Translational Research Program, Department of Anesthesiology and Center for Shock, Trauma and Anesthesiology Research, University of Maryland School of Medicine, Baltimore, Maryland.
Department of Surgery, University of Maryland School of Medicine, Baltimore, Maryland.
Shock. 2021 Oct 1;56(4):601-610. doi: 10.1097/SHK.0000000000001716.
Aeromedical evacuation can expose traumatically injured patients to low pressure (hypobaria) and hypoxia. Here, we sought to assess the impact of hypobaria on inflammation, organ injury, and mortality in a mouse model of polytrauma.
Eight to 12-week-old male C57BL/6J mice were subjected to sham or polytrauma consisting of bowel ischemia by superior mesenteric artery occlusion, hindlimb muscle crush, and tibia fracture. Two hours after injury, animals were randomized to undergo either 6 h of hypobaria or sea-level, room air conditions. At 8 or 24 h after injury, transthoracic echocardiography was performed. Acute kidney injury (AKI) biomarkers were measured by qRT-PCR. Plasma cytokine and endothelial injury markers were determined by enzyme-linked immunosorbent assay.
Eight hours after traumatic injury, mice exhibited a marked increase in plasma IL-6 (57 pg/mL vs. 1,216 pg/mL), AKI with increased Ngal and Kim-1, and endothelial injury as evidenced by significantly increased plasma hyaluronic acid (96 ng/mL vs.199 ng/mL), thrombomodulin (23.2 ng/mL vs. 58.9 ng/mL), syndecan-1 (0.99 ng/mL vs. 4.34 ng/mL), and E-selectin (38.6 ng/mL vs. 62.7 ng/mL). The trauma mice also developed cardiac dysfunction with decreased cardiac output and stroke volume at 8 h postinjury. Hypobaric exposure after polytrauma led to decreased ejection fraction (81.0% vs. 74.2%, P < 0.01) and increased plasma hyaluronic acid (199 ng/mL vs. 260 ng/mL, P < 0.05), thrombomodulin (58.9 ng/mL vs. 75.4 ng/mL, P < 0.05), and syndecan-1 (4.34 ng/mL vs. 8.33 ng/mL, P < 0.001) at 8 h postinjury.
Hypobaria exposure appeared to worsen cardiac dysfunction and endothelial injury following polytrauma and thus may represent a physiological "second hit" following traumatic injury.
航空医疗后送可能使创伤患者暴露于低压（低气压）和缺氧环境中。在这里，我们试图评估低压对创伤后多器官损伤模型中炎症、器官损伤和死亡率的影响。
8 至 12 周龄雄性 C57BL/6J 小鼠接受假手术或创伤后多器官损伤处理，包括肠系膜上动脉闭塞引起的肠缺血、后肢肌肉挤压伤和胫骨骨折。损伤后 2 小时，动物随机接受 6 小时低气压或海平面、室内空气条件处理。损伤后 8 或 24 小时，进行经胸超声心动图检查。通过 qRT-PCR 测定急性肾损伤（AKI）生物标志物。通过酶联免疫吸附试验测定血浆细胞因子和内皮损伤标志物。
创伤后 8 小时，小鼠的血浆白细胞介素 6（IL-6）水平显著升高（57 pg/mL 比 1216 pg/mL），AKI 标志物 Ngal 和 Kim-1 增加，内皮损伤的证据是血浆透明质酸（HA）（96 ng/mL 比 199 ng/mL）、血栓调节蛋白（TM）（23.2 ng/mL 比 58.9 ng/mL）、黏附素-1（syndecan-1）（0.99 ng/mL 比 4.34 ng/mL）和 E 选择素（E-selectin）（38.6 ng/mL 比 62.7 ng/mL）显著增加。创伤后多器官损伤的小鼠在损伤后 8 小时也出现心功能障碍，表现为心输出量和每搏输出量减少。多器官损伤后接受低压暴露导致射血分数降低（81.0%比 74.2%，P<0.01）和血浆透明质酸增加（199 ng/mL 比 260 ng/mL，P<0.05）、血栓调节蛋白（58.9 ng/mL 比 75.4 ng/mL，P<0.05）和黏附素-1（4.34 ng/mL 比 8.33 ng/mL，P<0.001）在损伤后 8 小时。
低气压暴露似乎加重了创伤后多器官损伤后的心脏功能障碍和内皮损伤，因此可能代表创伤后生理上的“二次打击”。
