveolus, which as shown by our results, covers a wide range of pressures, from several centimeters to dozens of centimeters of water, strongly depending on the underlying pulmonary conditions. The establishment of adequate regional ventilation-to-perfusion ratios may prevent recruited alveoli from reabsorption atelectasis and accordingly, reduce the required levels of PEEP. The present study and several recent animal experiments likewise suggest that a lung-protective ventilation strategy should not only include small tidal volume and plateau pressure limitations but also consider such cofactors as ventilation frequency and inflation rate.

scholarly journals Control of the development of the pulmonary surfactant system in the saltwater crocodile, Crocodylus porosus

2002 ◽  
Vol 283 (5) ◽  
pp. R1164-R1176 ◽  
Author(s):  
Lucy C. Sullivan ◽  
Sandra Orgeig ◽  
Christopher B. Daniels
Keyword(s):  
Surface Tension ◽  
Thyroid Hormones ◽  
Pulmonary Surfactant ◽  
Swimming Exercise ◽  
Type Ii Cells ◽  
Type Ii ◽  
In Ovo ◽  
Saltwater Crocodile ◽  
Crocodylus Porosus ◽  
Time Point

Pulmonary surfactant is a mixture of lipids and proteins that controls the surface tension of the fluid lining the inner lung. Its composition is conserved among the vertebrates. Here we hypothesize that the in ovo administration of glucocorticoids and thyroid hormones during late incubation will accelerate surfactant development in the saltwater crocodile, Crocodylus porosus. We also hypothesize that the increased maturation of the type II cells in response to hormone pretreatment will result in enhanced responsiveness of the cells to surfactant secretagogues. We sampled embryos at days 60, 68, and 75 of incubation and after hatching. We administered dexamethasone (Dex), 3,5,3′-triiodothyronine (T3), or a combination of both hormones (Dex + T3), 48 and 24 h before each prehatching time point. Lavage analysis indicated that the maturation of the phospholipids (PL) in the lungs of embryonic crocodiles occurs rapidly. Only T3 and Dex + T3 increased total PL in lavage at embryonic day 60, but Dex, T3, and Dex + T3increased PL at day 75. The saturation of the PLs was increased by T3 and Dex + T3 at day 68. Swimming exercise did not increase the amount or alter the saturation of the surfactant PLs. Pretreatment of embryos with Dex, T3, or Dex + T3 changed the secretion profiles of the isolated type II cells. Dex + T3increased the response of the cells to agonists at days 60and 68. Therefore, glucocorticoids and thyroid hormones regulate surfactant maturation in the crocodile.

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