scholarly journals Effect of Reconstituted Pulmonary Surfactant Containing the 6000-Dalton Hydrophobic Protein on Lung Compliance of Prematurely Delivered Rabbit Fetuses

1988 ◽  
Vol 23 (1) ◽  
pp. 23-30 ◽  
Author(s):  
Shou-Haw Yu ◽  
Duncan Wallace ◽  
Bhagu Bhavnani ◽  
Goran Enhorning ◽  
Paul G R Harding ◽  
...  
PEDIATRICS ◽  
1973 ◽  
Vol 51 (4) ◽  
pp. 655-659
Author(s):  
Robert V. Kotas

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.


1998 ◽  
Vol 84 (1) ◽  
pp. 146-156 ◽  
Author(s):  
Olga V. Lopatko ◽  
Sandra Orgeig ◽  
Christopher B. Daniels ◽  
David Palmer

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.


1996 ◽  
Vol 6 (4-5) ◽  
pp. 243-260 ◽  
Author(s):  
I. Panaiotov ◽  
Tz. Ivanova ◽  
J. Proust ◽  
F. Boury ◽  
B. Denizot ◽  
...  

2001 ◽  
Vol 23 (2) ◽  
pp. 319-327 ◽  
Author(s):  
Harald Bünger ◽  
Ralph-Peter Krüger ◽  
Sylvia Pietschmann ◽  
Nadeshda Wüstneck ◽  
Lutz Kaufner ◽  
...  

2002 ◽  
Vol 205 (3) ◽  
pp. 415-425
Author(s):  
Sonya D. Johnston ◽  
Christopher B. Daniels ◽  
David Cenzato ◽  
Jeffrey A. Whitsett ◽  
Sandra Orgeig

SUMMARY Pulmonary surfactant (PS), a mixture of phospholipids (PL), neutral lipids and surfactant proteins (SP), lowers surface tension within the lung, which increases lung compliance and improves the removal of fluid at birth. Here, we have examined the expression of thyroid transcription factor-1 (TTF-1) and the surfactant protein SP-B, and also the composition of pulmonary surfactant lipids in the developing lung of the turtle Chelydra serpentina. Lavage and lung tissue were collected from late embryonic, pipped and hatchling turtles. TTF-1, a regulator of gene expression of surfactant proteins and cell differentiation in mammals, was detected using immunohistochemistry in epithelia of the gas-exchange area and conducting airways during late development. Expression declined in hatchlings. SP-B was detected in subsets of cells within the respiratory epithelium at all stages sampled. The same cell types also stained for TTF-1. Turtle surfactant lipids matured toward the end of incubation. Maximal secretion of both total phospholipids and disaturated phospholipid (DSP) occurred at the time of pipping, coincident with the onset of breathing. The DSP/PL ratio increased after pipping, whereas cholesterol levels (Chol) increased prior to pipping. This resulted in a decrease in the Chol/PL and Chol/DSP ratios after pipping. Thus, TTF-1 and SP-B appear to be highly conserved within the vertebrates. Maturation of surfactant phospholipid content occurred with the commencement of pulmonary ventilation.


2017 ◽  
Vol 2 (2) ◽  
pp. 1-9 ◽  
Author(s):  
Guido Stichtenoth ◽  
Marie Haegerstrand-Björkman ◽  
Gabi Walter ◽  
Bim Linderholm ◽  
Egbert Herting ◽  
...  

Background: Ascending maternofetal bacterial infections often result in premature birth and neonatal respiratory distress. These neonates are treated with exogenous pulmonary surfactant (SF) and systemic antibiotics. Polymyxins are antimicrobiotic peptides that may bind to SF phospholipids. Objectives: Does topical administration of SF/polymyxin reduce bacterial growth in neonatal rabbit pneumonia and improve pulmonary function? Methods: Neonatal rabbits were tracheotomized and treated intratracheally with mixtures of porcine SF, SF/polymyxin E (PxE), or polymyxin B (PxB). Control animals received saline. Animals were then inoculated with Escherichia coli and ventilated for 4 h. During the experiment, peak insufflation pressures, dynamic lung compliance, and ECG were recorded. Pulmonary and renal bacterial load were determined. Lung histology was performed. Lung and kidney IL-8 were measured in subgroups. Results: Eighty-five animals were included in 2 experimental series, of which 78% survived 4 h of ventilation. E. coli inoculation caused severe neonatal pneumonia with median IL-8 levels of 2.2 ng/g in the lungs compared to a median of 0.2 ng/g in the lungs of the saline controls (p < 0.01). Lung compliance after 4 h was significantly increased at a mean of 0.48 ml/(kg·cm H2O) in the SF group and 0.43 in the SF + PxE group compared to 0.35 in the E. coli group (p < 0.01). In direct comparison, bacterial growth found in the E. coli group was reduced 20-fold in the SF + PxB group compared to 75-fold in the SF + PxE group. Conclusion: Addition of polymyxin to SF effectively promotes antimicrobial treatment and improves lung function in neonatal pneumonia of rabbits.


Author(s):  
Zaineb O. Ettarhouni ◽  
Aysha B. Mezoughi

Background: In Covid-19 the virus infects the respiratory tract in human. When lung tissue becomes diseased, the walls and lining of the alveoli and capillaries are damaged. At this point lung compliance and ventilation decrease. Pulmonary surfactant that is produced and dispersed into alveolar space, has a significant role in understanding how heavily covid-19 interferes and infects lung cells. The importance of pulmonary surfactant in alveoli is to lower surface tension at air/liquid interface in the lung. This is achieved by reducing the work of breathing and preventing alveolar collapse. The main constituent of pulmonary surfactant is dipalmitoylphosphatidylcholine (DPPC) (C40H80NO8P). It is a phospholipid containing two non polar palmitic acid C16 chains as hydrophobic tails linked to a polar head group of a phosphatidylcholine (also known as lecithin). Rationale of the Review and Objective Method: When DPPC molecules are in contact with a polar solvent, micelles which grow further into bilayers are formed considering their cylindrical structures. This trait makes the whole structure of pulmonary surfactant as amphipathic and surface active molecules. The head group of phosphatidylcholine in the pulmonary surfactant is attracted by polar liquid molecules causing a reduction of the liquid surface tension. Conclusion: This review complements the quoted information analysing them theoretically and integrates recent advances in pulmonary surfactant research with the global pandemic.


2008 ◽  
Vol 294 (4) ◽  
pp. L724-L732 ◽  
Author(s):  
Cory Yamashita ◽  
Amy Forbes ◽  
Jenna M. Tessolini ◽  
Li-Juan Yao ◽  
James F. Lewis ◽  
...  

Depletion of alveolar macrophages (AM) leads to an increase in endogenous surfactant that lasts several days beyond the repletion of AM. Furthermore, impairment to the endogenous pulmonary surfactant system contributes to ventilation-induced lung injury. The objective of the current study was to determine whether increased endogenous surfactant pools induced via AM depletion was protective against ventilation-induced lung injury. Adult rats were intratracheally instilled with either control or dichloromethylene diphosphonic acid (DMDP) containing liposomes to deplete AMs and thereby increase endogenous surfactant pools. Either 3 or 7 days following instillation, rats were exposed to 2 h of injurious ventilation using either an ex vivo or in vivo ventilation protocol and were compared with nonventilated controls. The measured outcomes were oxygenation, lung compliance, lavage protein, and inflammatory cytokine concentrations. Compared with controls, the DMDP-treated animals had significantly reduced AM numbers and increased surfactant pools 3 days after instillation. Seven days after instillation, AM numbers had returned to normal, but surfactant pools were still elevated. DMDP-treated animals at both time points exhibited protection against ventilation-induced lung injury, which included superior physiological parameters, lower protein leakage, and lower inflammatory mediator release into the air space, compared with animals not receiving DMDP. It is concluded that DMDP-liposome administration protects against ventilation-induced lung injury. This effect appears to be due to the presence of elevated endogenous surfactant pools.


1995 ◽  
Vol 269 (4) ◽  
pp. R838-R847 ◽  
Author(s):  
P. G. Wood ◽  
C. B. Daniels ◽  
S. Orgeig

The amount of pulmonary surfactant in the lungs of the bearded dragon (Pogona vitticeps) increases with increasing body temperature. This increase coincides with a decrease in lung compliance. The relationship between surfactant and lung compliance and the principal stimuli for surfactant release and composition (temperature, ventilatory pattern, and autonomic neurotransmitters) were investigated. We chose to investigate ventilatory pattern (which causes mechanical deformation of the type II cells) and adrenergic agents, because they are the major stimuli for surfactant release in mammals. To examine the effects of body temperature and ventilatory pattern, isolated lungs were ventilated at either 18 or 37 degrees C at different ventilatory regimens. An isolated perfused lung preparation at 27 degrees C was used to analyze the effects of autonomic neurotransmitters. Ventilatory pattern did not affect surfactant release, composition, or lung compliance at either 18 or 37 degrees C. An increase in temperature increased phospholipid reuptake and disproportionately increased cholesterol degradation/uptake. Epinephrine and acetylcholine stimulated phospholipid but not cholesterol release. Removal of surfactant caused a decrease in compliance, regardless of the experimental temperature. Temperature appears to be the principal determinant of lung compliance in the bearded dragon, acting directly to increase the tone of the smooth muscle. Increasing the ambient temperature may result in greater surfactant turnover by increasing cholesterol reuptake/degradation directly and by increasing circulating epinephrine, thereby indirectly increasing phospholipid secretion. We suggest that changing ventilatory pattern may be inadequate as a mechanism for maintaining surfactant homeostasis, given the discontinuous, highly variable reptilian breathing pattern.


1997 ◽  
Vol 70 (4) ◽  
pp. 444-455 ◽  
Author(s):  
Philip G. Wood ◽  
Lucy K. Andrew ◽  
Christopher B. Daniels ◽  
Sandra Orgeig ◽  
Claire T. Roberts

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