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The Chronobiology team works to understand the factors that contribute to poor lung and heart function in newborn infants and find ways to prevent heart and lung disease.
Investigators: Andrew Gill External collaborators: Assoc Prof David Tingay (Murdoch Children's Research Institute) The POLAR trial is an MRFF-funded
Since the first description of bronchopulmonary dysplasia (BPD), multiple definitions to diagnose BPD and its grading have been published. Several studies have compared the predictive performance of these definitions for long-term outcomes. The objective was to identify the BPD definition with the optimal predictive performance for long-term respiratory and neurological outcomes in preterm infants.
Jane Pillow BMedSci (Dist) MBBS, PhD (Dist) FRACP Head, Developmental Chronobiology jane.pillow@thekids.org.au Head, Developmental Chronobiology
Laboratory models provide an important tool in helping to understand the cellular and molecular drivers of respiratory disease. Many animal models exist that model the neonatal outcomes of preterm birth.
Inflammation and oxidative stress play a key role in the development of bronchopulmonary dysplasia (BPD), possibly contributing to persistent respiratory morbidity after preterm birth. We aimed to assess if inflammatory markers were elevated in exhaled breath condensate (EBC) of infants born very prematurely (< 32 weeks gestation) at 12-16 corrected months of age, and if increased levels were associated with BPD diagnosis and respiratory morbidity.
Preterm infants have immature control of breathing and impaired pulmonary gas exchange. We hypothesized that infants with bronchopulmonary dysplasia (BPD) have a blunted ventilatory response and peripheral oxygen saturation (SpO2 ) instability during a hypoxic challenge.
Normal in utero lung development and growth rely upon the expansion of airspaces and the controlled efflux of lung liquid into the amniotic space. Infants with congenital diaphragmatic hernia (CDH) also have lung hypoplasia due to occupation of the chest cavity by the stomach and bowel and, in the most severe cases, the liver. Balloon tracheal occlusion reduces the severity of lung hypoplasia in fetuses with CDH but increases the risk of premature birth.
Lung inflammation and impaired alveolarization precede bronchopulmonary dysplasia (BPD). Glucocorticoids are anti-inflammatory and reduce ventilator requirements in preterm infants. However, high-dose glucocorticoids inhibit alveolarization. The effect of glucocorticoids on lung function and structure in preterm newborns exposed to antenatal inflammation is unknown. We hypothesise that postnatal low-dose dexamethasone reduces ventilator requirements, prevents inflammation and BPD-like lung pathology, following antenatal inflammation.
Preterm infants are often vitamin A deficient, and vitamin A has functions that could mitigate the processes that lead to bronchopulmonary dysplasia. Therefore, supplementation of preterm infants with vitamin A to reduce the risk of bronchopulmonary dysplasia makes inherent sense.