Ventilation-induced lung injury is not exacerbated by growth restriction in preterm lambs

B.J. Allison, S.B. Hooper, E. Coia, V.A. Zahra, G. Jenkin, A. Malhotra, A. Sehgal, M. Kluckow, Andrew Gill, F. Sozo, S.L. Miller, G.R. Polglase

    Research output: Contribution to journalArticle

    13 Citations (Scopus)

    Abstract

    © 2016 the American Physiological Society. Intrauterine growth restriction (IUGR) and preterm birth are frequent comorbidities and, combined, increase the risk of adverse respiratory outcomes compared with that in appropriately grown (AG) infants. Potential underlying reasons for this increased respiratory morbidity in IUGR infants compared with AG infants include altered fetal lung development, fetal lung inflammation, increased respiratory requirements, and/or increased ventilation-induced lung injury. IUGR was surgically induced in preterm fetal sheep (0.7 gestation) by ligation of a single umbilical artery. Four weeks later, preterm lambs were euthanized at delivery or delivered and ventilated for 2 h before euthanasia. Ventilator requirements, lung inflammation, early markers of lung injury, and morphological changes in lung parenchymal and vascular structure and surfactant composition were analyzed. IUGR preterm lambs weighed 30% less than AG preterm lambs, with increased brain-tobody weight ratio, indicating brain sparing. IUGR did not induce lung inflammation or injury or alter lung parenchymal and vascular structure compared with AG fetuses. IUGR and AG lambs had similar oxygenation and respiratory requirements after birth and had significant, but similar, increases in proinflammatory cytokine expression, lung injury markers, gene expression, and surfactant phosphatidylcholine species compared with unventilated controls. IUGR does not induce pulmonary structural changes in our model. Furthermore, IUGR and AG preterm lambs have similar ventilator requirements in the immediate postnatal period. This study suggests that increased morbidity and mortality in IUGR infants is not due to altered lung tissue or vascular structure, or to an altered response to early ventilation.
    Original languageEnglish
    Pages (from-to)L213-L223
    Number of pages11
    JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
    Volume310
    Issue number3
    DOIs
    Publication statusPublished - 2016

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