Effects of inhaled nitric oxide on pulmonary edema and lung neutrophil accumulation in severe experimental hyaline membrane disease

Effects of inhaled nitric oxide on pulmonary edema and lung neutrophil accumulation in severe experimental hyaline membrane disease
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DOI:
10.1203/00006450-199704000-00002
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发表时间:
1997-04-01
期刊:
影响因子:
3.6
通讯作者:
Abman, SH
Abman, SH
中科院分区:
医学3区
文献类型:
--
作者:
Kinsella, JP;Parker, TA;Abman, SH

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为了确定吸入NO(iNO)对实验性肺透明膜病(HMD)肺水肿和肺部炎症的影响,我们测定了极早产羔羊(妊娠115 d,0.78足月)吸入NO对肺血流动力学、气体交换、肺水肿和肺髓过氧化物酶(MPO)活性的影响。在方案I中,我们测量了在Fio(2)= 1.00的常规机械通气1 h(n = 10)和3 h(n = 14)期间iNO(20 ppm)对肺血管内皮细胞对I-125标记白蛋白(使用Cr-57标记红细胞指数化血容量)的通透性的影响。与对照组相比,iNO改善了肺血流动力学和气体交换,但在机械通气1或3小时后并没有改变肺重干重比或血管对白蛋白的通透性。为了确定低剂量iNO(5 ppm)是否会减少严重HMD中的肺中性粒细胞积聚,我们在有或没有iNO的机械通气4小时后测量肺MPO活性(方案2)。低剂量iNO改善了4小时机械通气期间的气体交换(Pao,4小时:119 +/- 35 mmHg iNO vs 41 +/- 7 mmHg对照,p < 0.05),并使MPO活性降低79%(p < 0.05)。我们得出结论,低剂量iNO增加肺血流量,而不恶化肺水肿,并减少肺中性粒细胞积聚在严重的实验性HMD。我们推测,除了其血流动力学效应,低剂量iNO减少早期中性粒细胞募集,并可能减轻严重HMD的肺损伤。
To determine the effects of inhaled NO (iNO) on pulmonary edema and lung inflammation in experimental hyaline membrane disease (HMD), we measured the effects of iNO on pulmonary hemodynamics, gas exchange, pulmonary edema, and lung myeloperoxidase (MPO) activity in extremely premature lambs (115 d of gestation, 0.78 term). In protocol I, we measured the effects of iNO (20 ppm) on lung vascular endothelial permeability to I-125-labeled albumin (indexed to blood volume using Cr-57-tagged red blood cells) during 1 h (n = 10) and 3 h (n = 14) of conventional mechanical ventilation with Fio(2) = 1.00. In comparison with controls, iNO improved pulmonary hemodynamics and gas exchange, but did not alter lung weight-to-dry weight ratio or vascular permeability to albumin after 1 or 3 h of mechanical ventilation. To determine whether low dose iNO (5 ppm) would decrease lung neutrophil accumulation in severe HMD, we measured lung MPO activity after 4 h of mechanical ventilation with or without iNO (protocol 2). Low dose iNO improved gas exchange during 4 h of mechanical ventilation (Pao, at 4 h: 119 +/- 35 mm Hg iNO versus 41 +/- 7 mmHg control, p < 0.05), and reduced MPO activity by 79% (p < 0.05). We conclude that low dose iNO increases pulmonary blood flow, without worsening pulmonary edema, and decreases lung neutrophil accumulation in severe experimental HMD. We speculate that in addition to its hemodynamic effects, low dose iNO decreases early neutrophil recruitment and may attenuate lung injury in severe HMD.