Lung Surfactant Apoprotein and Fetal Lung Maturity1

2015 ◽  
pp. 106-111
Author(s):  
S. L. Katyal ◽  
J. S. Amenta ◽  
G. Singh ◽  
J. A. Silverman
Keyword(s):  
Lung Surfactant ◽  
Fetal Lung ◽  
Surfactant Apoprotein

Prostaglandins mediate the fetal pulmonary response to intrauterine inflammation

2012 ◽  
Vol 302 (7) ◽  
pp. L664-L678 ◽  
Author(s):  
Alana J. Westover ◽  
Stuart B. Hooper ◽  
Megan J. Wallace ◽  
Timothy J. M. Moss
Keyword(s):  
Amniotic Fluid ◽  
Lung Inflammation ◽  
Lung Surfactant ◽  
Fetal Lung ◽  
Surfactant Protein ◽  
Fetal Plasma ◽  
Pulmonary Response ◽  
Surfactant Production ◽  
Prostaglandin Dehydrogenase ◽  
Prostaglandin H

Intra-amniotic (IA) lipopolysaccharide (LPS) induces intrauterine and fetal lung inflammation and increases lung surfactant and compliance in preterm sheep; however, the mechanisms are unknown. Prostaglandins (PGs) are inflammatory mediators, and PGE2 has established roles in fetal lung surfactant production. The aim of our first study was to determine PGE2 concentrations in response to IA LPS and pulmonary gene expression for PG synthetic [prostaglandin H synthase-2 (PGHS-2) and PGE synthase (PGES)] and PG-metabolizing [prostaglandin dehydrogenase (PGDH)] enzymes and PGE2 receptors. Our second study aimed to block LPS-induced increases in PGE2 with a PGHS-2 inhibitor (nimesulide) and determine lung inflammation and surfactant protein mRNA expression. Pregnant ewes received an IA saline or LPS injection at 118 days of gestation. In study 1, fetal plasma and amniotic fluid were sampled before and at 2, 4, 6, 12, and 24 h after injection and then daily, and fetuses were delivered 2 or 7 days later. Amniotic fluid PGE2 concentrations increased ( P < 0.05) 12 h and 3–6 days after LPS. Fetal lung PGHS-2 mRNA and PGES mRNA increased 2 ( P = 0.0084) and 7 ( P = 0.014) days after LPS, respectively. In study 2, maternal intravenous nimesulide or vehicle infusion began immediately before LPS or saline injection and continued until delivery 2 days later. Nimesulide inhibited LPS-induced increases in PGE2 and decreased fetal lung IL-1β and IL-8 mRNA ( P ≤ 0.002) without altering lung inflammatory cell infiltration. Nimesulide decreased surfactant protein (SP)-A ( P = 0.05), -B ( P = 0.05), and -D ( P = 0.0015) but increased SP-C mRNA ( P = 0.023). Thus PGHS-2 mediates, at least in part, fetal pulmonary responses to inflammation.

Clearance of intra-amniotic lung surfactant: uptake and utilization by the fetal rabbit lung

1997 ◽  
Vol 273 (1) ◽  
pp. L55-L63 ◽  
Author(s):  
M. Hallman ◽  
U. Lappalainen ◽  
K. Bry
Keyword(s):  
Amniotic Fluid ◽  
Lung Surfactant ◽  
Protein A ◽  
Alveolar Epithelium ◽  
Fetal Lung ◽  
Surfactant Protein ◽  
Lung Compliance ◽  
Rabbit Lung ◽  
Lower Lung ◽  
Lung Surfactant Protein

To investigate the metabolism of intra-amniotic surfactant, surfactant containing double-labeled dipalmitoylphosphatidylcholine (DPPC) was injected in amniotic fluid on days 23-27 of gestation. Within 44 h, DPPC was distributed to the gastrointestinal tract (45.9%), fetal membranes and placenta (8.2%), fetal lung (6.6%), and liver (1.9%). DPPC uptake was higher in the upper than in the lower lung lobes. The mixture of phosphatidylglycerol and DPPC increased the uptake of DPPC that was not saturable (range 15-60 mg phospholipid). There was no detectable metabolism of DPPC taken up by the fetal lung. Surfactant protein A, originating from intra-amniotic heterplogous surfactant, was detected immunohistochemically in alveolar epithelium. Intra-amniotic surfactants did not affect the expression of surfactant protein mRNAs. Intra-amniotic surfactant (1,500-2,000 mg/kg on day 25.3) improved lung compliance of ventilated 27.0-day premature rabbits less than intratracheal surfactant at birth (75-100 mg/kg). Reutilization by the alveolar epithelium of surfactant secreted to future airspaces, airways, and amniotic fluid may be a mechanism that increases intracellular surfactant pool before birth.

Biochemistry of Lung Surfactant: Apoprotein-Phospholipid Interaction1

2015 ◽  
pp. 84-92
Author(s):  
K. S. Z�nker ◽  
V. Breuninger ◽  
D. Hegner ◽  
G. Bl�mel ◽  
J. Probst
Keyword(s):  
Lung Surfactant ◽  
Surfactant Apoprotein

Fluorometric procedure for determining "lamellar body" phospholipids in the particulate fraction of amniotic fluid after filtration.

1983 ◽  
Vol 29 (2) ◽  
pp. 362-365 ◽  
Author(s):  
J Egberts ◽  
W Soederhuizen ◽  
D O Gebhardt
Keyword(s):  
Amniotic Fluid ◽  
Lung Surfactant ◽  
Lamellar Body ◽  
Fetal Lung ◽  
Human Amniotic Fluid ◽  
Wide Range ◽  
Before And After ◽  
The Difference ◽  
Filtration Step ◽  
Good Agreement

Abstract A rapid (30-min) semiautomated continuous-flow procedure is described for use in assessing the phospholipids of the particulate ("lamellar body") fraction of human amniotic fluid. The method is based on measuring the difference in fluorescence of 1,6,-diphenyl-1,3,5-hexatriene added to amniotic fluid before and after micropore filtration. The filtration step removes "lamellar body" particles, which are considered to contain the fetal lung surfactant. The phospholipid values for the filtered particles are independent of background fluorescence, which increases when amniotic fluid is contaminated by bilirubin pigments or blood components. Over a wide range (3-150 mumols/L) the fluorescence increases linearly with the phospholipid concentration of the amniotic fluid. There is a good agreement between the value for particulate "lamellar body" phospholipid, the ratio of the "lamellar body" phospholipids to total amniotic fluid phospholipids, and the lecithin/sphingomyelin ratio.

scholarly journals 289 INSULIN INHIBITS THE SYNTHESIS OF THE MAJOR SURFACTANT APOPROTEIN IN HUMAN FETAL LUNG IN VITRO

1985 ◽  
Vol 19 (4) ◽  
pp. 159A-159A
Author(s):  
Carole R Mendelson ◽  
Jeanne M Snyder ◽  
C R Rosenfeld
Keyword(s):  
Fetal Lung ◽  
Human Fetal Lung ◽  
Surfactant Apoprotein

Isoxsuprine Infusion to the Pregnant Rabbit and Its Effect on Fetal Lung Surfactant

Neonatology ◽  
1979 ◽  
Vol 35 (1-2) ◽  
pp. 43-51 ◽  
Author(s):  
Goran Enhorning ◽  
Dean Chamberlain ◽  
Carlos Contreras ◽  
Rosmarie Burgoyne ◽  
Bengt Robertson
Keyword(s):  
Lung Surfactant ◽  
Fetal Lung ◽  
Pregnant Rabbit

Degree of unsaturation of the fatty acid chains of phospholipids influences the fluorescence polarization: implications for evaluating fetal lung maturity.

1986 ◽  
Vol 32 (3) ◽  
pp. 425-428 ◽  
Author(s):  
J C Dohnal ◽  
L J Bowie ◽  
H J Burstein
Keyword(s):  
Fatty Acid ◽  
Fluorescence Polarization ◽  
Unsaturated Fatty Acids ◽  
Lung Surfactant ◽  
Fetal Lung ◽  
Fetal Lung Maturity ◽  
Fatty Acid Chain ◽  
Surface Active ◽  
Fluorescence Polarization Assay ◽  
Lung Maturity

Abstract To study the effect of fatty acid chain saturation on the fluorescence polarization assay as a measure of fetal lung maturity, we used purified phospholipids isolated from human amniotic fluid and various commercial phospholipids. We found that the fluorescence polarization value decreased as the concentration of unsaturated fatty acids increased. In contrast, the lecithin/sphingomyelin ratio increases with increasing amounts of saturated lecithin, produced as the fetal lung matures. Since only saturated lecithins are surface active, the two indices of fetal respiratory status must reflect different properties of lung surfactant.

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