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  • Title: Experimental hyaline membrane disease in the premature monkey: effects of antenatal dexamethasone.
    Author: Kessler DL, Truog WE, Murphy JH, Palmer S, Standaert TA, Woodrum DE, Hodson WA.
    Journal: Am Rev Respir Dis; 1982 Jul; 126(1):62-9. PubMed ID: 6920252.
    Abstract:
    A blind, randomized trial of antenatal glucocorticoid treatment was conducted using the premature monkey (Macaca nemestrina) model of hyaline membrane disease (HMD). Twelve dams received dexamethasone (2 mg/dose) 72, 48, and 24 h before abdominal delivery at 135 +/- 1 days of gestation. Twelve control animals received saline. Infants of dexamethasone-treated dams had significantly lower incidence and severity of HMD than did infants of control animals (50 versus 92%, p less than 0.05). Improvement with treatment was markedly greater for males than for females. Differences in volume-pressure behavior of the excised lungs included greater distensibility in the infants from dexamethasone-treated dams (20.6 +/- 7.1 ml/g dry lung versus 14.7 +/- 6.1, p less than 0.05) and enhanced deflation stability with treatment. Accelerated production of surface active material (SAM) phospholipids in infants from dexamethasone-treated dams was indicated by increases in total lung phospholipid (84.5 +/- 8.1 mg/g dry lung versus 75.1 +/- 9.9, p less than 0.025), alveolar lavage fluid phospholipid (5.65 +/- 3.33 mg/g dry lung versus 3.01 +/- 1.84, p less than 0.05), and alveolar lavage fluid disaturated phosphatidylcholine (DPC) (2.47 +/- 1.84 mg/g dry lung versus 1.06 +/- 1.05, p less than 0.05). Incorporation of 14C-palmitate into lung lipid was not influenced by dexamethasone, but a significantly greater portion of the label appeared in the DPC fraction with treatment. Antenatal dexamethasone treatment was successful in reducing the incidence and severity of experimental HMD in this animal model; the beneficial effects of treatment were associated with accelerated maturation of fetal pulmonary functions, including, but not limited to, synthetic metabolism of SAM phospholipid.
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