Swim-bladder surfactants of Amazon air-breathing fishes

1978 ◽  
Vol 56 (4) ◽  
pp. 946-952 ◽  
Author(s):  
C. F. Phleger ◽  
B. S. Saunders
Keyword(s):  
Surface Tension ◽  
Lung Tissue ◽  
Phospholipid Composition ◽  
Vascular Supply ◽  
Swim Bladder ◽  
Tissue Slices ◽  
Minimum Surface ◽  
Arapaima Gigas ◽  
Minimum Surface Tension ◽  
Hoplerythrinus Unitaeniatus

Minimum surface tension and phospholipid composition of fish lung and swim-bladder wash and tissue extract were determined on an obligate water breather, Hoplias malabaricus, two species of facultative air breathers, Hoplerythrinus unitaeniatus and Erythrinus erythrinus, and two species of obligate air breathers, Arapaima gigas and Lepidosiren paradoxa. In addition, lung tissue slices were incubated with [1-14C]acetale and [1-14C]palmitate.All lung and swim-bladder wash lipid extracts showed a minimum surface tension of 20–25 dyn/cm (1 dyn = 10 μN). The principle phospholipid of all species is phosphatidylcholine; no phosphatidylglycerol was detected in any sample.The two obligate air breathers had higher rates of incorporation of isotope in tissue slices than facultative air breathers and nonair breathers. This observation correlates well with the greater vascular supply to their lungs.The phospholipid patterns of these fishes are significantly different from those of mammals. We speculate that these lipids recovered from saline wash may not be important in the maintenance of lung stability. Perhaps their function is keeping water from leaking into the lung and swim bladder.

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

Gill phospholipids of Amazon fishes

1978 ◽  
Vol 56 (4) ◽  
pp. 793-794 ◽  
Author(s):  
Charles F. Phleger
Keyword(s):  
Phospholipid Composition ◽  
Hoplias Malabaricus ◽  
Arapaima Gigas ◽  
Hoplerythrinus Unitaeniatus

Gill phospholipid composition was quantitatively determined for four Amazon fishes. The fishes included Hoplias malabaricus (obligate water breather), Hoplerythrinus unitaeniatus and Erythrinus erythrinus (facultative air breathers), and Arapaima gigas (obligate air breather). Phosphatidylcholine and phosphatidylethanolamine were the principal gill phospholipids (49–64% and 12–27% of the total phospholipids, respectively). Other phospholipids present included sphingomyelin (5–16%), phosphatidylserine(1–13%), lysophosphatidylcholine (0–6%), phosphatidylinositol (0–5%), and diphosphatidylglycerol (0–3%). The gill phospholipid composition was similarfor these four species of fish.

Altered surface tension of lung extracts and lung mechanics

1965 ◽  
Vol 20 (6) ◽  
pp. 1253-1260 ◽  
Author(s):  
D. F. Tierney ◽  
R. P. Johnson
Keyword(s):  
Surface Tension ◽  
Phospholipase C ◽  
Transpulmonary Pressure ◽  
Lung Mechanics ◽  
Elastic Recoil ◽  
Rat Serum ◽  
Minimum Surface ◽  
Rat Lungs ◽  
Minimum Surface Tension ◽  
Volume Characteristics

Reduction of the surface area of 24 extracts of rabbit lungs by four-fifths decreased the surface tension to a minimum value of 0–5 dynes/cm at 18–22 C. However, minimum surface tension was above 15 dynes/cm if 1) the temperature was raised to 42 C, 2) the extract was prepared with distilled water, 3) phospholipase C was incubated with the extract, and 4) cholesterol or oleic acid was added to the surface. If blood or serum was added during the extraction, minimum surface tension was usually (although not invariably) elevated. Rinsing diluted rat serum or chylomicrons through the airways increases elastic recoil of excised rat lungs. Other reports show that heating a lung above 42 C or rinsing a solution of phospholipase C through the airways also increases elastic recoil of excised rat lungs. Therefore, these conditions alter the surface tension of lung extracts and the pressure-volume characteristics of the lungs concordantly. In addition, we found that the surface tension of lung extracts was not stable below 24 dynes/cm. Similar instability of the surface within the lung should lead to gradual atelectasis if a low transpulmonary pressure is maintained. elastic recoil; atelectasis; compliance; lung surface Submitted on January 21, 1965

Mechanisms of peroxynitrite-induced injury to pulmonary surfactants

1993 ◽  
Vol 265 (6) ◽  
pp. L555-L564 ◽  
Author(s):  
I. Y. Haddad ◽  
H. Ischiropoulos ◽  
B. A. Holm ◽  
J. S. Beckman ◽  
J. R. Baker ◽  
...  
Keyword(s):  
Surface Tension ◽  
Dynamic Compression ◽  
Lung Surfactant ◽  
Thiobarbituric Acid ◽  
Surfactant Protein ◽  
Surfactant Proteins ◽  
Minimum Surface ◽  
Surfactant Protein B ◽  
Minimum Surface Tension ◽  
By Products

Activated alveolar macrophages secrete both nitric oxide and superoxide in the alveolar lining fluid which combine rapidly to form peroxynitrite, a potent oxidizing agent capable of damaging lipids and proteins in biological membranes. Peroxynitrite (1 mM) plus 100 microM Fe3+EDTA inhibited calf lung surfactant extract (CLSE) from reaching a minimum surface tension below 10 mN/m on dynamic compression. Peroxynitrite and its by-products reacted with the unsaturated lipid components of CLSE, as evidenced by the appearance of conjugated dienes and thiobarbituric acid products, and damaged all surfactant proteins. A mixture of the hydrophobic proteins [surfactant protein B (SP-B) and surfactant protein C (SP-C)] exposed to peroxynitrite became incapable of lowering phospholipid minimum surface tension on dynamic compression. Exposure of SP-A to peroxynitrite decreased its ability to cause lipid aggregation and to act synergistically with SP-B and SP-C in lowering surface tension of surfactant lipids. Western blot analysis of SP-A exposed to peroxynitrite was consistent with fragmentation and polymerization of the 28- to 36-kDa triplet band, and amino acid analysis revealed the presence of significant levels of 3-nitro-L-tyrosine. We conclude that peroxynitrite and its reactive intermediates inhibit pulmonary surfactant function by lipid peroxidation and damaging surfactant proteins.

Long-term cycling of surfactant films in Wilhelmy balance

1996 ◽  
Vol 8 (1) ◽  
pp. 173 ◽  
Author(s):  
B Sun ◽  
T Curstedt ◽  
B Robertson
Keyword(s):  
Surface Tension ◽  
Dependent Manner ◽  
Minimum Surface ◽  
Stable Period ◽  
Other Substances ◽  
Minimum Surface Tension ◽  
Surfactant Activity ◽  
Number Of Cycles ◽  
Dose Dependent

Surface properties of porcine surfactant were observed during long-term cycling in Wilhelmy balance. Various amounts of surfactant were applied onto the surface as dry particles or droplets, or were suspended in the hypophase, and the films generated by this material were subjected to 50% cyclic compression at a rate of 1 cycle per min. Film spreading was faster from a droplet than from a particle of lyophilized surfactant, but the 'stable period' during which minimum surface tension of the compressed film remained below 5 mN/m was significantly longer for the dry material. For surfactant suspensions the period of film 'refinement', defined as the number of cycles required to reduce minimum surface tension to a level below 5 mN/m, was inversely correlated with the concentration of surfactant in the hypophase. Thirteen batches of porcine surfactant, used successfully in clinical trials for treatment of neonatal respiratory distress syndrome, were evaluated in the same system suspended in the hypophase at a concentration of 0.5 mg/ml. Films adsorbed from these batches had a median refinement period of 4 cycles, and a median stable period of 2160 cycles (36 h). In the same assay system, surfactant activity was inhibited in a dose-dependent manner by serum, fibrinogen, meconium, and bilirubin, but the specific inhibitory activity was significantly higher for bilirubin than for the other substances tested.

A species comparison of alveolar size and surface forces

1987 ◽  
Vol 62 (5) ◽  
pp. 1865-1871 ◽  
Author(s):  
H. Lum ◽  
W. Mitzner
Keyword(s):  
Surface Tension ◽  
Static Pressure ◽  
Total Lung Capacity ◽  
Mammalian Species ◽  
Lung Capacity ◽  
Minimum Surface ◽  
Minimum Surface Tension ◽  
Mean Linear Intercept ◽  
The Mean ◽  
Complex Manner

The independent roles of alveolar size and surface tension in relation to lung stability were investigated in 11 different mammalian species whose body weight ranged from 0.03 to 50 kg. This range in species provided a wide variation in subgross anatomy as well as a fourfold range in alveolar diameter. Alveolar diameter was estimated from the mean linear intercept (Lm) of fixed lungs. Quasi-static pressure-volume curves were determined in excised lungs and the percent volume remaining on deflation from total lung capacity at 30 cmH2O to 10 cmH2O (%V10) provided an index of deflation stability related to functional surfactant. Surface tension of lung extract was measured in the Wilhelmy balance, and the minimum surface tension measured provided an index of surface tension lowering capacity of surfactant. Relationships of %V10 with alveolar diameter and surface tension with alveolar diameter were examined for correlations. Our results indicated that despite a range in Lm between 31 and 133 micron (mouse to pig), %V10 did not change in proportion with Lm across species. Similarly, minimum surface tension was about the same (6.1 to 8.8 dyn/cm) across a threefold difference in alveolar diameter. These results suggest that a stable alveolar configuration is maintained by both surface and tissue forces in a complex manner yet to be analyzed.

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.

The effect of methylation of phosphatidylethanolamine on the behaviour of lipid monolayers at the air–water interface

1988 ◽  
Vol 66 (5) ◽  
pp. 405-417 ◽  
Author(s):  
K. M. W. Keough ◽  
M. W. Hawco ◽  
C. S. Parsons
Keyword(s):  
Surface Tension ◽  
Dynamic Compression ◽  
High Surface ◽  
Head Group ◽  
Surface Tensions ◽  
Minimum Surface ◽  
Ideal Mixing ◽  
Compression And Expansion ◽  
Minimum Surface Tension ◽  
Mixed Systems

Monolayers of DPPE and its N-methylated derivatives including DPPC have been investigated at 23 and 37 °C using a modified Langmuir–Wilhelmy surface balance. The monolayers have been subjected to dynamic compression and expansion, and some characteristics of the surfaces have been determined. The minimum surface tension attained by surfaces containing the lipids (maximum surface pressures sustained by the films) depended on the extent of methylation of the head group. Monolayers of DPPE or N-MeDPPE collapsed at surface tensions of 12–16 mN∙m−1, whereas those containing N,N-diMeDPPE and DPPC could be compressed to near zero surface tension. The areas per molecule occupied by these lipids under high compression varied slightly and not systematically with head-group methylation. Monolayers containing mixtures of DPPC and DPPE were also studied under the same conditions. The monolayers showed some deviation from the behaviour expected if they were to have characteristics of ideally mixed systems. The minimum surface tensions attained suggested that monolayers containing 50 mol% or more DPPC might be further enriched during compression by some selective exclusion of the DPPE. At high surface pressures, some positive deviations in nominal areas per molecule from that expected for ideal mixing were observed in the monolayers made with 50 mol% or more DPPC. These deviations might be caused by packing disruptions associated with the explosion of lipid from the films.

scholarly journals Pulmonary Inflammation Disrupts Surfactant Function during Pneumocystis carinii Pneumonia

2001 ◽  
Vol 69 (2) ◽  
pp. 758-764 ◽  
Author(s):  
Terry W. Wright ◽  
Robert H. Notter ◽  
Zhengdong Wang ◽  
Allen G. Harmsen ◽  
Francis Gigliotti
Keyword(s):  
Surface Tension ◽  
Inflammatory Response ◽  
Pulmonary Inflammation ◽  
Pneumocystis Carinii ◽  
Lavage Fluid ◽  
Respiratory Impairment ◽  
Minimum Surface ◽  
Minimum Surface Tension ◽  
Surfactant Activity ◽  
Surfactant Dysfunction

ABSTRACT During Pneumocystis carinii pneumonia (PCP) in mice, the degree of pulmonary inflammation correlates directly with the severity of lung function deficits. Therefore, studies were undertaken to determine whether the host inflammatory response contributes to PCP-related respiratory impairment, at least in part, by disrupting the pulmonary surfactant system. Protein and phospholipid content and surfactant activity were measured in the lavage fluid of infected mice in either the absence or presence of an inflammatory response. At 9 weeks postinfection with P. carinii, nonreconstituted SCID mice exhibited no signs of pulmonary inflammation, respiratory impairment, or surfactant dysfunction. Lavage fluid obtained from these mice had protein/phospholipid (Pr/PL) ratios (64% ± 4.7%) and minimum surface tension values (4.0 ± 0.9 mN/m) similar to those of P. carinii-free control mice. However, when infected SCID mice were immunologically reconstituted, an intense inflammatory response ensued. Pr/PL ratios (218% ± 42%) and minimum surface tension values (27.2 ± 2.7 mN/m) of the lavage fluid were significantly elevated compared to those of the lavage fluid from infected, nonreconstituted mice (P < 0.05). To examine the specific role of CD8+ T-cell-mediated inflammation in surfactant dysfunction during PCP, mice with defined T-cell populations were studied. P. carinii-infected, CD4+-depleted mice had elevated lavage fluid Pr/PL ratios (126% ± 20%) and elevated minimum surface tension values (16.3 ± 1.0 mN/m) compared to normal mice (P < 0.05). However, when infected mice were additionally depleted of CD8+ cells, Pr/PL ratios were normal and surfactant activity was improved. These findings demonstrate that the surfactant pathology associated with PCP is related to the inflammatory process rather than being a direct effect of P. carinii. Moreover, CD8+ lymphocytes are involved in the mechanism leading to surfactant dysfunction.

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