Maturation of the Fetal Lung

Gc, Liggins; Ja, Kitterman

doi:10.1016/b978-0-08-027341-9.50010-4

Cited by 7 publications

(5 citation statements)

References 18 publications

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“…The prolonged absence of FBM-related diaphragmatic activity in high-cord transected foetuses significantly reduced lung growth, whereas low spinal cord transections had no effect. It was concluded that FBM are important for normal fetal lung growth (Wigglesworth & Desai 1979;Liggins et al 1981) and these results led to the suggestion that FBM stimulate lung growth by causing phasic stretch of lung tissue (Liggins 1984;Skinner 1989). In support of this concept, phasic stretch of isolated pulmonary epithelial cells in vitro has been shown to increase [3H]-thymidine incorporation into DNA (Skinner 1989;Liu et al 1992).…”

Section: Fetal Breathing Movements Lung Liquid Volume and Lung Growthmentioning

confidence: 99%

Fetal Lung Liquid: A Major Determinant of the Growth and Functional Development of the Fetal Lung

Hooper

Harding

1995

Clin Exp Pharma Physio

240

176

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1. During fetal life the lung develops as a liquid-filled organ. This liquid is produced by the fetal lung and leaves via the trachea from where it is either swallowed or enters the amniotic sac. Fetal lung liquid plays a crucial role in the growth and development of the lungs by maintaining them in a distended state. It is now recognized that the retention of liquid within the future airways is required to maintain the lungs at an appropriate level of expansion in order to stimulate their growth. Indeed, it is likely that most, if not all, of the conditions and malformations that lead to inadequate growth of the fetal lung do so by reducing the volume of lung liquid and hence the degree of lung expansion. 2. The volume of fetal lung liquid is principally regulated by the resistance to lung liquid efflux through the fetal upper airway and by the presence of diaphragmatic activity associated with fetal breathing movements (FBM). During non-breathing periods, the relatively high resistance offered by the upper airway to the efflux of lung liquid opposes the loss of liquid from the lung, thereby maintaining fetal lung expansion. During episodes of FBM, when the larynx is actively dilated and the resistance to lung liquid efflux is reduced, lung liquid leaves the lungs at an increased rate. However, selective inhibition of diaphragmatic muscle activity in the foetus leads to a reduction in lung liquid volume, rather than an increase. This finding indicates that during periods of FBM, rhythmical contractions of the diaphragm retard the loss of lung liquid and help to maintain lung expansion when the upper airway resistance is reduced. It is now apparent that the maintenance of lung expansion by FBM is the basis for their role in promoting fetal lung growth. 3. Successful transition from intra-uterine to extra-uterine life is dependent upon the clearance of liquid from the fetal lungs at the time of birth so that the lungs may effectively function as an organ of gas exchange.(ABSTRACT TRUNCATED AT 400 WORDS)

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Section: Fetal Breathing Movements Lung Liquid Volume and Lung Growthmentioning

confidence: 99%

Fetal Lung Liquid: A Major Determinant of the Growth and Functional Development of the Fetal Lung

Hooper

Harding

1995

Clin Exp Pharma Physio

240

176

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“…Episodic fetal breathing movements and pulmonary fluid production make an important contribution to the structural changes and morphological maturation of fetal lungs in addition to the hormonal factors (Alcorn, Adamson, Lambert, Maloney, Ritchie & Robinson, 1977;Liggins, 1984). Lung liquid secretion, which passes into the alveolar lumen and thence to the amniotic cavity throughout gestation, declines near term and normally ceases at birth (Liggins & Kitterman, 1981;Liggins, 1984;Dickson, Maloney & Berger, 1986). This secretion can be inhibited or even reversed experimentally by very low concentrations of adrenaline (Walters & Olver, 1978).…”

Section: Fetal Changesmentioning

confidence: 99%

Prenatal maturation, the timing of birth and how it may be regulated in domestic animals

Silver¹

1990

Experimental Physiology

115

111

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“…The dual nature of corticosteroid action in the lung of the avian embryo is similar to that seen in the fetal mammal, in which cortisol inhibited increased pulmonary cell number while simultaneously promoting DSPC synthesis . As in the chick embryo, physiological concentrations of glucocorticoid specifically attenuated the mitotic rate of lung cells in the fetus (Liggins and Kitterman, 1981).…”

Section: Discussionmentioning

confidence: 93%

Ontogeny of embryonic chicken lung: Effects of pituitary gland, corticosterone, and other hormones upon pulmonary growth and synthesis of surfactant phospholipids

Hylka

Doneen

1983

General and Comparative Endocrinology

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The actions of hormones on growth, cellular proliferation, and on synthetic rates of the major surfactant phospholipids, phosphatidylcholine (PC) and disaturated PC (DSPC), were studied in the lung of the chick embryo. Particular emphasis was placed on the effects of hypophysectomy, pituitary transplantation, and treatment with corticosterone (CORT). One study was concerned with hydrocortisone (HYCORT), estrogen (E2), thyroxine (T4), ovine prolactin (oPRL), and insulin. Hypophysectomy interfered with the normal gain in protein, the progressive dehydration of the embryonic lung, and also caused a reduction in the number of pulmonary cells on Days 16 and 18 of incubation. Absence of the pituitary gland diminished pulmonary PC by Day 16. Transplantation of one pituitary gland or exogenous CORT partially restored pulmonary phospholipid and PC (normalized per wet weight) in hypophysectomized (hypox) embryos. Transplantation also restored relative protein content in lungs of hypox individuals. Beyond this, transplantation was generally ineffective in reversing deficits of hypox individuals. All concentrations of CORT administered (30-100-300 micrograms) reduced the rate of pulmonary cell division. The highest dose was toxic as judged by its capacity to cause cellular death. Treatment of intact chicken embryos with CORT or E2 for two days stimulated incorporation of [14C]choline into PC and DSPC (the most surface-active component of PC) in the lungs of Day 17 embryos. CORT, but not E2, stimulated DSPC synthesis when treatment was increased to 3 days. Other hormones tested (T4, oPRL, insulin, and HYCORT) had no effect upon the rate of incorporation of [14C]choline into PC or DSPC. These results indicate that during ontogeny the avian lung becomes sensitive to CORT, and possibly E2, prior to 16 days of incubation. CORT, in particular, acts both to trigger the prehatching stimulation of surfactant phospholipid synthesis, especially the vital DSPC fraction, and to slow the rate of pulmonary cellular division coincident with biochemical differentiation of the surfactant system.

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Maturation of the Fetal Lung

Cited by 7 publications

References 18 publications

Fetal Lung Liquid: A Major Determinant of the Growth and Functional Development of the Fetal Lung

Fetal Lung Liquid: A Major Determinant of the Growth and Functional Development of the Fetal Lung

Prenatal maturation, the timing of birth and how it may be regulated in domestic animals

Ontogeny of embryonic chicken lung: Effects of pituitary gland, corticosterone, and other hormones upon pulmonary growth and synthesis of surfactant phospholipids

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