Hai-Feng Zong1,2, Guo Guo2,3,4, Jing Liu2, Chuan-Zhong Yang1, Lin-Lin Bao5. 1. Neonatal Intensive Care Unit, Affiliated Shenzhen Maternity & Child Healthcare Hospital, Southern Medical University, Shenzhen, China. 2. Department of Neonatology and NICU, Beijing Chaoyang District Maternal and Child Healthcare Hospital, Beijing, China. 3. Department of Pediatrics, Medical School of Chinese PLA, Beijing, China. 4. Department of Neonatology, The Fifth Medical Center of The PLA General Hospital, Beijing, China. 5. Department of dermatology, Shenzhen People's Hospital, Shenzhen, China.
Abstract
BACKGROUND: 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. METHODS: 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) via 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. RESULTS: 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 (p < .05). IHC staining displayed the same findings. CONCLUSIONS: 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.
BACKGROUND: 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. METHODS: 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) via 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. RESULTS: 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 (p < .05). IHC staining displayed the same findings. CONCLUSIONS: 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.