Inflammation and lung maturation from stretch injury in preterm fetal sheep
Inflammation and lung maturation from stretch injury in preterm fetal sheep
复制标题
DOI：
10.1152/ajplung.00294.2010
复制
发表时间：
2011-02-01
影响因子：
4.9
通讯作者：
Jobe, Alan H.
中科院分区：
文献类型：
--
作者：
Hillman, Noah H.;Polglase, Graeme R.;Jobe, Alan H.
Hillman NH、Polglase GR、Pillow JJ、Saito M、Kallapur SG、Jobe AH。早产胎羊拉伸损伤引起的炎症和肺成熟。 Am J Physiol Lung Cell Mol Physiol 300：L232-L241，2011。首次发表于 2010 年 12 月 3 日； doi:10.1152/ajplung.00294.2010.-机械通气是早产儿发生支气管肺发育不良的危险因素。 15 分钟的高潮气量 (V-T) 通气可在 3 小时内诱导小气道和肺实质中炎症细胞因子的表达。我们的目的是描述暴露于规定的 15 分钟拉伸损伤的胎羊中细胞因子的时间进展和对肺损伤的成熟反应。产妇麻醉和子宫切开后，将妊娠 129 天的胎羔（n = 7-8/组）的头部和胸部取出。对每个胎儿进行插管，并轻轻去除气道液体。在维持胎盘支持的同时，胎儿使用加热、加湿的 100% 氮气接受通气 15 分钟，VT 逐渐升高至 15 ml/kg，无呼气末正压 (PEEP)。然后将胎儿放回子宫1、6或24小时。对照羔羊接受 2 cmH(2)O 的 PEEP 15 分钟。对来自肺和全身器官的组织样本进行了评估。拉伸损伤增加了早期反应基因 Egr-1，并在 1 小时内增加了促炎和抗炎细胞因子的表达。损伤诱导粒细胞/巨噬细胞集落刺激因子 mRNA 和成熟的单核细胞在 24 小时内形成肺泡巨噬细胞。 24 小时后，肺部表面活性蛋白 A、B 和 C 的 mRNA 增加。气道上皮的热休克蛋白 70 (HSP70) 随着时间的推移呈现动态变化。血清皮质醇水平没有增加，全身炎症的诱发也很小。我们得出的结论是，短暂的高潮气量通气会导致促炎级联反应、肺单核细胞的成熟以及表面活性剂蛋白 mRNA 的诱导。
Hillman NH, Polglase GR, Pillow JJ, Saito M, Kallapur SG, Jobe AH. Inflammation and lung maturation from stretch injury in preterm fetal sheep. Am J Physiol Lung Cell Mol Physiol 300: L232-L241, 2011. First published December 3, 2010; doi:10.1152/ajplung.00294.2010.-Mechanical ventilation is a risk factor for the development of bronchopulmonary dysplasia in premature infants. Fifteen minutes of high tidal volume (V-T) ventilation induces inflammatory cytokine expression in small airways and lung parenchyma within 3 h. Our objective was to describe the temporal progression of cytokine and maturation responses to lung injury in fetal sheep exposed to a defined 15-min stretch injury. After maternal anesthesia and hysterotomy, 129-day gestation fetal lambs (n = 7-8/group) had the head and chest exteriorized. Each fetus was intubated, and airway fluid was gently removed. While placental support was maintained, the fetus received ventilation with an escalating VT to 15 ml/kg without positive end-expiratory pressure (PEEP) for 15 min using heated, humidified 100% nitrogen. The fetus was then returned to the uterus for 1, 6, or 24 h. Control lambs received a PEEP of 2 cmH(2)O for 15 min. Tissue samples from the lung and systemic organs were evaluated. Stretch injury increased the early response gene Egr-1 and increased expression of pro-and anti-inflammatory cytokines within 1 h. The injury induced granulocyte/macrophage colony-stimulating factor mRNA and matured monocytes to alveolar macrophages by 24 h. The mRNA for the surfactant proteins A, B, and C increased in the lungs by 24 h. The airway epithelium demonstrated dynamic changes in heat shock protein 70 (HSP70) over time. Serum cortisol levels did not increase, and induction of systemic inflammation was minimal. We conclude that a brief period of high VT ventilation causes a proinflammatory cascade, a maturation of lung monocytic cells, and an induction of surfactant protein mRNA.