From the CAP trial we know that caffeine administration leads to less bronchopulmonary dysplasia. The question is how? The mechanism could help to design other studies, or help in a decision about clinical use where the question hasn’t been directly answered by CAP. One possibility is just that improving respiratory drive allows earlier more successful extubation, and less exposure to positive pressures; I think this is likely to be part of the mechanism. On the other hand there is now evidence of direct effects of caffeine on inflammation, which are mostly anti-inflammatory, and on apoptosis. This new study in neonatal rabbits (Nagatomo T, et al. Caffeine Prevents Hyperoxia-Induced Functional and Structural Lung Damage in Preterm Rabbits. Neonatology. 2016;109(4):274-81) exposed preterm cesarean delivered rabbits to 95% oxygen, and randomly divided into groups receiving either caffeine or control. Without going into all the methodologic details of this excellent study, the authors found that caffeine was highly protective against the reductions in lung function caused by hyperoxia. Caffeine use also reduced the size of the alveoli, but prevented the reduction in alveolar numbers caused by hyperoxia.
With other data this suggest that caffeine helps to protect immature lungs from the effects of too much oxygen. The impact of caffeine on bronchopulmonary dysplasia could be partly as a result of this effect.