Welty S E
Children's Research Institute, The Ohio State University, 700 Children's Drive, Columbus, OH 43205, USA.
J Nutr. 2001 Mar;131(3):947S-950S. doi: 10.1093/jn/131.3.947S.
Bronchopulmonary dysplasia (BPD) is a chronic lung disease first described in 1967 as a complication of therapy for premature infants with hyaline membrane disease, and treatment with high concentrations of oxygen was thought to be a major contributor to its development. Thus, interventions to enhance lung antioxidants to prevent the development of BPD were considered appropriate therapeutic strategies. In the last decades, advances in the acute care of premature infants has reduced the reliance on therapy with high concentrations of supplemental oxygen. However, the incidence of BPD has not changed significantly. The changing clinical context in which BPD develops begs the question of whether oxidation is important in the development of BPD and, therefore, whether designing interventions enhancing lung antioxidants is still warranted. This review presents evidence that premature infants that will develop BPD have qualitative and quantitative differences in oxidation of lipids and proteins when compared to infants that do not develop BPD. Such differences in oxidation patterns are the most obvious in the first few days of life. The emerging evidence thus supports the concept that the lung injury process leading to the development of BPD occurs within hours to days of delivery and that oxidation is a major contributor to this pathological process. Unfortunately, early attempts at delivery of antioxidants to the lung have not been successful, perhaps because of an inability to deliver antioxidants in a timely manner to the areas in the lung in which deleterious oxidations are occurring. Further research is necessary to determine both the nature and the location of the oxidative events that lead to the development of early lung injury, so that more appropriate and specific antioxidant interventions can be designed.
支气管肺发育不良（BPD）是一种慢性肺部疾病，于1967年首次被描述为患有透明膜病的早产儿治疗的并发症，高浓度氧气治疗被认为是其发展的主要促成因素。因此，增强肺部抗氧化剂以预防BPD发展的干预措施被认为是合适的治疗策略。在过去几十年中，早产儿急性护理方面的进展减少了对高浓度补充氧气治疗的依赖。然而，BPD的发病率并没有显著变化。BPD发生的临床背景变化引发了一个问题，即氧化在BPD的发展中是否重要，因此，设计增强肺部抗氧化剂的干预措施是否仍然有必要。这篇综述提供的证据表明，与未患BPD的婴儿相比，将患BPD的早产儿在脂质和蛋白质氧化方面存在质和量的差异。这种氧化模式的差异在生命的最初几天最为明显。因此，新出现的证据支持这样一种概念，即导致BPD发展的肺损伤过程发生在分娩后的数小时至数天内，并且氧化是这一病理过程的主要促成因素。不幸的是，早期将抗氧化剂输送到肺部的尝试并不成功，可能是因为无法及时将抗氧化剂输送到肺部发生有害氧化的区域。有必要进行进一步的研究，以确定导致早期肺损伤发展的氧化事件的性质和位置，以便能够设计出更合适、更具体的抗氧化干预措施。
