新生儿高氧肺损伤机制研究进展  

Recent advances in hyperoxia-induced lung injury in newborn

作　　者：彭琼玲[1] 常立文[1] 

机构地区：[1]华中科技大学同济医学院附属同济医院儿科,湖北武汉430030

出　　处：《临床儿科杂志》2008年第6期542-544,共3页Journal of Clinical Pediatrics

摘　　要：新生儿高氧肺损伤是一个极其复杂的病理生理过程,其损伤机制涉及炎性水肿、血管生成、细胞外基质重建、组织异常修复和细胞凋亡等多种因素,且这些因素交织成网,相互影响,共同形成了高氧肺损伤的病理特征。文章综述了近年研究较多且在高氧肺损伤病理过程中发挥重要作用的分子系统,包括水通道蛋白、基质金属蛋白酶、血管内皮生长因子、单核细胞趋化因子和细胞凋亡相关因子。The pathophysiology of hyperoxia-induced lung injury in the newborns is very complicated. The mechanisms involve inflammatory edema, angiogenesis, extracellular matrix regeneration, abnormal repair of tissues, and apoptosis of cells. These factors affect each other and form the pathological characteristics of this injury. This article reviewed the recent extensively studied molecular systems that have important effects on the process of hyperoxia-induced lung injury, including aquaporins, matrix metalloproteinases, vascular endothelial growth factor, chemokines and apoptosis-associatedfactors.

关 键 词：新生儿 高氧肺损伤 基质金属蛋白酶 细胞凋亡 

分 类 号：R722.1[医药卫生—儿科]