Inhaled NO improves early pulmonary function and modifies lung growth and elastin deposition in a baboon model of neonatal chronic lung disease
Inhaled NO improves early pulmonary function and modifies lung growth and elastin deposition in a baboon model of neonatal chronic lung disease
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DOI：
10.1152/ajplung.00347.2004
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发表时间：
2005-03-01
影响因子：
4.9
通讯作者：
Shaul, PW
中科院分区：
文献类型：
--
作者：
McCurnin, DC;Pierce, RA;Shaul, PW
一氧化氮（NO）在发育中的肺中发挥多种功能，并且在妊娠125天（d）（足月= 185天）早产的慢性肺病（CLD）狒狒模型中，肺NO产生减少。为了确定出生后NO给药是否改变CLD的发生，在狒狒模型中评估了吸入NO（iNO，5 ppm）超过14天的作用。iNO在第一个2d引起肺动脉压降低，动脉导管自发闭合率增加，肺顺应性增加，第一周呼气阻力改善。与iNO，死后的压力-容积曲线上移，肺DNA含量和细胞增殖增加，肺生长被保存到等于发生在同一时期在子宫内。此外，CLD的过度弹性蛋白沉积特征通过iNO正常化，并且有刺激次级嵴发育的证据。因此，在CLD的狒狒模型中，iNO改善早期肺功能并改变肺生长和细胞外基质沉积。因此，NO生物合成途径功能障碍可能有助于CLD的发病机制。
Nitric oxide (NO) serves multiple functions in the developing lung, and pulmonary NO production is decreased in a baboon model of chronic lung disease (CLD) after premature birth at 125 days (d) gestation (term=185d). To determine whether postnatal NO administration alters the genesis of CLD, the effects of inhaled NO (iNO, 5 ppm) were assessed in the baboon model over 14d. iNO caused a decrease in pulmonary artery pressure in the first 2d and a greater rate of spontaneous closure of the ductus arteriosus, and lung compliance was greater and expiratory resistance was improved during the first week. With iNO, postmortem pressure-volume curves were shifted upward, lung DNA content and cell proliferation were increased, and lung growth was preserved to equal that which occurs during the same period in utero. In addition, the excessive elastin deposition characteristic of CLD was normalized by iNO, and there was evidence of stimulation of secondary crest development. Thus, in the baboon model of CLD, iNO improves early pulmonary function and alters lung growth and extracellular matrix deposition. As such, NO biosynthetic pathway dysfunction may contribute to the pathogenesis of CLD.