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Inflammation is one of the main causes of preterm birth, frequently associated to intrauterine infection or chorioamnionitis. Oxidative stress is involved in preterm birth. On the one hand, reactive oxygen species are released by inflammatory cells against infection; on the other hand it is responsible of placental tissue damage after chorioamnionitis. Because of improvement in obstetric and perinatal care, survival rate in preterm births has increased, leading to changes in pathology of several processes, such as bronchopulmonary dysplasia. Bronchopulmonary dysplasia is a multifactorial entity which is consequence of multiple mechanisms, including perinatal inflammation and oxygen free radicals. Preterm newborn is very susceptible to chronic lung damage because of both, low antioxidant capacity, and exposure to high oxygen fractions during postnatal life. Modest lung oxidative stress damage after exposure to fetal endotoxin in premature newborns has been shown. Postnatal injury is needed to amplify the intrauterine inflammatory damage. Cell death induction by reactive oxygen species has been suggested as mechanism of lung damage. Several antioxidant therapies have been used in experimental studies in order to reduce or prevent bronchopulmonary dysplasia. So far, care is needed to standardize its use, because of its undesirable effects on inflammatory defense and development.
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Reference：
Quinuclidine – Wikipedia,
Quinuclidine | C7H648N | ChemSpider