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At least 433 records · Page 24Linked to original sources
PubMed2007

Predicting inadequate long-term lung development in children with congenital diaphragmatic hernia: an analysis of longitudinal changes in ventilation and perfusion.

PURPOSE: Infants born with congenital diaphragmatic hernia (CDH) demonstrate a wide variability in postnatal catch-up lung growth. The goals of this study were to assess the pulmonary development of children born with CDH using sequential ventilation-perfusion (V/Q) scintigraphy and to identify the perinatal factors that correspond to a progressive V/Q mismatch. METHODS: The records of 137 patients seen between 1990 and 2005 in a multidisciplinary CDH clinic were reviewed. Changes in the ipsilateral V/Q quotient were compared in 46 patients who had 2 or more studies with the following variables: sex, patch repair, laterality, gestational age, and use of extracorporeal membrane oxygenation. An abnormal V/Q quotient was defined as greater than 1.2 (reference range, 0.8-1.2). RESULTS: Abnormal V/Q scans were identified in 28 (61%) of the 46 patients at the time of the last V/Q study. Patients who underwent a patch repair had nearly 7 times the risk (P < .001) of developing an ipsilateral V/Q mismatch. The use of extracorporeal membrane oxygenation had a variable effect on the probability of an abnormal V/Q study finding. No other variable was significant. CONCLUSIONS: Many children with CDH develop significant and progressive V/Q mismatches. Although some perinatal variables appear to be predictive of this phenomenon, they may simply be surrogates for a greater degree of pulmonary hypoplasia present at birth. This subpopulation of CDH survivors is an identifiable group clearly at risk and thus requires long-term follow-up.

Adolescent↗
PubMed1990

Relationships among surfactant fraction lipids, proteins and biophysical properties in the developing rat lung.

Lung development is associated with increases in specific phospholipids and proteins that function as critical pulmonary surfactant components. Attempts to characterize the pattern of surfactant development in fetal rat lungs have been hampered by the lack of a micromethod which will permit quantitative isolation of surface active components from small tissue specimens. As part of studies designed to elucidate the metabolic regulation of lung development in the rat, we developed sucrose density gradient centrifugation procedures to separate pulmonary phospholipids and proteins into a presumed surfactant (S) fraction and a residual (R) fraction. Electron microscopy of S pellets from mature fetuses identified predominant lamellar bodies and minimal contamination; incubation with 5 mM CaCl2 induced the appearance of tubular myelin figures, implying functional potential. This was confirmed by demonstrating low surface tension (less than 1 dyn/cm) in S, but not R, fractions at term gestation (21.5 days) and in 1-day-old neonatal lung isolates, based on dynamic measurements using the oscillating bubble technique. Surface activity was also high in the S pellets from fetuses at 20.5 days of gestation; however, at 19.5 days, minimum surface tension values of at least 19 dyne/cm were seen. These results correlated directly with biochemical analyses which indicated striking increases in three surfactant-associated proteins (SP-A, SP-B, and SP-C) after 19.5 days of gestation; a finding in agreement with previously reported data on the developmental increase of disaturated phosphatidylcholine in fetal rat lung. We conclude that isolation of S fraction components is valuable for demonstrating maturation of the fetal rat lung and may provide a useful tool for the study of regulatory mechanisms influencing surfactant production and function.

Animals↗
PubMed1984

The effect of amniocentesis and drainage of amniotic fluid on lung development in Macaca fascicularis.

Amniocentesis and withdrawal of amniotic fluid was performed on pregnant monkeys (Macaca fascicularis) at two stages in development, either between 47 and 64, or between 85 and 95 days gestation. After birth the lungs of each infant monkey were studied using precise morphometric techniques, and compared with those in a control group of animals. The lungs after amniocentesis had alveoli of normal maturity but reduced in number and increased in size, features which both reduce the relative area for gas exchange. There was also a reduction in the number of respiratory airways. These changes occurred regardless of the time of amniocentesis, the amount of fluid removed and even if the membranes were simply punctured with no fluid removal. There is some evidence to suggest that similar sublethal effects may be present in human infants after maternal amniocentesis.

Amniocentesis↗
PubMed1980

The effect of beta-aminopropionitrile on lung development in the rat.

beta-Aminopropionitrile (beta APN) was administered intraperitoneally to rats on postnatal days 1, 3, and 5. Body weight, lung volume, lung weight, number of alveoli per unit area and volume, total number of alveoli in the lung, and the total length of elastic fibers in the lung decreased, and the average alveolar volume increased in comparison with control animals similarly treated with saline. From Day 2 of age to Day 6 the total length of elastic fibers increased in control lungs but remained almost the same following beta APN treatment. Ultrastructurally, both the quality and quantity of elastin in lung alveolar wall were affected. beta APN also inhibited the synthesis of deoxyribonucleic acid in interstitial, endothelial, and Type II epithelial cells of the lung alveolar wall. The diminished number of alveoli gives support to the hypothesis that the elastin-collagen network may play a key role in postnatal alveolar multiplication.

Aminopropionitrile↗
PubMed1991

Fetal lung development in rats with a glycogen storage disorder.

A New Zealand strain of rats (NZR/Mh) is unable to mobilize liver glycogen due to a deficiency of phosphorylase b kinase. Affected homozygous rats (gsd/gsd) were used to assess the developmental relationship between lung glycogen loss and surfactant phospholipid and protein biosynthesis. Phosphorylase a and phosphorylase b kinase activities were negligible in gsd/gsd fetal lungs compared with controls from gestational day (D18) until postnatal day 1 (D + 1). At D20, tissue glycogen content was 158 +/- 5 and 181 +/- 6 mumol/g lung for control and gsd/gsd, respectively. Control rats mobilized 84% of their lung glycogen by D + 1, whereas the gsd/gsd strain retained 70-80% of D19-20 levels. This apparent fall in gsd/gsd glycogen per gram lung was due to an increase in cellular protein and size. Thus, in controls, total glycogen per lung decreased 65% from D20 to D + 1, whereas DNA doubled. In contrast, gsd/gsd lung growth resulted in a doubling of total lung glycogen, whereas the glycogen-to-DNA ratio remained constant. A lack of cellular glycogenolysis was confirmed by electron microscopy where gsd/gsd type II cells remained large and glycogen-rich over the entire perinatal interval. The potential for glycogen breakdown by a lysosomal alpha-amyloglucosidase in gsd/gsd lungs was estimated in tissue homogenates, whereas rates of hydrolysis of glycogen or p-nitrophenylglucoside were significant and equal to controls at all ages tested. Incorporation of [14C]choline into phosphatidylcholine (PC) of incubated lung slices increased 1.7-fold in control lungs from D20-D21. Over the same interval, PC synthesis in gsd/gsd lungs was 40% lower and did not change.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1980

Transplacental stimulation of lung development in the fetal rabbit by 3,5-dimethyl-3'-isopropyl-L-thyronine.

The effect of thyroid hormone on maturation of fetal rabbit lung was studied with maternal treatment using 3,5-dimethyl-3'-isopropyl-L-thyronine (DIMIT), a synthetic analogue of triiodothyronine. To investigate the in vivo kinetics and distribution of DIMIT, we prepared [3H]DIMIT and injected both pregnant rats (18-21 d gestation) and rabbits (25 d gestation). In the rat, maximal concentrations of radioactivity in maternal plasma, fetal plasma, and amniotic fluid occurred within 10 min, 1-2 h, and 4-6 h, respectively, after intramuscular injection. After 7 h the concentration of radioactivity in fetal plasma was 163 and 71% of the maternal level in rats and rabbits, respectively, indicating that DIMIT readily crosses the placenta. We treated pregnant rabbits for 1-2 d with DIMIT in doses of 0.5-3 mg/kg per d and examined the fetuses at 26 and 27 d gestation. Treatment did not affect fetal growth or viability. In fetal liver, DIMIT increased the activity of NADPH cytochromeac reductase by 64% and decreased the glycogen content by 73% compared to controls. The rate of choline incorporation by lung minces increased in dose-dependent manner to a maximum of +104% at 3 mg/kg DIMIT; this does stimulated by 38% the activity of lung phosphatidic acid phosphatase (PAPase), a corticosteroid-responsive enzyme, but there was no increase in tissue PAPase activity at most lower doses of DIMIT that enhanced choline incorporation. Treated lungs had 38% less glycogen tha controls, but there was no effect on tissue levels of DNA, protein, or phospholipid. DIMIT treatment increased the amount of total phospholipid (+163%). saturated phosphatidylcholine (+330%), and PAPase activity (+134%) in lung lavage fluid. The DIMIT effects on both choline incorporation by lung minces and phospholipid content of lavage fluid were substantially greater than what had occurred with an optimal dose of betamethasone. DIMIT also increased corticosteroid binding capacity in fetal plasma and produced a dose-dependent increase (maximal threefold) in total and free corticoids of both maternal and fetal plasma. It is estimated that elevated endogenous corticoids probably account for less than one-third of the increases in phospholipid synthesis and secretion observed at the higher doses of DIMIT. These data indicate that administration of DIMIT to pregnant rabbits accelertes maturation of the surfactant system in fetal lung. The magnitude of the effects on phospholipid synthesis and secretion, along with the minimal effect of PAPase activity in fetal lung tissue, suggest that thyroid hormones affect different biochemical processes from those influenced by glucocorticoids.

Adrenal Cortex Hormones↗
PubMed1998

Significance of ion transport during lung development and in respiratory disease of the newborn.

Active ion transport plays a critical role in the liquid movement across the fetal and perinatal lung epithelium. The fetal lung liquid production is coupled with active secretion of Cl- into the luminal space. The potential for fluid absorbing mechanisms related to active Na+ transport from the apical to the basolateral side of the epithelium appears near the end of gestation. At birth there is a dramatic change of environment with commencement of air-breathing, sudden increase in oxygen partial pressure (PO2) and profound changes in the pulmonary circulation. A concurrent switch from fluid secretion to maintenance of low amounts of alveolar fluid is another major physiological adjustment taking place in the perinatal distal lung epithelium. The fluid-absorbing mechanism is a result of a well-synchronized co-operation between the basolateral membrane Na-K-ATPase and the apical membrane Na+ channels and it promotes salt and water movement from the airspace. Inability of the fetal lung epithelium to switch from fluid secretion to Na+ transport-dependent absorption seems to be an important factor adversely contributing to the respiratory distress of the newborn premature infant.

Epithelium↗