Surfactant fetal

Beneficial effects have also been attributed to PAF. In reproduction, PAF secreted by the fertilized egg is instrumental in the implantation of the egg in the uterine wall. PAF is produced in significant quantities in the lungs of the fetus late in pregnancy and may stimulate the production of fetal lung surfactant, a protein-lipid complex that prevents collapse of the lungs in a newborn infant. 

Uterine relaxants tocolytic drugs) are administered where prolonged intrauterine life would greatly benefit the fetus or would permit additional time to allow treatment with drugs such as corticosteroids, which promote the production of fetal lung surfactant. Tocolytics are also used when temporary uterine relaxation is be desirable (e.g., intrauterine fetal resuscitation). While hydration, bed rest, and sedation have been used to inhibit uterine contractions, tocolytics are more likely to inhibit labor early in gestation, especially before labor is far... 

Alfonso LF, Arnaiz A, Alvarez FJ, Qi BQ, Dies-Pardo JA, Vallisi-Soler A, Tovar JA (1996) Lung hypoplasia and surfactant system immaturity induced in the fetal rat by prenatal exposure to nitrofen. Biol Neonate 69 94-100... 

Glucocorticoids have important effects on the development of the fetal lungs. Indeed, the structural and functional changes in the lungs near term, including the production of pulmonary surface-active material required for air breathing (surfactant), are stimulated by glucocorticoids. 

The pulmonary alveolar epithelium is comprised of two morphologically distinct cells, type I and type II cells. Type I cells are extremely large, squamous cells that make up 95% of the alveolar surface. Type II cells are smaller cuboidal cells that secrete and recycle surfactant and cover the remaining 5% of the alveolar surface. Mechanical distention of fetal lung tissue has been shown to stimulate expression of the type I cell phenotype and inhibit expression of the type II phenotype. Lumenal mechanical stim-... 

The cause of preterm labor is unknown, but recent evidence in a mouse model indicates that a maternal serum surfactant protein, SP-A, may trigger labor. Fetal fibronectin and cervical ultrasound have proven value for evaluating patients suspected of having preterm labor. The fetal fibronectin test is described later in the section entitled Laboratory Tests. Use of salivary estriol, corticotropin-releasing hormone, and interleukin-6 for preterm labor prediction is being investigated. 

Surfactant proteins (SP-A and SP-B) have been evaluated as potential fetal lung maturity tests, but the results are disappointing. ... 

Fluorescence polarization is a dimensionless ratio with values from 0.000 to 0.500 for dilute solutions containing fluorescing compounds (see Chapter 3). Polarization (P) measures the rotational diffusion of the fluorophore relative to its fluorescent half-life. If the half-life is short compared with the rate of rotational diffusion, P will be high. In contrast, if molecular rotation is faster than the excited state decay, then P wfll be low. Shinitzky proposed that for amni-otic fluid, lower polarization values reflected a decrease in the microviscosity of surfactant phospholipids. The fluidity of these phospholipids paralleled the change in lipid composition with maturation of the fetal lungs. This mechanism is incorrect for the NBD-PC method. NBD-PC binds to albumin and to surfactant thus the resulting polarization is a function of the surfactant/albumin ratio. ... 

The exact role of PG in lung surfactant is unclear. Many claim that the appearance of PG in the amniotic fluid indicates the final biochemical maturation of surfactant, but PG can be found in measurable quantities in amniotic fluid as early as 32 weeks, and its presence in small quantities does not necessarily imply that the fetal lungs are mature. The concentration of PG in amniotic fluid increases with gestational age. Most thm-layer chromatography techniques are positive when PG exceeds about 2 xmol/L. At this cutoff, results indicating maturity are almost always correct, but results indicating immaturity are frequently wrong. 

Lamellar bodies avidly scatter light, producing a haziness in mature amniotic fluid. These particles can be counted dfrecdy using the platelet channel of most whole blood cell counters. This technique is termed lamellar body count (LBC). LBC is a direct reflection of surfactant concentration in amniotic fluid, in contrast to L/S ratio and TDx FLM II, which are ratios. Fetal urination lowers LBC, but does not affect results of the other two methods. 

Condon JC, Jeyasuria P, Faust JM, Mendelson CR. Surfactant protein secreted by the maturing mouse fetal lung acts as a hormone that signals the initiation of parturition. Proc Natl Acad Sci USA 2004 101 4978-83. 

Holt JA, Ryan DF, Russell JC, et al. Automated rapid assessment of surfactant and fetal lung maturity. Lab Med 1990 21 359-66. 

Pryhuber GS, Hull WM, Fink I, McMahan MJ, Whit-sett JA. Ontogeny of surfactant proteins A and B in human amniotic fluid as indices of fetal lung maturity. Pediatr Res 1991 30 597-605. 

Thyroid hormones also accelerate fetal lung maturation. Fetal thyroid hormone levels may be increased by antenatal administration of thyrotropin-releasing hormone (TRH), a tripeptide that crosses the placental barrier, stimulates fetal pituitary production of thyroid stimulating hormone (TSH), and which, in turn, increases fetal thyroid hormone production (Chapter 33). This indirect method of enhancement of fetal thyroid hormone production is utilized because thyroid hormones do not readily cross the placental barrier. Insulin delays surfactant synthesis and so fetal hyperinsulinemia in diabetic mothers may increase the incidence of RDS even in the full-term infant. Androgen synthesized in the fetal testis is the probable cause of a slower onset of surfactant production in male fetuses. Prophylactic, or after onset of RDS, administration of synthetic or natural pulmonary surfactants intratracheally to preterm infants improves oxygenation and decreases pulmonary morbidity. 

Pulmonary surfactant in amniotic fluid can also be measured by its ability to generate stable foam in the presence of ethanol. This/oam stability test (FST), or shake test, correlates well with the L/S ratio and with fetal lung maturity. In some instances, in the presence of an L/S ratio of less than 2, the FST has indicated lung maturity (without subsequent respiratory distress). This discrepancy may be due to the presence of surfactants other than lecithin that stabilize the neonatal alveoli, namely, phosphatidyl-glycerol (PG) and phosphatidylinositol (PI). These acidic phospholipids are synthesized in stepwise fashion during the last trimester of normal pregnancy. 

Fetal lung maturation can be accelerated with antenatal corticosteroids. The National Institutes of Health (NIH) consensus conference in 1994 concluded that all fetuses between 24 and 34 weeks gestation at risk for preterm delivery should receive corticosteroids regardless of gender, race, maternal infection, and availability of surfactant. A report by the National Institutes of Child Health and Development Neonatal Research Network noted that antenatal steroid use was associated with fewer pulmonary problems and mortality. Many women who are appropriate candidates are... 

The administration of synthetic corticosteroids 48 to 72 hours before delivery of a fetus of less than 33 weeks of gestation in women who have toxemia of pregnancy, diabetes mellitus, or chronic renal disease may reduce the incidence or mortality of RDS by stimulating fetal synthesis of lung surfactant. 

Sul fetal 4069 Fatty alcohol sulfate. Anionic surfactant Zsch i m... 

Steroids accelerate lung maturation, resulting in fetal surfactant development. 

Celestone is a medication used to increase surfactant in fetal lungs and would be administered to a client who is less than 36 weeks pregnant therefore, the nurse would not question administering this medication. 

Pulmonary and Peripheral Gas Exchange in Health and Disease, edited by J. Roca, R. Rodriguez-Roisen, and P. D. Wagner Lung Surfactants Basic Science and Clinical Applications, R. H. Natter Nosocomial Pneumonia, edited by W. R. Jarvis Fetal Origins of Cardiovascular and Lung Disease, edited by David J. P. Barker... 

An important aspect in all drug delivery is the toxicity of the drug as well as that of the drug carrier. Therefore, toxicity has to be assessed also for microemulsion formulations. In microemulsion systems, the main concern regarding toxicity has to do with the cosurfactants used. For example, the majority of the work on the pharmaceutical application of microemulsions has involved the use of short- or medium-chain alcohols, e.g., butanol. In a range of studies it has been shown that these cause toxic side effects. For example, inhalation studies of the toxicity of 1-butanol, 2-butanol, and / -butanol in rats showed a dose-dependent reduction in fetal weight [56]. Furthermore, aqueous solutions of ethanol, propanol, and butanol were shown to result in elongated mitochondria in hepatocytes after 1 month of exposure [57]. (In addition to the toxicity aspects of these alcohols, microemulsions formed in their presence are often destabilized on dilution of the continuous phase.) Furthermore, many studies so far have involved aliphatic or aromatic oils, such as hexane or benzene, which obviously are unsuitable for pharmaceutical use. Moreover, ionic surfactants could in themselves be toxic and irritant [58]. 

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