Effects of betamethasone on phospholipid content, composition and biosynthesis in the fetal rabbit lung

Rooney, Seamus A.; Gobran, Laurice I.; Mariño, P; Maniscalco, William M.; Gross, Ian

doi:10.1016/0005-2760(79)90200-5

Cited by 130 publications

(41 citation statements)

References 36 publications

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“…Although glucocorticoids (17)(18)(19)(20), thyroid hormone (20), estrogen (44,45), and aminophylline (46,47) have previously been reported to accelerate the normal developmental decrease in lung glycogen, an acceleration of the earlier increase in lung glycogen was reported in only one previous study. Alescio and Dani (48) reported that the glycogen content of 1 1-day fetal mouse lung explants was increased when cultured in the presence of cortisol for 48 h. Effects of hormones on fatty acid synthesis in developing fetal lung have not been extensively examined.…”

Section: Discussionmentioning

confidence: 96%

“…Nevertheless, hormones that accelerate lung Abbreviations maturation and stimulate surfactant production in the fetus also promote glycogen depletion (1). Glucocorticoids decreased lung T3, triiodothyronine glycogen in vivo in the fetal rabbit (17,18) and mouse (19) while RDS, respiratory distress syndrome dexamethasone and thyroxine had a similar effect in cultured fetal rat lung explants (20). The influence of a combination of these two hormones on this parameter of lung maturation, however, has not previously been reported.…”

mentioning

confidence: 86%

“…The rate of [methyl-'4C]choline incorporation into phosphatidylcholine in lung slices was measured in Krebs-Ringer phosphate buffer as described previously (17,19). Because of possible differences in the intracellular pool sizes of choline or phosphorylated choline intermediates it is possible that this measurement is not a true reflection of phosphatidylcholine synthesis.…”

Section: Rate Of Choline Incorporation Into Phosphatidylcholinementioning

confidence: 99%

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Thyroid Hormone Opposes Some Glucocorticoid Effects on Glycogen Content and Lipid Synthesis in Developing Fetal Rat Lung

1986

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ABSTRACT. Because of current interest in use of a com-used prophylactically to accelerate fetal lung maturation and bination of glucocorticoid and thyroid hormones for pre-prevent RDS in human newborns (2, 3) and in at least one vention of respiratory distress syndrome we examined the clinical study (4) thyroxine was also reported to be effective in effects of dexamethasone and triiodothyronine (T3), alone this regard. However, the findings in a recent multicenter study and in combination, on glycogen content and rates of fatty that glucocorticoids are not as efficacious in preventing RDS as acid and phosphatidylcholine synthesis in fetal rat lung. earlier believed and that its effects may be largely confined to The hormones were administered to the mothers on the 2 female infants (5) has led to interest in use of a combination of days before delivery on days 17-22 of gestation. Both glucocorticoids and thyroid hormone for prevention of RDS (6).hormones increased the rate of choline incorporation into Prior to such clinical use, however, it is desirable to have inforphosphatidylcholine, an index of surfactant synthesis, on mation on the interaction of these hormones in the acceleration day 20 just prior to the normal developmental surge but of lung maturation in animals. had no effect on this parameter on days 19, 21, or 22.Previous studies in animals have shown that a combination of There is a developmental increase in lung glycogen on days glucocorticoid and thyroid hormones is more effective than either 17-20 with a decrease thereafter and a developmental hormone alone in accelerating fetal lung maturation and stimuincrease in the rate of fatty acid synthesis between days 20 lating surfactant production. In a morphological study in the and 21. The increases in glycogen content and fatty acid fetal rat, Hitchcock (7) reported maximal acceleration of lung synthesis were accelerated by dexamethasone and pre-maturation when glucocorticoids and thyroxine were both presvented by T3 and when the hormones were administered ent. Similarly, a synergistic interaction between glucocorticoids together T3 antagonized the stimulatory effects of dexa-and thyroid hormone in stimulating synthesis of phosphatidylmethasone on these parameters. Both dexamethasone and choline and disaturated phosphatidylcholine, the major compo-T3 accelerated the normal developmental decrease in lung nent of pulmonary surfactant (I), was demonstrated in fetal rat glycogen later in gestation and the effects of the two lung in vivo (8,9) and in fetal rat (10, 1 I), rabbit (12), and hormones on this parameter were additive. The combina-human (1 3) lung in culture. tion of dexamethasone and T3 led to significantly smaller In addition to morphology and synthesis of surfactant phosfetuses and increased mortality late in gestation. These pholipids, lung maturation may also be assessed by other criteria. data show that glucocorticoid and thyroid hormones have An increase followed by a decrease in glycogen content is a opposite as well as common effects on...

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Section: Discussionmentioning

confidence: 96%

mentioning

confidence: 86%

Section: Rate Of Choline Incorporation Into Phosphatidylcholinementioning

confidence: 99%

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Thyroid Hormone Opposes Some Glucocorticoid Effects on Glycogen Content and Lipid Synthesis in Developing Fetal Rat Lung

1986

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“…Effects of prenatal corticosteroids on surfactant synthesis in preterm infants with RDS In many in vitro studies corticosteroids have been found to increase the activity of the enzymes involved in surfactant PC synthesis [42][43][44][45][46] and also increase surfactant protein synthesis. 44 In in vitro experiments with lung slices and isolated type II cells, corticosteroids were found to increase the incorporation of radiolabel precursors into surfactant PC, reflecting increased PC synthesis.…”

Section: Surfactant Pool Sizementioning

confidence: 99%

“…44 In in vitro experiments with lung slices and isolated type II cells, corticosteroids were found to increase the incorporation of radiolabel precursors into surfactant PC, reflecting increased PC synthesis. 43,46,47 Prenatal corticosteroid treatment in preterm lambs rapidly increases surfactant protein mRNAs and surfactant proteins in lung tissue. 48 In a study by Kessler et al 49 in premature baboons, a 72-h treatment with prenatal dexamethasone did not increase radioactive palmitate incorporation in lung lipids, but increased total lung phospholipids and alveolar lavage DPPC in lung lavage fluid at birth.…”

Section: Surfactant Pool Sizementioning

confidence: 99%

Pulmonary surfactant kinetics of the newborn infant: novel insights from studies with stable isotopes

et al. 2009

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Deficiency or dysfunction of the pulmonary surfactant plays a critical role in the pathogenesis of respiratory diseases of the newborn. After a short review of the pulmonary surfactant, including its role in selected neonatal respiratory conditions, we describe a series of studies conducted by applying two recently developed methods to measure surfactant kinetics. In the first set of studies, namely 'endogenous studies', which used stable isotope-labeled intravenous surfactant precursors, we have shown the feasibility of measuring surfactant synthesis and kinetics in infants using several metabolic precursors, including plasma glucose, plasma fatty acids and body water. In the second set of studies, namely 'exogenous studies', which used a stable isotope-labeled phosphatidylcholine (PC) tracer given endotracheally, we estimated the surfactant disaturated phosphatidylcholine (DSPC) pool size and half-life. The major findings of our studies are presented here and can be summarized as follows: (a) the de novo synthesis and turnover rates of the surfactant (DSPC) in preterm infants with respiratory distress syndrome (RDS) are very low with either precursor; (b) in preterm infants with RDS, pool size is very small and half-life much longer than what has been reported in animal studies; (c) patients recovering from RDS who required higher continuous positive airway pressure pressure after extubation or reintubation have a lower level of intrapulmonary surfactant than those who did well after extubation; (d) term newborn infants with pneumonia have greatly accelerated surfactant catabolism; and (e) infants with uncomplicated congenital diaphragmatic hernia (CDH) and on conventional mechanical ventilation have normal surfactant synthesis, but those requiring extracorporeal membrane oxygenated (ECMO) do not. Information obtained from these studies in infants will help to better tailor exogenous surfactant treatment in neonatal lung diseases.

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Hormonal Influences During Fetal Lung Development

Ballard

1980

Novartis Foundation Symposia

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Effects of betamethasone on phospholipid content, composition and biosynthesis in the fetal rabbit lung

Cited by 130 publications

References 36 publications

Thyroid Hormone Opposes Some Glucocorticoid Effects on Glycogen Content and Lipid Synthesis in Developing Fetal Rat Lung

Thyroid Hormone Opposes Some Glucocorticoid Effects on Glycogen Content and Lipid Synthesis in Developing Fetal Rat Lung

Pulmonary surfactant kinetics of the newborn infant: novel insights from studies with stable isotopes

Hormonal Influences During Fetal Lung Development

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