The Clinical Medicine Department, Xi'an Medical University, Xi'an, 710021, Shaanxi, P.R. China.
Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, 277 Yanta West Road, Xi'an, 710061, Shaanxi, P.R. China.
J Mol Histol. 2024 Oct;55(5):793-801. doi: 10.1007/s10735-024-10231-3. Epub 2024 Aug 7.
Many people sustain acute lung injuries in road traffic collisions, but few studies have dealt with such injuries in live models. This study aimed to explore the basic pathophysiological and inflammatory changes in adult rabbits following acute thoracic trauma. We randomly assigned 50 rabbits to control and injury groups. Rabbits in the injury group were subjected to right chest pressure (2600 g) using a Hopkinson bar. Measurements were taken in the control group and 0, 24, 48, and 72 h after injury in the injury group. Injury severity was evaluated in gross view; with haematoxylin and eosin (H&E) staining; and through the serum changes of tumor necrosis factor alpha (TNF-α), surfactant protein D (SP-D), and neutrophils. Secretion changes in SP-D in right lung injured tissues were estimated by western blotting and qPCR. Serum TNF-α levels increased rapidly immediately after injury, gradually recovering after 24, 48, and 72 h (p < 0.01). The percentage of neutrophils in the accompanying blood showed a consistent trend. Gross necropsy and H&E staining indicated different levels of bleeding, alveoli exudation, and inflammatory transformation after impact. ELISA depicted the same trend in circulation (F = 22.902, p < 0.01). Western blotting showed that SP-D protein levels in tissues decreased at 0 h and increased at 24, 48, and 72 h. We demonstrate the feasibility of a model of impact lung injury. Primary impact caused injury without external signs. Inflammation began immediately, and the lungs began recovering at 24, 48, and 72 h, as shown by increased SP-D levels in circulation and tissues.With complaints of ALI and inflammation, SP-D may be a potential biomarker after chest trauma.
许多人在道路交通碰撞中遭受急性肺损伤，但很少有研究涉及活体模型中的此类损伤。本研究旨在探讨急性胸部创伤后成年兔基本病理生理和炎症变化。我们将 50 只兔子随机分为对照组和损伤组。损伤组的兔子使用 Hopkinson 杆接受右胸压力（2600g）。在对照组和损伤组中，分别在损伤后 0、24、48 和 72h 进行测量。通过大体观察、苏木精和伊红（H&E）染色以及肿瘤坏死因子 alpha（TNF-α）、表面活性蛋白 D（SP-D）和中性粒细胞血清变化来评估损伤严重程度。通过 Western blot 和 qPCR 估计右肺损伤组织中 SP-D 的分泌变化。损伤后 TNF-α 水平迅速升高，24、48 和 72h 后逐渐恢复（p<0.01）。伴随血液中中性粒细胞的百分比呈一致趋势。大体尸检和 H&E 染色表明冲击后有不同程度的出血、肺泡渗出和炎症转化。ELISA 显示循环中存在相同趋势（F=22.902，p<0.01）。Western blot 显示组织中 SP-D 蛋白水平在 0h 时降低，在 24、48 和 72h 时增加。我们证明了冲击性肺损伤模型的可行性。原发性冲击造成无外部迹象的损伤。炎症立即开始，24、48 和 72h 时肺部开始恢复，循环和组织中 SP-D 水平升高。伴有 ALI 和炎症的主诉，SP-D 可能是胸部创伤后的潜在生物标志物。
