The influence of hormones on the biochemical development of fetal rat lung in organ culture

Gross, Ian; Wilson, C. M.; Ingleson, Linda D.; Brehier, Arlette; Rooney, Seamus A.

doi:10.1016/0005-2760(79)90106-1

Cited by 89 publications

(41 citation statements)

References 20 publications

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“…In summary, the data in this paper together with previous data from this laboratory (12,16,17) show that estrogen can accelerate fetal lung maturation and stimulate pulmonary surfactant production. Estrogen levels are known to increase towards the end of gestation in many species.…”

Section: Effect Of I7p-estradiol On Fetal Rabbit Lung and Liver Glycosupporting

confidence: 67%

“…Thus, maternal estrogen administration has the following effects on the fetal lung: it increases the amount of total phospholipid and phosphatidylcholine as well as the phosphatidylcholine:sphingomyelin ratio in lung lavage (17), it increases the rate of choline incorporation into phosphatidylcholine in lung slices (16), and it increases the activities of pulmonary cholinephosphate cytidylyltransferase and lysolecithin acyltransferase (16), enzymes involved in the synthesis of total and disaturated phosphatidylcholine, respectively (33). Gross et al (12) reported that estrogen accelerates maturation of fetal rat lung in organ culture. This fmding suggests that estrogen has a direct effect on the fetal lung.…”

Section: Speculationmentioning

confidence: 99%

“…Thus, estrogens must act via another mechanism. Inasmuch as estrogen accelerates the maturation of fetal rat lung explants in vitro (12), it is likely that it acts directly on the lung rather than y 25 of gestation, and the fetuses were delivered on day 26. The fetal weight are from three control and three estrogen-treated litters.…”

Section: Effect Of I7p-estradiol On Fetal Rabbit Lung and Liver Glycomentioning

confidence: 99%

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Effects of Estrogen on Fetal Rabbit Lung Maturation: Morphological and Biochemical Studies

et al. 1981

Pediatr Res

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Summary17P-Estradiol (0.44 to 4.4 &kg) was intramuscularly administered to pregnant rabbits on day 25 or 26 of gestation, and the fetuses were delivered by cesarean section 24 hr later. On light microscopy, the lungs from the treated group had larger alveoli and thinner interalveolar septa than did those from the controls at the same gestational age. The 1umen:septa ratio was 0.62 + 0.06 in the control group and 0.88 + 0.05 in the treated group ( P < 0.01). Blood vessels in the lungs of the treated group were also more mature than were those in the control group. Alveolar epithelial cells consisted of 52% undifferentiated, 21% type 11, and 27% type I cells in the control group. In the estrogen-treated group, the corresponding distribution was 25, 29, and 45%. There were 0.82 -+ 0.16 lamellar bodies per alveolar cell in the treated group compared to 0.38 k 0.06 in the controls (P < 0.05). Estrogen decreased fetal lung glycogen content from 247 + 15 pg/mg protein to 70 9 on day 26 and from 103 -+ 13 to 13 + 2 on day 27 ( P < 0.001). Estrogen administration increased the rate of incdrporation of choliie into phosphatidylcholine in fetal lung slices. decreased the rate of thymidine incorporation into DNA, but had no effect on the rates bf incorporatibn of ethanolamine into phosphatidylethanolamine or of leucine into protein. These data indicate that estrogen accelerates the rate of fetal lung maturation. It appears to stimulate lung differentiation at the expense of lung growth. SpeculationEstrogen may be involved in the physiologic control of fetal lung maturation and pulmonary surfactant production.We have previously shown that administration of 17/3-estradiol to pregnant rabbits at 25 to 26 days gestation (term is 31 days) accelerates fetal lung maturation and stimulates production of pulmonary surfactant (16,17). Thus, maternal estrogen administration has the following effects on the fetal lung: it increases the amount of total phospholipid and phosphatidylcholine as well as the phosphatidylcholine:sphingomyelin ratio in lung lavage (17), it increases the rate of choline incorporation into phosphatidylcholine in lung slices (16), and it increases the activities of pulmonary cholinephosphate cytidylyltransferase and lysolecithin acyltransferase (16), enzymes involved in the synthesis of total and disaturated phosphatidylcholine, respectively (33). Gross et al. (12) reported that estrogen accelerates maturation of fetal rat lung in organ culture. This fmding suggests that estrogen has a direct effect on the fetal lung.The purpose of the present study was to further characterize the effects of estrogen on fetal lung maturation. Inasmuch as there are distinct morphological changes during maturation of the fetal lung (2), we examined the effects of estrogen on these parameters of lung maturation. In addition, we determined the effect of estrogen on lung glycogen content because this decreases toward the end of gestation in a number of species (4,23,36), and it has been postulated that glycogen may provide substrate o...

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Section: Effect Of I7p-estradiol On Fetal Rabbit Lung and Liver Glycosupporting

confidence: 67%

Section: Speculationmentioning

confidence: 99%

Section: Effect Of I7p-estradiol On Fetal Rabbit Lung and Liver Glycomentioning

confidence: 99%

See 1 more Smart Citation

Effects of Estrogen on Fetal Rabbit Lung Maturation: Morphological and Biochemical Studies

et al. 1981

Pediatr Res

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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: 97%

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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“…Gross et at. (10) also have reported that treatment of fetal rat lung explants in organ culture with 10-5 M estrogen results in increased incorporation of pH]acetate into PC and phosphatidylglycerol (10). Recently, Thuresson-KJein et at.…”

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confidence: 97%

Failure to Detect a Stimulatory Effect of Estradiol-17β on Ovine Fetal Lung Maturation

et al. 1987

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MATERIALS AND METHODSAnimals. Fourteen pregnant ewes of mixed Western breed were studied between the 106th and 127th days of gestation. 145 ABSTRACT. It has been reported that estradiol-17P (E2) stimulates rat and rabbit fetal lung maturation; however, E2 was not directly administered to the fetus in these experiments. Therefore, we used the chronically instrumented fetal sheep to study the effects of 14 days of continuous E2 infusion on fetal lung maturation. Animals were instrumented on days 104-106 of gestation, then infused with either saline or E2 (100~g/day) from 111 to 127 days of gestation. Fetal plasma concentrations of E2, estrone, and cortisol, and tracheal fluid phosphatidylcholine:sphingomyelin ratios and phosphatidylcholine flux were measured daily in E2-infused (n = 8) and salineinfused (n = 6) control animals. At 127 days of gestation, fetuses were sacrificed and lung tissue samples obtained for biochemical and morphological analyses. Plasma E2 levels rose from 0.045 ± 0.001 (x ± SE) to 7.45 ± 5.31 ng/ml (p < 0.05) in E2-infused animals whereas levels remained < 0.06 ng/ml in saline-infused animals. Plasma estrone concentrations also were significantly elevated by E2 infusion. Plasma contisol concentrations increased from 0.58 ± 0.08 to 0.88 ± 0.40 Itg/dl in E2-treated fetuses during the last week of infusion whereas values in control animals were unchanged. The ratio of acetone-precipitated phosphatidylcholine to sphingomyelin and the flux of acetone-precipitated phosphatidylcholine in tracheal fluid were not affected by E2 infusion. Fetal lung tissue phospholipid content was also unaffected by E2 infusion. Furthermore, there was no consistent effect of E2 infusion on the histological structure of the fetal lung tissue as determined by morphometric methods. Therefore, we conclude that prolonged elevations in plasma E2 in the early to middle 3rd trimester of gestation, i.e., prior to 128 days of gestation, do not stimulate lung maturation in the intact ovine fetus. (Pediatr Res 22: 145-149, 1987) Abbreviations RDS, respiratory distress syndrome E2, estradiol-17P PC, phosphatidylcholine EI, estrone iv, intravenous RIA, radioimmunoassay DSPC, disaturated phosphatidylcholine S, sphingomyelin

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The influence of hormones on the biochemical development of fetal rat lung in organ culture

Cited by 89 publications

References 20 publications

Effects of Estrogen on Fetal Rabbit Lung Maturation: Morphological and Biochemical Studies

Effects of Estrogen on Fetal Rabbit Lung Maturation: Morphological and Biochemical Studies

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

Failure to Detect a Stimulatory Effect of Estradiol-17β on Ovine Fetal Lung Maturation

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