Decreased surfactant level in the lung with oligohydramnios: A morphometric and biochemical study

Nakamura, Yasuhiro; Yamamoto, Iwahiko; Funatsu, Yoshiyuki; Motomura, Kazunori; Fukuda, Seiichi; Hasegawa, T.; Morimatsu, Minoru

doi:10.1016/s0022-3476(88)80340-8

Cited by 14 publications

(5 citation statements)

References 8 publications

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“…Crs adjusted for LW (Crs/LW) and Crs adjusted for LV (Crs/LV) were not different between the groups. Alterations in the development of type I and II alveolar epithelial cells and in the production of surfactant in LH are controversial (12,35). However, the above results suggest that the change in lung compliance was due to the change in lung size and not to any superimposed factors such as a deficiency in surfactant production or release.…”

Section: Discussionmentioning

confidence: 95%

Effect of Lung Hypoplasia on Birth-Related Changes in the Pulmonary Circulation in Sheep

et al. 2005

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Lung hypoplasia (LH) is a serious cause of neonatal compromise, but little is known of its functional effects on the pulmonary circulation. Our aim was to characterize birth-related changes in the pulmonary circulation of newborn lambs with LH and to compare them with alterations in respiratory function. LH was induced in six ovine fetuses by the creation of a tracheoamniotic shunt as well as amniotic fluid drainage starting at 105.6 Ϯ 1.5 (mean Ϯ SEM) days of gestation (term~147 d). At 139.9 Ϯ 0.3 d, fetuses were exteriorized under anesthesia to implant vascular catheters and an ultrasonic flow probe around the left pulmonary artery. The lambs then were delivered and ventilated for 2 h, during which systemic and pulmonary artery pressures, left pulmonary blood flow, and measures of respiratory function were recorded. At autopsy, lungs were weighed and volume was measured at 20 cm H 2 O. In LH lambs, lung weight was 25% lower and respiratory system compliance was 30% lower than in controls. Mean pulmonary blood flow in LH lambs was 42% lower and pulmonary vascular resistance was 138% higher than in controls. Morphometry showed that volume density of pulmonary arteries in LH was 30% lower than in controls. We conclude that, in this LH model, changes in ventilatory indices were proportional to the change in lung size, whereas changes in the pulmonary circulation were greater than the change in lung size and were associated with reduced density of pulmonary arteries. Abbreviations AaDO 2 , alveolar-arterial difference of oxygen tension BW, body weight CDH, congenital diaphragmatic hernia Crs, total respiratory system compliance EEP, end-expiratory pressure FIO 2 , fraction of inspired oxygen LH, lung hypoplasia LV, lung volume LW, lung weight MAP, mean airway pressure PaCO 2 , partial pressure of carbon dioxide in the arterial blood PaO 2 , partial pressure of oxygen in the arterial blood PAP, pulmonary artery pressure PBF, pulmonary blood flow PIP, peak inspiratory pressure PVR, pulmonary vascular resistance SAP, systemic artery pressure V a , volume density of arteries in the lung (tissue and airspace) V at , volume density of arteries in lung tissue alone VEI, ventilatory efficiency index V t , tidal volume Fetal lung hypoplasia (LH) results from impaired lung tissue growth during fetal development and can result in severe respiratory insufficiency in the neonate. LH is present in approximately one in 1000 human live births (1,2), and, despite recent advances in the treatment of newborn infants with respiratory insufficiency, it remains one of the major causes of neonatal mortality and morbidity (3-5). The incidence of LH in neonatal autopsies is reportedly increasing because death rates as a result of other neonatal diseases are decreasing (6).LH is associated with many predisposing conditions (7), including chronic oligohydramnios, as a result of fetal anuria or amniotic fluid leakage (8 -10), intrathoracic masses, as in congenital diaphragmatic hernia (CDH), and decreased fetal breathing movements (5,11). The...

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Section: Discussionmentioning

confidence: 95%

Effect of Lung Hypoplasia on Birth-Related Changes in the Pulmonary Circulation in Sheep

et al. 2005

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“…Insults occurring after the pseudoglandular stage (after 16 weeks' gestation) impair acinar complexity and maturation 8 . In a morphometric and biochemical study on hypoplastic lungs from human fetuses associated with oligohydramnios, Wigglesworth et al 6 as well as Nakamura et al 12,13 confirmed not only lung growth arrest but also impairment of lung maturation based on low surfactant phospholipid concentrations. Reale et al 11 stated that changes in the histologic appearance were correlated with severity and were independent of the type of associated malformations.…”

Section: Abnormal Lung Development: Pulmonary Hypoplasia Definition Amentioning

confidence: 95%

The fetal lung 2: pulmonary hypoplasia

Laudy

Wladimiroff

2000

Ultrasound in Obstet & Gyne

139

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This review describes the pathogenesis of pulmonary hypoplasia and highlights its clinical, radiological and pathologic features, with emphasis on oligohydramniosrelated pulmonary hypoplasia. Since pulmonary hypoplasia may lead to severe respiratory distress immediately after birth and even to neonatal death, an accurate and patient-friendly prenatal test for early detection and distinction between lethal and non-lethal pulmonary hypoplasia is still highly desirable. An extended overview of the proposed methods for the prenatal prediction of pulmonary hypoplasia is presented.

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“…5614 There also is a decrease or delay in surfactant maturation, but response to therapy has been poor. 15 Haldar et al 14 further give indirect evidence that the decrease of type I pneumocytes seen with PH from PROM indicates a failure of development of the normal blood-air barrier. 14 In contrast to specific airway and airspace structural and maturational changes associated with various etiologies of PH, including PROM, pulmonary vascular changes appear to be nonspecific.…”

Section: Discussionmentioning

confidence: 98%

Increased Acinar Arterial Wall Muscle in Preterm Infants with Prom and Pulmonary Hypoplasia

Thibeault

Kilbride²

1997

Amer J Perinatol

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Pulmonary hypoplasia (PH), secondary to premature rupture of fetal membranes (PROM), is a frequent cause of pulmonary insufficiency in preterm infants. Pulmonary hypoplasia of diverse causes is usually associated with pulmonary hypertension. The objective of this study was to quantitate the acinar arterial wall thickness and muscularization in preterm infants with PROM that died with PH in comparison to age-matched controls. The left lung and pulmonary vasculature were perfused and fixed in a standard method in 16 infants with PROM and PH, and in 16 controls. In infants with PH, the alveolar ductal artery walls were nearly twice as thick as those of controls, 15.1 +/- 5.1% versus 7.4 +/- 1.3%, p < 0.0001. Ninety-one percent had muscle in the wall compared to 18% of controls. We conclude that infants with PROM and PH have increased pulmonary arterial muscularization, placing them at significant risk to have pulmonary hypertension. For these infants, therapy to reduce pulmonary vascular resistance should be instituted early.

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Decreased surfactant level in the lung with oligohydramnios: A morphometric and biochemical study

Cited by 14 publications

References 8 publications

Effect of Lung Hypoplasia on Birth-Related Changes in the Pulmonary Circulation in Sheep

Effect of Lung Hypoplasia on Birth-Related Changes in the Pulmonary Circulation in Sheep

The fetal lung 2: pulmonary hypoplasia

Increased Acinar Arterial Wall Muscle in Preterm Infants with Prom and Pulmonary Hypoplasia

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