摘要部分患有呼吸窘迫综合征的晚期早产儿,给予外源性肺表面活性物质疗效不佳,且此类患儿无感染或其他可能导致呼吸窘迫综合征的危险因素,可能存在不同于早产儿呼吸窘迫综合征的发病机制.研究表明,作为肺液经由上皮转运过程中核心部分的α-钠离子通道,可通过抑制肺液吸收和肺表面活性物质活性而在晚期早产儿呼吸窘迫综合征发病机制中起着重要作用.该文就肺液吸收障碍在晚期早产儿呼吸窘迫综合征中的作用作一综述.

abstractsIn recent studies,it has been demonstrated that the clinical efficacy of surfactant is poor for late protein infants.Besides,this kind of infants have not infection or other risk factors that may lead to respiratory distress syndrome(RDS).Thus,it is speculated that the pathogenesis of RDS of late preterm infants is different from preterm infants.New researches show that,as the key point of Lung fluid transport via Epithelium,α-ENaC plays an important role in the pathogenesis of RDS of late preterm infants through the inhibition of lung fluid clearance and activity of surfactant.This review highlights the most important mechanisms of Lung fluid absorption barrier in RDS of late preterm infants.