Neonatal Intensive Care Unit, Affiliated Shenzhen Maternity & Child Healthcare Hospital, Southern Medical University, Shenzhen, China.
Department of Neonatology and NICU, Beijing Chaoyang District Maternal and Child Healthcare Hospital, Beijing, China.
J Matern Fetal Neonatal Med. 2021 Jul;34(13):2197-2205. doi: 10.1080/14767058.2020.1846711. Epub 2020 Nov 17.
Clinically, the lung ultrasound (LUS) showed wet lung could cause respiratory distress syndrome (RDS) in newborns. This work aimed to investigate LUS changes over time and its potential mechanism as alveolar fluid increase in a rabbit model.
A total of 35 New Zealand Rabbits were randomly assigned to seven groups. Models of various alveolar fluid levels were induced by infusion of different volumes of normal saline (NS) the endotracheal tube. LUS was performed before NS infusion, immediately after NS infusion and 4 h after NS infusion. To appraise LUS changes and its potential mechanism as alveolar fluid increase, histopathological examination, the mRNA and protein expression of surfactant protein (SP), and immunohistochemistry (IHC) were performed. The expression levels of SP-B and SP-C proteins were detected using western blotting, and the relative expression levels of SP-B and SP-C mRNA were detected using qRT-PCR.
The results showed that LUS changed from B-line to lung consolidations accompanied by air-bronchograms in some locations of lungs at 4 h when the injection volume ≥ 6 ml/kg. Histopathological examination showed alveoli collapse, inflammatory cell infiltration and alveolar wall thickened. SP-B and SP-C mRNA and protein expression were statistically significantly reduced when the injection volume ≥6 ml/kg ( < .05). IHC staining displayed the same findings.
As alveolar fluid increase, LUS changed from wet lung to RDS after 4 h. The possible mechanism was that the SP protein expression was significantly reduced. LUS can be used to guide the administration of exogenous surfactant in this situation.
临床上，肺部超声（LUS）显示湿肺可导致新生儿呼吸窘迫综合征（RDS）。本研究旨在探讨兔模型中肺泡液增加时 LUS 的时变变化及其潜在机制。
共 35 只新西兰兔随机分为 7 组。通过气管内管输注不同体积的生理盐水（NS）来诱导不同肺泡液水平的模型。在 NS 输注前、NS 输注后即刻和 NS 输注后 4 小时进行 LUS 检查。为评估 LUS 变化及其作为肺泡液增加的潜在机制，进行了组织病理学检查、表面活性蛋白（SP）的 mRNA 和蛋白表达以及免疫组织化学（IHC）检查。使用 Western blot 检测 SP-B 和 SP-C 蛋白的表达水平，使用 qRT-PCR 检测 SP-B 和 SP-C mRNA 的相对表达水平。
结果显示，当注射量≥6ml/kg 时，LUS 从 B 线变为肺实变，并伴有肺部某些部位的空气支气管征。4 小时时，组织病理学检查显示肺泡塌陷、炎症细胞浸润和肺泡壁增厚。当注射量≥6ml/kg 时，SP-B 和 SP-C mRNA 和蛋白表达均显著降低（ < .05）。IHC 染色显示相同的结果。
随着肺泡液的增加，4 小时后 LUS 从湿肺变为 RDS。可能的机制是 SP 蛋白表达显著降低。LUS 可用于指导这种情况下外源性表面活性剂的给药。
