Effects of intrauterine growth retardation and prematurity on spirometric flow values and lung volumes at school age in twin pairs

Nikolajev, Kari; Heinonen, Kirsti; Hakulinen, A.; Länsimies, Esko

doi:10.1002/(sici)1099-0496(199806)25:6<367::aid-ppul2>3.0.co;2-e

Cited by 48 publications

(35 citation statements)

References 10 publications

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“…Our study may help explain why IUGR increases the risk for impaired respiratory function in infants, children and adults (2)(3)(4)(5)49). It may also help explain why maternal cigarette smoking, a common cause of IUGR, leads to altered lung function in offspring (32,33).…”

Section: Discussionmentioning

confidence: 80%

“…Recent studies of neonates and infants who have been growth restricted in utero indicate that they have an increased risk of mortality and morbidity (1), including respiratory distress (2,3). Respiratory compromise may persist during postnatal development as it has been shown that children with evidence of growth restriction in utero have reduced forced expiratory flow rates (4,5) indicative of impaired airway function. In addition, adults who were of low birth weight and, therefore, likely to have been growth restricted in utero, have reduced expiratory flow rates and an increased risk of respiratory morbidity and mortality (6,7).…”

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confidence: 99%

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Compromised Respiratory Function in Postnatal Lambs after Placental Insufficiency and Intrauterine Growth Restriction

et al. 2001

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Epidemiologic studies have shown persistent effects of low birth weight on respiratory function and lung health, but underlying mechanisms are not understood. Our aim was to determine the effects of intrauterine growth restriction (IUGR), a major cause of low birth weight, on postnatal respiratory function. IUGR was induced by umbilico-placental embolization during late gestation in chronically catheterized sheep. Umbilicoplacental embolization was performed between 120 d of gestation and term (~146 d) during which fetuses were hypoxemic and hypoglycemic relative to controls. Umbilico-placental embolization led to a 48% reduction in birth weight compared with controls, and throughout the postnatal study period IUGR lambs (n ϭ 8) remained lighter than controls (n ϭ 8). Respiratory function was repeatedly studied in lambs for 8 wk after birth; during this period, IUGR lambs were mildly hypoxemic and tended to be hypercapnic compared with controls. In IUGR lambs, relative to controls, O 2 consumption (mL/min/kg) and minute ventilation (mL/kg) were increased and pulmonary diffusing capacity (adjusted for functional residual capacity) was decreased. Functional residual capacity, measured by helium dilution, and total lung capacity (measured at 30 cm H 2 O) were smaller in IUGR lambs than in controls. When adjusted for functional residual capacity, static lung compliance was reduced and chest wall compliance was increased in IUGR lambs. Restricted fetal growth, resulting in low birth weight, has been associated with altered lung development and impaired respiratory function after birth. Recent studies of neonates and infants who have been growth restricted in utero indicate that they have an increased risk of mortality and morbidity (1), including respiratory distress (2, 3). Respiratory compromise may persist during postnatal development as it has been shown that children with evidence of growth restriction in utero have reduced forced expiratory flow rates (4, 5) indicative of impaired airway function. In addition, adults who were of low birth weight and, therefore, likely to have been growth restricted in utero, have reduced expiratory flow rates and an increased risk of respiratory morbidity and mortality (6, 7). Thus, a number of epidemiologic studies suggest that pulmonary gas exchange and airway function after birth may be affected by IUGR.Placental insufficiency and IUGR are common causes of low birth weight, and are associated with pregnancy-induced hypertension, maternal tobacco smoking, and placental pathology (8, 9). Fetuses identified as being growth restricted have been found to be hypoxemic, hypoglycemic, and to have elevated

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Section: Discussionmentioning

confidence: 80%

mentioning

confidence: 99%

Compromised Respiratory Function in Postnatal Lambs after Placental Insufficiency and Intrauterine Growth Restriction

et al. 2001

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“…It is likely that altered lung development may be a contributing factor as it has been shown that the risk of respiratory illness and the requirement for ventilatory support is increased in FGR infants (3,4). Respiratory impairments may persist into later life because low birth weight children who were growth-restricted in utero (5,6), as well as adults having low birth weights (7,8), have evidence of impaired lung function. At present, however, the structural basis for a relationship between FGR and later pulmonary dysfunction is poorly understood.…”

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confidence: 99%

Fetal Growth Restriction Has Long-Term Effects on Postnatal Lung Structure in Sheep

et al. 2004

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We have previously shown that fetal growth restriction (FGR) during late gestation in sheep affects lung development in the near-term fetus and at 8 wk after birth. In the present study, our aim was to determine the effects of FGR on the structure of the lungs at 2 y after birth; our hypothesis was that changes observed at 8 wk after birth would persist until maturity. FGR was induced in sheep by umbilicoplacental embolization, which was maintained from 120 d until delivery at term (approximately 147 d); birth weights of FGR lambs were 41% lower than in controls. At 2 y after birth, body and lung weights were not different, but there were 28% fewer alveoli and alveoli were significantly larger than in controls; hence there was a 10% reduction in the internal surface area relative to lung volume in FGR sheep compared with controls. The lungs of FGR sheep, compared with controls, had thicker interalveolar septa as a result of increased extracellular matrix deposition; the alveolar blood-air barrier was also thicker, largely because of an 82% increase in basement membrane thickness. These changes are qualitatively similar to those observed at 8 wk. Our data show that structural alterations in the lungs induced by FGR that were apparent at 8 wk were still evident at 2 y after birth, indicating that FGR may result in permanent changes in the structure of the lungs of the offspring and may affect respiratory health and lung aging later in life. Low birth weight as a result of FGR has been associated with an increased risk of morbidity and mortality during infancy (1, 2). It is likely that altered lung development may be a contributing factor as it has been shown that the risk of respiratory illness and the requirement for ventilatory support is increased in FGR infants (3, 4). Respiratory impairments may persist into later life because low birth weight children who were growth-restricted in utero (5, 6), as well as adults having low birth weights (7,8), have evidence of impaired lung function. At present, however, the structural basis for a relationship between FGR and later pulmonary dysfunction is poorly understood.The sheep is a suitable animal model in which to study the effects of FGR on lung development; it is a long-gestation species in which alveolar formation begins before birth (9), as in the human (10), and which reaches sexual maturity 6 mo after birth. Recently we found, in developing sheep, that fundamental aspects of respiratory function were impaired after FGR; FGR lambs were hypoxemic and hypercapnic soon after birth and had reduced pulmonary diffusing capacity and lung compliance up to 8 wk (11). In addition to these functional alterations, we found that FGR induced structural changes in lung parenchyma that were evident in the near-term fetus and became more pronounced at 8 wk after birth (12). In particular, the blood-air barrier and structure of interalveolar septa were affected after FGR. It is possible that structural

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“…After restriction of placental growth, the tracheas of growth-restricted sheep fetuses were found to have thinner mucosal and submucosal layers, reduced ciliation of epithelial cells, and reduced extent of mucosal folding near term (Rees et al 1991). Children with evidence of growth restriction in utero have reduced forced expiratory flow rates, indicative of impaired airway function (Nikolajev et al 1998, Magness & Poston 2005, a condition persisting into adulthood with increased risk of respiratory morbidity and mortality (Barker et al 1991, Stein et al 1997. While the molecular bases for these detrimental effects on lung development and function have to be fully elucidated, there is evidence that a cascade of inflammatory markers, including TNF-and interleukin (IL)-1 , which are also known to upregulate UCP2 in the lung (Pecqueur et al 2001), may underlie the development of chronic lung disease (Ozdemir et al 1997, Allen 2003.…”

Section: Maternal Nutrient Restriction Between Early and Midgestationmentioning

confidence: 99%

Developmental regulation of the lung in preparation for life after birth: hormonal and nutritional manipulation of local glucocorticoid action and uncoupling protein–2

Gnanalingham

Mostyn²,

Gardner³

et al. 2006

Journal of Endocrinology

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Glucocorticoid action has a major role in regulating fetal and postnatal lung development, although its impact on mitochondrial development is less well understood. Critically, the consequences of any change in glucocorticoid action and mitochondrial function in early life may not be limited to the postnatal period, but may extend into later life. This paper focuses on more recent findings on the impact of ontogeny, fetal cortisol status, maternal nutrient restriction and postnatal leptin administration on mitochondrial uncoupling protein (UCP)-2, glucocorticoid receptor (GR) and 11 -hydroxysteroid dehydrogenase type 1 (11 HSD1) isoform abundance in the lung. For example, in sheep, GR and 11 HSD1 mRNA are maximal at 140 days' gestation (term 147 days), while UCP2 mRNA peaks at 1 day after birth and then decreases with advancing age. In the fetus, chronic umbilical cord compression enhances the abundance of these genes, an outcome that can also be produced after birth following chronic, but not acute, leptin administration. Irrespective of the timing of maternal nutrient restriction in pregnancy, glucocorticoid sensitivity and UCP2 abundance are both upregulated in the lungs of the resulting offspring. In conclusion, prenatal and postnatal endocrine challenges have distinct effects on mitochondrial development in the lung resulting from changes in glucocorticoid action, which can persist into later life. As a consequence, changes in glucocorticoid sensitivity and mitochondrial protein abundance have the potential to be used to identify those at greatest risk of developing later lung disease.

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Effects of intrauterine growth retardation and prematurity on spirometric flow values and lung volumes at school age in twin pairs

Cited by 48 publications

References 10 publications

Compromised Respiratory Function in Postnatal Lambs after Placental Insufficiency and Intrauterine Growth Restriction

Compromised Respiratory Function in Postnatal Lambs after Placental Insufficiency and Intrauterine Growth Restriction

Fetal Growth Restriction Has Long-Term Effects on Postnatal Lung Structure in Sheep

Developmental regulation of the lung in preparation for life after birth: hormonal and nutritional manipulation of local glucocorticoid action and uncoupling protein–2

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