Massachusetts General Hospital, Department of Anesthesia, Critical Care and Pain Medicine, 55 Fruit St. Boston, MA; Tokyo Medical and Dental University, Department of Intensive Care Medicine, Tokyo, Japan.
University of São Paulo, Cardio-Pulmonary Department, São Paulo, Brazil.
Acad Radiol. 2020 Dec;27(12):1679-1690. doi: 10.1016/j.acra.2019.12.022. Epub 2020 Mar 12.
Pulmonary atelectasis presumably promotes and facilitates lung injury. However, data are limited on its direct and remote relation to inflammation. We aimed to assess regional 2-deoxy-2-[F]-fluoro-D-glucose (F-FDG) kinetics representative of inflammation in atelectatic and normally aerated regions in models of early lung injury.
We studied supine sheep in four groups: Permissive Atelectasis (n = 6)-16 hours protective tidal volume (V) and zero positive end-expiratory pressure; Mild (n = 5) and Moderate Endotoxemia (n = 6)- 20-24 hours protective ventilation and intravenous lipopolysaccharide (Mild = 2.5 and Moderate = 10.0 ng/kg/min), and Surfactant Depletion (n = 6)-saline lung lavage and 4 hours high V. Measurements performed immediately after anesthesia induction served as controls (n = 8). Atelectasis was defined as regions of gas fraction <0.1 in transmission or computed tomography scans. F-FDG kinetics measured with positron emission tomography were analyzed with a three-compartment model.
F-FDG net uptake rate in atelectatic tissue was larger during Moderate Endotoxemia (0.0092 ± 0.0019/min) than controls (0.0051 ± 0.0014/min, p = 0.01). F-FDG phosphorylation rate in atelectatic tissue was larger in both endotoxemia groups (0.0287 ± 0.0075/min) than controls (0.0198 ± 0.0039/min, p = 0.05) while the F-FDG volume of distribution was not significantly different among groups. Additionally, normally aerated regions showed larger F-FDG uptake during Permissive Atelectasis (0.0031 ± 0.0005/min, p < 0.01), Mild (0.0028 ± 0.0006/min, p = 0.04), and Moderate Endotoxemia (0.0039 ± 0.0005/min, p < 0.01) than controls (0.0020 ± 0.0003/min).
Atelectatic regions present increased metabolic activation during moderate endotoxemia mostly due to increased F-FDG phosphorylation, indicative of increased cellular metabolic activation. Increased F-FDG uptake in normally aerated regions during permissive atelectasis suggests an injurious remote effect of atelectasis even with protective tidal volumes.
肺不张可能会促进和加重肺损伤。然而，关于其与炎症的直接和间接关系的数据有限。本研究旨在评估早期肺损伤模型中肺不张和正常充气区域的代表炎症的 2-脱氧-2-[F]-氟-D-葡萄糖（F-FDG）动力学。
我们研究了仰卧位绵羊的四个组：允许性肺不张组（n=6）-16 小时保护性潮气量（V）和零呼气末正压；轻度（n=5）和中度内毒素血症组（n=6）-20-24 小时保护性通气和静脉内脂多糖（轻度=2.5ng/kg/min，中度=10.0ng/kg/min）和表面活性剂耗竭组（n=6）-生理盐水肺灌洗和 4 小时高 V。麻醉诱导后立即进行的测量作为对照（n=8）。用传输或计算机断层扫描定义不张区域的气体分数<0.1。用正电子发射断层扫描测量 F-FDG 动力学，并采用三房室模型进行分析。
中度内毒素血症时（0.0092±0.0019/min），不张组织中的 F-FDG 净摄取率大于对照组（0.0051±0.0014/min，p=0.01）。两组内毒素血症中，不张组织中的 F-FDG 磷酸化率均大于对照组（0.0287±0.0075/min）（p=0.05），而 F-FDG 分布容积在各组之间无显著差异。此外，允许性肺不张时，正常充气区的 F-FDG 摄取量增加（0.0031±0.0005/min，p<0.01），轻度（0.0028±0.0006/min，p=0.04）和中度内毒素血症（0.0039±0.0005/min，p<0.01）时大于对照组（0.0020±0.0003/min）。
中度内毒素血症时，不张区域的代谢激活增加，主要是由于 F-FDG 磷酸化增加，表明细胞代谢激活增加。允许性肺不张时正常充气区 F-FDG 摄取增加提示肺不张存在损伤的远程效应，即使采用保护性潮气量。
