Jobe A H, Ikegami M
Pulmonary Biology/Neonatology, Children's Hospital Medical Center, Cincinnati, Ohio 45229, USA.
Annu Rev Physiol. 2000;62:825-46. doi: 10.1146/annurev.physiol.62.1.825.
Mortality of infants of < 1-kg birth weight has decreased because of surfactant treatments, antenatal glucocorticoid treatments, and new ventilation strategies. However, many of these infants develop a chronic lung disease characterized by an arrest of lung development and interference with alveolarization. Antenatal glucocorticoids can induce early lung maturation clinically, but new information from transgenic and other experimental models indicates that traditional explanations for glucocorticoid effects on the developing lung are inadequate. These very preterm infants have lungs with small lung gas volumes and delicate lung tissue that are susceptible to injury with the initiation of ventilation and subsequent ventilation. Antenatal proinflammatory exposures are frequent in very preterm infants, and postnatal injury is associated with elevations of proinflammatory cytokines in the lungs. One hypothesis is that proinflammatory cytokines can promote or interfere with lung development as well as promote lung injury. Mechanisms of lung injury being characterized in the adult lung may have unique characteristics in the developing lung.
由于表面活性剂治疗、产前糖皮质激素治疗和新的通气策略，出生体重<1千克的婴儿死亡率有所下降。然而，这些婴儿中的许多人会患上一种慢性肺病，其特征是肺发育停滞和肺泡化受到干扰。产前糖皮质激素可在临床上诱导早期肺成熟，但来自转基因和其他实验模型的新信息表明，对糖皮质激素对发育中肺的作用的传统解释并不充分。这些极早产儿的肺气体量小，肺组织脆弱，在开始通气及随后的通气过程中易受损伤。极早产儿产前经常暴露于促炎环境中，产后损伤与肺中促炎细胞因子升高有关。一种假设是，促炎细胞因子可促进或干扰肺发育以及促进肺损伤。在成年肺中所确定的肺损伤机制在发育中的肺中可能具有独特特征。
