Physiology of Transition from Intrauterine to Extrauterine Life

Hillman, Noah H.; Kallapur, Suhas G.; Jobe, Alan H.

doi:10.1016/j.clp.2012.09.009

Cited by 343 publications

(377 citation statements)

References 56 publications

(72 reference statements)

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“…In particular, thyroid hormones promote synthesis of surfactant proteins B and C. They also increase the phospholipid content of lung liquid, although this effect may be mediated via upregulation of pulmonary b-adrenergic receptor expression and, hence, enhanced epinephrine-stimulated surfactant release (Das et al 1984, Warburton et al 1988. Similar to lung liquid resorption, the effects of T 3 and cortisol on surfactant production appear to be synergistic with greater effects on lung stability when the two hormones are given together than when either hormone is given alone (Warburton et al 1988, Mendelson & Boggaram 1991, Hillman et al 2012.…”

Section: The Lungs and Respiratory Functionmentioning

confidence: 97%

“…Maturation of surfactant synthesis and release by the type II pneumocytes also depends, in part, on the increasing T 3 bioavailability toward term (Mendelson & Boggaram 1991, Hillman et al 2012. Thyroidectomy of fetal sheep reduces the number of type II pneumocytes in the lungs at term as well as the number of surfactantcontaining lamellar bodies in these cells (Ayromlooi et al 1983).…”

Section: The Lungs and Respiratory Functionmentioning

confidence: 99%

“…Ventilation of the lungs and gas exchange in the newborn animal depend on a number of structural and functional changes, including removal of lung liquid and production of surfactant (Olver et al 1981, Wilson et al 2007, Hillman et al 2012. Thyroid hormones have an important role in determining the sensitivity of the fluid absorption system to catecholamines released during birth (Barker et al 1988(Barker et al , 1990(Barker et al , 1991.…”

Section: The Lungs and Respiratory Functionmentioning

confidence: 99%

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Thyroid hormones in fetal growth and prepartum maturation

Forhead

Fowden

2014

Journal of Endocrinology

328

267

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The thyroid hormones, thyroxine (T 4 ) and triiodothyronine (T 3 ), are essential for normal growth and development of the fetus. Their bioavailability in utero depends on development of the fetal hypothalamic-pituitary-thyroid gland axis and the abundance of thyroid hormone transporters and deiodinases that influence tissue levels of bioactive hormone. Fetal T 4 and T 3 concentrations are also affected by gestational age, nutritional and endocrine conditions in utero, and placental permeability to maternal thyroid hormones, which varies among species with placental morphology. Thyroid hormones are required for the general accretion of fetal mass and to trigger discrete developmental events in the fetal brain and somatic tissues from early in gestation. They also promote terminal differentiation of fetal tissues closer to term and are important in mediating the prepartum maturational effects of the glucocorticoids that ensure neonatal viability. Thyroid hormones act directly through anabolic effects on fetal metabolism and the stimulation of fetal oxygen consumption. They also act indirectly by controlling the bioavailability and effectiveness of other hormones and growth factors that influence fetal development such as the catecholamines and insulin-like growth factors (IGFs). By regulating tissue accretion and differentiation near term, fetal thyroid hormones ensure activation of physiological processes essential for survival at birth such as pulmonary gas exchange, thermogenesis, hepatic glucogenesis, and cardiac adaptations. This review examines the developmental control of fetal T 4 and T 3 bioavailability and discusses the role of these hormones in fetal growth and development with particular emphasis on maturation of somatic tissues critical for survival immediately at birth.

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Section: The Lungs and Respiratory Functionmentioning

confidence: 97%

Section: The Lungs and Respiratory Functionmentioning

confidence: 99%

Section: The Lungs and Respiratory Functionmentioning

confidence: 99%

See 1 more Smart Citation

Thyroid hormones in fetal growth and prepartum maturation

Forhead

Fowden

2014

Journal of Endocrinology

328

267

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“…Pulmonary vascular resistance is high during gestation and decreases rapidly after birth under the influence of breathing movements, gas exchange and the release of vasoactive factors of the endothelin (ET), nitric oxide (NO) and prostacyclin (PGI 2 ) pathways [8,9] (figure 1). The ET pathway is activated by three ligands: ET-1, ET-2 and ET-3, of which ET-1 is the most common isoform [10,11].…”

mentioning

confidence: 99%

Pulmonary vascular development in congenital diaphragmatic hernia

et al. 2018

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Congenital diaphragmatic hernia (CDH) is a rare congenital anomaly characterised by a diaphragmatic defect, persistent pulmonary hypertension (PH) and lung hypoplasia. The relative contribution of these three elements can vary considerably in individual patients. Most affected children suffer primarily from the associated PH, for which the therapeutic modalities are limited and frequently not evidence based. The vascular defects associated with PH, which is characterised by increased muscularisation of arterioles and capillaries, start to develop early in gestation. Pulmonary vascular development is integrated with the development of the airway epithelium. Although our knowledge is still incomplete, the processes involved in the growth and expansion of the vasculature are beginning to be unravelled. It is clear that early disturbances of this process lead to major pulmonary growth abnormalities, resulting in serious clinical challenges and in many cases death in the newborn. Here we provide an overview of the current molecular pathways involved in pulmonary vascular development. Moreover, we describe the abnormalities associated with CDH and the potential therapeutic approaches for this severe abnormality. Normal pulmonary vascular developmentHuman lung development can be divided into different stages based on histology, starting with the embryonic stage at 4 weeks of gestation, followed by the pseudoglandular stage in which branching of the lung buds continues. During the canalicular stage, starting at ∼16 weeks of gestation, the terminal bronchioli are formed. From 24 weeks of gestation until term, the saccular stage, airspaces widen and alveoli are formed. During the alveolar stage, which persists into the postnatal period up to 3 years of age, maturation of the airways occurs [1]. Concomitant with the expansion of the airways is the adaptation of the microvasculature to optimise the exchange of oxygen and carbon dioxide between the blood and the airways. We and others have shown that very early in lung development pulmonary vessels are present and connected to the systemic circulation. The vasculature develops in close relation with the airways and is a rate-limiting factor in branching morphogenesis [2][3][4]. This implies that the pulmonary vasculature plays an important role in lung development. The formation of new blood vessels primarily occurs through

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“…Scheduled birth (via labour induction or elective cesarean) impairs this process 10 . Anticipating birth can increase vulnerability to hypoxia and to fetal distress during induction.…”

Section: Introductionmentioning

confidence: 99%