Department of Pharmacology and Toxicology, University of Kansas Medical Center, Kansas City, MO 64108-2792, USA.
J Trauma Acute Care Surg. 2012 Apr;72(4):992-8. doi: 10.1097/TA.0b013e31823c96b0.
Fat embolism (FE) after trauma and some orthopedic procedures is known to cause acute lung injury, including acute respiratory distress syndrome. However, its potential long-term effects on the lung are unknown. A previous study using a rat model of FE found significant histopathologic changes in the lungs after intravenous injection of triolein for up to 11 days. This study detailed the persistence of the lung damage and investigated the input of the renin-angiotensin system in its pathology.
Unanesthetized rats were injected via the tail vein with 0.2 mL saline or triolein. After euthanasia, at 3 weeks or 6 weeks, lung sections were stained to highlight cellular structure, presence of collagen and fat, or immunolabeled for smooth muscle actin or angiotensin peptides.
At 3 weeks or 6 weeks after triolein injection, there was no dilatation of the heart or inferior vena cava, no congestion of the liver or spleen, no adventitial edema, nor was fluid present in alveoli or pleural cavity as reported in animals at earlier time points. Persisting pathology included reduced lumen patency, thickening of the media of small arteries and arterioles, and vascular and septal inflammation. Although the fat content of the lung decreased from week 3 to week 6, there was a progressive increase in collagen, smooth muscle actin, and angiotensin peptides.
This model extends the effect of FE on pulmonary pathology to 6 weeks, revealing persistent vasculitis, septal inflammation, and progressive fibrotic changes which are associated with increased presence of angiotensin peptides.
创伤和一些骨科手术后脂肪栓塞（FE）已知会导致急性肺损伤，包括急性呼吸窘迫综合征。然而，其对肺部的潜在长期影响尚不清楚。先前使用 FE 大鼠模型的一项研究发现，静脉注射三油酸甘油酯后长达 11 天，肺部会出现明显的组织病理学变化。本研究详细描述了肺部损伤的持续存在，并研究了肾素-血管紧张素系统在其发病机制中的作用。
未麻醉大鼠通过尾静脉注射 0.2mL 生理盐水或三油酸甘油酯。安乐死后，在 3 周或 6 周时，对肺组织切片进行染色以突出细胞结构、胶原和脂肪的存在，或免疫标记平滑肌肌动蛋白或血管紧张素肽。
在三油酸甘油酯注射后 3 周或 6 周时，心脏或下腔静脉无扩张，肝脏或脾脏无充血，外膜无水肿，肺泡或胸腔内无液体。与早期时间点的动物相比，报告中没有报道。持续存在的病理学包括管腔通畅性降低、小动脉和小动脉中层变厚以及血管和间隔炎症。尽管肺内脂肪含量从第 3 周降至第 6 周，但胶原、平滑肌肌动蛋白和血管紧张素肽的含量逐渐增加。
该模型将 FE 对肺病理学的影响延长至 6 周，显示出持续的血管炎、间隔炎症和进行性纤维化变化，这些变化与血管紧张素肽的增加有关。
