Objective To assess the role of nasal continuous positive airway pressure (CPAP) initiated at birth for prevention of death and bronchopulmonary dysplasia in very preterm infants. Design Systematic review.Data sources PubMed, Embase, the Cochrane Central Register of Controlled Trials, and online Pediatric Academic Society abstracts from the year of inception to June 2013.Eligibility criteria for selecting studies Randomised controlled trials evaluating the effect of nasal CPAP compared with intubation in preterm infants born at less than 32 weeks' gestation and presenting the outcomes of either death or bronchopulmonary dysplasia, or both (defined as the need for oxygen support or mechanical ventilation at 36 weeks corrected gestation), during hospital stay.Results Four randomised controlled trials (2782 participants) met the inclusion criteria, with 1296 infants in the nasal CPAP group and 1486 in the intubation group. All the trials reported bronchopulmonary dysplasia independently at 36 weeks corrected gestation, with borderline significance in favour of the nasal CPAP group (relative risk 0.91, 95% confidence interval 0.82 to 1.01, risk difference −0.03, 95% confidence interval −0.07 to 0.01). No difference in death was observed (relative risk 0.88, 0.68 to 1.14, risk difference −0.02, −0.04 to 0.01, respectively). Pooled analysis showed a significant benefit for the combined outcome of death or bronchopulmonary dysplasia, or both, at 36 weeks corrected gestation for babies treated with nasal CPAP (relative risk 0.91, 0.84 to 0.99, risk difference −0.04, -0.07 to 0.00), number needed to treat of 25). ConclusionOne additional infant could survive to 36 weeks without bronchopulmonary dysplasia for every 25 babies treated with nasal CPAP in the delivery room rather than being intubated.

O'Reilly M, Thébaud B. Animal models of bronchopulmonary dysplasia. The term rat models. Am J Physiol Lung Cell Mol Physiol 307: L948 -L958, 2014. First published October 10, 2014; doi:10.1152/ajplung.00160.2014.-Bronchopulmonary dysplasia (BPD) is the chronic lung disease of prematurity that affects very preterm infants. Although advances in perinatal care have enabled the survival of infants born as early as 23-24 wk of gestation, the challenge of promoting lung growth while protecting the ever more immature lung from injury is now bigger. Consequently, BPD remains one of the most common complications of extreme prematurity and still lacks specific treatments. Progress in our understanding of BPD and the potential of developing therapeutic strategies have arisen from large (baboons, sheep, and pigs) and small (rabbits, rats, and mice) animal models. This review focuses specifically on the use of the rat to model BPD and summarizes how the model is used in various research studies and the advantages and limitations of this particular model, and it highlights recent therapeutic advances in BPD by using this rat model. hyperoxia; lung development; premature birth BRONCHOPULMONARY DYSPLASIA (BPD) is the most common chronic lung disease of very preterm infants. BPD interrupts lung development and has serious long-term respiratory complications that reach beyond childhood and into adult life (8,25,26,41,53). The multifactorial etiology of BPD has prompted research to investigate the many factors contributing to the pathogenesis of BPD (reviewed in Ref. 38), with the ultimate aim of developing effective therapies to prevent longterm pulmonary sequelae. To investigate the effectiveness of various therapeutic strategies on the development, structure, and function of the lungs, it is important to have animal models that reliably reproduce some of the features observed in very preterm infants developing BPD. To achieve this, known contributing factors of BPD, such as perinatal inflammation, growth restriction, hyperoxia, and mechanical ventilation, have been used in both large and small animals to mimic the BPD-like lung injury. In particular, exposure of neonatal rats to hyperoxia is extensively utilized as a small animal model of experimental BPD. Characterization of the Rat Model of Experimental BPDExposing the immature rat lung to hyperoxic gas through neonatal life closely reproduces the histopathology observed in human infants with BPD. Studies have shown that exposure of the developing rat lung to hyperoxic gas can have detrimental effects, particularly on the structure of the gas-exchanging region (14,30,34,46,62,66). The main overall finding, which is common to each study, is that exposure of the immature lung to hyperoxic gas impairs alveolarization, resulting in fewer and enlarged alveolar air spaces. Pulmonary hypertension, disrupted vascular growth, vascular leakage, accumulation of plasma proteins, extravascular fibrin deposition, increased lung collagen content, increased inflammatory cell influx, and diso...

Background Bronchopulmonary dysplasia and emphysema are life-threatening diseases resulting from impaired alveolar development or alveolar destruction. Both conditions lack effective therapies. Angiogenic growth factors promote alveolar growth and contribute to alveolar maintenance. Endothelial colony-forming cells (ECFCs) represent a subset of circulating and resident endothelial cells capable of self-renewal and de novo vessel formation. We hypothesized that resident ECFCs exist in the developing lung, that they are impaired during arrested alveolar growth in experimental bronchopulmonary dysplasia, and that exogenous ECFCs restore disrupted alveolar growth. Methods and Results Human fetal and neonatal rat lungs contain ECFCs with robust proliferative potential, secondary colony formation on replating, and de novo blood vessel formation in vivo when transplanted into immunodeficient mice. In contrast, human fetal lung ECFCs exposed to hyperoxia in vitro and neonatal rat ECFCs isolated from hyperoxic alveolar growth–arrested rat lungs mimicking bronchopulmonary dysplasia proliferated less, showed decreased clonogenic capacity, and formed fewer capillary-like networks. Intrajugular administration of human cord blood–derived ECFCs after established arrested alveolar growth restored lung function, alveolar and lung vascular growth, and attenuated pulmonary hypertension. Lung ECFC colony- and capillary-like network-forming capabilities were also restored. Low ECFC engraftment and the protective effect of cell-free ECFC-derived conditioned media suggest a paracrine effect. Long-term (10 months) assessment of ECFC therapy showed no adverse effects with persistent improvement in lung structure, exercise capacity, and pulmonary hypertension. Conclusions Impaired ECFC function may contribute to arrested alveolar growth. Cord blood–derived ECFC therapy may offer new therapeutic options for lung diseases characterized by alveolar damage.

Non‐native species can have adverse impacts on native species. Predicting the potential extent of distributional expansion and abundance of an invading non‐native species can inform appropriate conservation and management actions. Non‐native mountain goats (Oreamnos americanus) in the greater Yellowstone area (GYA) have substantial potential to occupy similar habitats to native Rocky Mountain bighorn sheep (Ovis canadensis canadensis). To understand the potential for expansion of mountain goats in the GYA, this study evaluated detection‐nondetection data derived from ground‐based occupancy surveys of viewsheds partitioned into a grid of 100 × 100 m sampling units. Surveys were conducted over three summer seasons (2011–2013) in two study areas with well‐established mountain goat populations. Relationships between scale‐specific habitat covariates and mountain goat selection were evaluated to model occupancy and detection probabilities based on mountain goat detections in 505 of the 53,098 sampling units surveyed. Habitat selection was most strongly associated with terrain covariates, including mean slope and slope variance, at a spatial scale of 500 × 500 m, and canopy cover, heat load, and normalized difference vegetation index at a spatial scale of 100 × 100 m. These results provide new insight into multi‐scale patterns of mountain goat habitat selection, as well as evidence that mean slope and slope variance are more informative terrain covariates than distance to escape terrain, which has been commonly used in published mountain goat habitat models. The model predicted 9,035 km2 of suitable habitat within the GYA, of which 57% is currently un‐colonized. Seventy‐five percent of all bighorn observations recorded in the GYA fall within predicted suitable mountain goat habitat. We also estimated that the GYA might have the potential to support 5,331–8,854 mountain goats when all predicted habitat is occupied, or approximately 2.5–4.2 times the most recent abundance estimate of 2,354.

Compared with IPPV, preterm infants initially treated with SI at birth required less mechanical ventilation with no improvement in the rate of BPD and/or death. The use of SI should be restricted to randomised trials until future studies demonstrate the efficacy and safety of this lung aeration manoeuvre.

Background-Guidelines on neonatal resuscitation recommend 90 chest compressions (CCs) and 30 manual inflations (3:1) per minute in newborns. The study aimed to determine whether CC s during sustained inflations (SIs) improves the recovery of asphyxiated newborn piglets in comparison with coordinated 3:1 resuscitation. Methods and Results-Term newborn piglets (n=8/group) were anesthetized, intubated, instrumented, and exposed to 45-minute normocapnic hypoxia followed by asphyxia. Piglets were randomly assigned to receive either 3:1 resuscitation (3:1 group) or CCs during SIs (SI group) when the heart rate decreased to 25% of baseline.

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Preterm birth affects 8-10% of human pregnancies and is a major cause of long-term disability. Individuals who are born very preterm, especially if they develop bronchopulmonary dysplasia (BPD), have an increased risk of impaired lung function in infancy, childhood and adulthood, as well as an increased risk of respiratory illness. Our aim is to briefly review current understanding of the basis for long-term impairments in lung function and respiratory health following preterm birth and BPD. Histopathology of the lungs of infants and children following preterm birth and BPD shows altered development of the lung parenchyma, conducting airways and pulmonary vasculature. Owing to improvements in the care of preterm infants, especially the use of exogenous surfactant and lower concentrations of administered oxygen, lung pathology following preterm birth and BPD is less severe than in the past. Recent studies indicate that very preterm birth and BPD can lead to hyperplasia of airway smooth muscle, impaired alveolarization, pulmonary inflammation and an increase in pulmonary artery muscularization. Imaging of adult lungs suggests that the deficit in alveoli can persist into later life. Long-term lung injury apparently relates to the use of mechanical ventilation and the use of supplemental oxygen in infancy. Impaired lung function in later life is due to airway hyper-reactivity and fewer alveoli, resulting in reductions in the surface area for gas exchange and physical support for bronchioles. Because the incidence of preterm birth is not declining, it will continue to be a major cause of respiratory ill-health in adults.