Ehlert Carey A, Truog William E, Thibeault Donald W, Garg Uttam, Norberg Mike, Rezaiekhaligh Mo, Mabry Sherry, Ekekezie Ikechukwu I
Section of Neonatal-Perinatal Medicine, Department of Pediatrics, Children's Mercy Hospitals and Clinics, Kansas City, Mo., USA.
Biol Neonate. 2006;90(2):89-97. doi: 10.1159/000092005. Epub 2006 Mar 14.
Hyperoxia and tidal volume mechanical ventilation are independent factors in the genesis of lung injury, but it remains unclear the extent to which each is responsible or contributes to this process in newborns.
To study the independent and combined effects of hyperoxia and tidal volume mechanical ventilation on the induction of lung inflammation in a newborn piglet model of ventilator-induced lung injury.
Following exposure to either ambient air or F(I)O2 = 1.0 for a period of 3 days, newborn piglets were randomized to receive mechanical ventilation with either high tidal volume (20 ml/kg) or low tidal volume (6 ml/kg) for 4 h while controlling for pH.
Monocyte chemoattractant protein-1 level in the lungs of animals randomized to hyperoxia with high tidal volume ventilation was significantly elevated, compared to all other groups (p < 0.05). Myeloperoxidase assayed in lung homogenate was found to be significantly higher in nonventilated animals exposed to hyperoxia (p < 0.01). Only in animals previously exposed to hyperoxia did the addition of high tidal volume ventilation further increase the level of myeloperoxidase present (p < 0.05). Pulmonary vascular resistance was significantly elevated after 4 h of mechanical ventilation compared to 1 h (p < 0.001).
We conclude that in neonatal piglets undergoing hyperoxic stress, superimposition of high tidal volume ventilation exacerbates the lung inflammation as assessed by lung monocyte chemoattractant protein-1 and level of myeloperoxidase.
高氧和潮气量机械通气是肺损伤发生的独立因素，但在新生儿中，二者各自对这一过程的责任程度或贡献程度仍不明确。
在呼吸机诱导的肺损伤新生仔猪模型中，研究高氧和潮气量机械通气对肺炎症诱导的独立及联合作用。
将新生仔猪暴露于室内空气或F(I)O₂ = 1.0 3天后，随机分为接受高潮气量（20 ml/kg）或低潮气量（6 ml/kg）机械通气4小时两组，同时控制pH值。
与所有其他组相比，随机分配至高氧高潮气量通气组动物肺内单核细胞趋化蛋白-1水平显著升高（p < 0.05）。在暴露于高氧的未通气动物中，肺匀浆中检测到的髓过氧化物酶显著更高（p < 0.01）。仅在先前暴露于高氧的动物中，增加高潮气量通气会进一步提高髓过氧化物酶水平（p < 0.05）。与机械通气1小时后相比，机械通气4小时后肺血管阻力显著升高（p < 0.001）。
我们得出结论，在遭受高氧应激的新生仔猪中，通过肺单核细胞趋化蛋白-1和髓过氧化物酶水平评估，高潮气量通气的叠加会加剧肺部炎症。
