Oestrogens in fetal and maternal fluids throughout pregnancy in the pig and comparisons with the ewe and cow

Robertson, H. A.; Dwyer, R. J.; King, G. J.

doi:10.1677/joe.0.1060355

Cited by 38 publications

(17 citation statements)

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“…Similarly, low FSH concentrations during that period had also been reported by others (Mc Coard et al 2003). The high concentrations of estrogens in umbilical artery plasma during the last trimester are paralleled by a similar course of estrogen concentrations in amniotic fluid (Robertson et al 1985) and in the urine of sows along pregnancy (Velle 1958). However, these concentrations were attributed to steroid formation and aromatization in placental tissue (e.g., Rombauts 1964, Knight 1994) and do not require contribution by the fetus.…”

Section: Discussionsupporting

confidence: 72%

Changes of testicular aromatase expression during fetal development in male pigs (sus scrofa)

Haeussler

Wagner²,

Welter³

et al. 2007

Reproduction

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Male pig fetuses secrete considerable amounts of estrogens, but the location of aromatase activity within the fetal testis is not known. The location of aromatase expression was investigated by immunocytochemistry in fetal testes from week 6 (nZ5), weeks 10, 13, and 15 (each: nZ6) of gestation and additionally in neonates (nZ4). Blood was sampled from the umbilical artery of fetuses and jugular vein of neonates. Histological evaluation of testes involved morphological criteria and counting of Leydig cells, Sertoli cells, and gonocytes. Aromatase activity was localized immunocytochemically and quantified by the percentage of positive stained cells within the same cell type. Aromatase expression was further characterized by quantitative RT-PCR. Concentrations of estrogens, testosterone, FSH, and LH were measured in blood plasma. Total estrogens increased from week 10 to a maximum of 31.03 nmol/l in week 15. Increased testosterone concentrations were only measured at week 6 and were paralleled by slightly elevated estrogens. Thereafter, testosterone dropped and was low throughout. The increase of estrogens was not paralleled by a similar increase of FSH and LH but was related to the increase of the total number of Leydig cells. This increase was also found for mRNA expression. Both Leydig cells and gonocytes were identified as contributors to estrogen formation. Gonocytes were the main source of aromatase at week 10, when gene expression by Leydig cells is low due to the preparation of a wave of Leydig cell mitosis. Reproduction (2007) 133 323-330

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Section: Discussionsupporting

confidence: 72%

Changes of testicular aromatase expression during fetal development in male pigs (sus scrofa)

Haeussler

Wagner²,

Welter³

et al. 2007

Reproduction

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“…Fetal plasma levels of estrogen are in abundance in the latter stages of gestation in many species (9,18,61). Maternal administration of estrogen accelerates lung maturation and stimulates surfactant production in the fetal rabbit and rat (21, 29 -31, 54).…”

Section: Lung Developmentmentioning

confidence: 99%

The impact of sex and sex hormones on lung physiology and disease: lessons from animal studies

Carey¹,

Card²,

Voltz³

et al. 2007

American Journal of Physiology-Lung Cellular and Molecular Phys

199

144

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Numerous animal studies have revealed significant effects of sex and sex hormones on normal lung development, lung physiology, and various lung diseases. The primary goal of this review is to summarize knowledge to date on the effects of sex and sex hormones on lung development, physiology, and disease in animals. Specific emphasis will be placed on fibrosis, allergic airway disease, acute lung injury models, respiratory infection, and lung toxicology studies.

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“…Fetal plasma estradiol (E 2 ) levels increase progressively during late gestation, they rise further with the onset of parturition at term, and they fall in the early postnatal period due to the loss of the placentally derived hormone (22,23). These cumulative observations suggest that there is relative estrogen deprivation following preterm birth that may adversely impact lung NOS and thereby impair pulmonary development and function.…”

Section: What This Study Adds To the Fieldmentioning

confidence: 99%

Postnatal Estradiol Up-regulates Lung Nitric Oxide Synthases and Improves Lung Function in Bronchopulmonary Dysplasia

McCurnin

Pierce

Willis³

et al. 2009

Am J Respir Crit Care Med

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Rationale: Nitric oxide (NO) plays an important role in lung development and perinatal lung function, and pulmonary NO synthases (NOS) are decreased in bronchopulmonary dysplasia (BPD) following preterm birth. Fetal estradiol levels increase during late gestation and estradiol up-regulates NOS, suggesting that after preterm birth estradiol deprivation causes attenuated lung NOS resulting in impaired pulmonary function. Objective: To test the effects of postnatal estradiol administration in a primate model of BPD over 14 days after delivery at 125 days of gestation (term 5 185 d). Methods: Cardiopulmonary function was assessed by echocardiography and whole body plethysmography. Lung morphometric and histopathologic analyses were performed, and NOS enzymatic activity and abundance were measured. Measurements and Main Results: Estradiol caused an increase in blood pressure and ductus arteriosus closure. Expiratory resistance and lung compliance were also improved, and this occurred before spontaneous ductal closure. Furthermore, both oxygenation and ventilation indices were improved with estradiol, and the changes in lung function and ventilatory support requirements persisted throughout the study period. Whereas estradiol had negligible effect on indicators of lung inflammation and on lung structure assessed after the initial 14 days of ventilatory support, it caused an increase in lung neuronal and endothelial NOS enzymatic activity. Conclusions: In a primate model of BPD, postnatal estradiol treatment had favorable cardiovascular impact, enhanced pulmonary function, and lowered requirements for ventilatory support in association with an up-regulation of lung NOS. Estradiol may be an efficacious postnatal therapy to improve lung function and outcome in preterm infants.The signaling molecule nitric oxide (NO), generated by nitric oxide synthase (NOS), plays a key role in multiple processes in the mature lung (1, 2). In the developing lung, NO participates in pulmonary vascularization, alveolarization, and airway branching, and also counteracts apoptosis in multiple lung cell types (3-6). In the perinatal period, epithelium-derived NO is critically involved in the regulation of lung liquid production and of peripheral contractile elements (7, 8), and it also mediates pulmonary vasomotor tone (9). In studies of lungs from fetal baboons, we showed that all three NOS isoforms, neuronal NOS (nNOS), endothelial NOS (eNOS), and inducible NOS (iNOS), are principally expressed in proximal respiratory epithelium, and that there are maturational increases in their abundance and in NO production during the early third trimester (10). Thus, pulmonary NOS expression is up-regulated during fetal development in the primate, and this process may be critical to lung structural development and airway, parenchymal, and pulmonary vascular function in the early postnatal period.Bronchopulmonary dysplasia (BPD) is a devastating primary complication of premature birth that develops in the preterm human lung following ventilatory and oxyg...

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Oestrogens in fetal and maternal fluids throughout pregnancy in the pig and comparisons with the ewe and cow

Cited by 38 publications

References 0 publications

Changes of testicular aromatase expression during fetal development in male pigs (sus scrofa)

Changes of testicular aromatase expression during fetal development in male pigs (sus scrofa)

The impact of sex and sex hormones on lung physiology and disease: lessons from animal studies

Postnatal Estradiol Up-regulates Lung Nitric Oxide Synthases and Improves Lung Function in Bronchopulmonary Dysplasia

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