Pulmonary oxygen toxicity plays an important role in the lung injury process that leads to the development of bronchopulmonary dysplasia. Connective tissue growth factor (CTGF) is a fibroblast mitogen and promoter of collagen deposition. We investigated the effects of postnatal hyperoxia on lung collagen and CTGF expression in rats. Rat pups were exposed to 7 d of >95% O2 and a further 3 wk of 60% O2. CTGF mRNA and protein expression increased after hyperoxia treatment, and the values were significantly higher in hyperoxia-exposed rats on postnatal d 7 and 14. Lung collagen levels increased as rats aged, and the values were comparable between room air-exposed and hyperoxia-exposed rats on postnatal d 7 and 14 and were significantly higher in hyperoxia-exposed rats on postnatal d 21 and 28. Increases in CTGF mRNA and protein expressions preceded the onset of increased lung collagen. These data demonstrate that CTGF is up-regulated at time points preceding the fibrotic phase of the lung injury adding credence to the hypothesis that CTGF seems to be involved in the pathogenesis of hyperoxia-induced lung fibrosis and an anti-CTGF strategy might attenuate hyperoxia-induced lung fibrosis.

Pulmonary hypoplasia is a substantial cause of death in newborn infants, and oligohydramnios is one of the most commonly associated abnormalities. Lung growth is influenced by physical factors such as the intrauterine space, lung liquid volume and pressure, and fetal breathing movements. During lung development, the main physical force experienced by the lungs is stretching induced by breathing movements and the lung fluid in the airspaces. Oligohydramnios reduces the intrathoracic cavity size, thus disrupting fetal lung growth and leading to pulmonary hypoplasia. The exact mechanism by which oligohydramnios alters the respiratory system structure and the effect of oligohydramnios on long-term respiratory outcomes remain unknown. In this review, we summarize the effects of oligohydramnios on lung development, discuss the mechanisms of oligohydramnios-induced pulmonary hypoplasia identified in various animal studies, and describe the long-term respiratory outcomes in childhood of oligohydramnios-exposed fetuses reported by a population-based study.

Despite significant progress in the treatment of preterm neonates, bronchopulmonary dysplasia (BPD) continues to be a major cause of neonatal morbidity. Affected infants suffered from long-term pulmonary and nonpulmonary sequel. The pulmonary sequels include reactive airway disease and asthma during childhood and adolescence. Nonpulmonary sequels include poor coordination and muscle tone, difficulty in walking, vision and hearing problems, delayed cognitive development, and poor academic achievement. As inflammation seems to be a primary mediator of injury in pathogenesis of BPD, role of steroids as antiinflammatory agent has been extensively studied and proven to be efficacious in management. However, evidence is insufficient to make a recommendation regarding other glucocorticoid doses and preparations. Numerous studies have been performed to investigate the effects of steroid. The purpose of this paper is to evaluate these studies in order to elucidate the beneficial and harmful effects of steroid on the prevention and treatment of BPD.