School of Nursing, University of Nevada, Las Vegas, NV 89154, USA.
Department of Population Health Sciences, College of Medicine, University of Central Florida, Orlando, FL 32827, USA.
Exp Biol Med (Maywood). 2022 Mar;247(6):509-518. doi: 10.1177/15353702211060775. Epub 2021 Dec 14.
Tissue trauma and hemorrhagic shock are common battlefield injuries that can induce hypoxia, inflammation, and/or anemia. Inflammation and hypoxia can initiate adaptive mechanisms, such as stress erythropoiesis in the spleen, to produce red blood cells and restore the oxygen supply. In a military context, mild hypobaric hypoxia-part of the environmental milieu during aeromedical evacuation or en route care-may influence adaptive mechanisms, such as stress erythropoiesis, and host defense. In the present study, healthy (control), muscle trauma, and polytrauma (muscle trauma and hemorrhagic shock) mice were exposed to normobaric normoxia or hypobaric hypoxia for ∼17.5 h to test the hypothesis that hypobaric hypoxia exposure influences splenic erythropoiesis and splenic inflammation after polytrauma. This hypothesis was partially supported. The polytrauma + hypobaric hypoxia group exhibited more splenic neutrophils, fewer total spleen cells, and fewer splenic proliferating cells than the polytrauma+normobaric normoxia group; however, no splenic erythroid cell differences were detected between the two polytrauma groups. We also compared splenic erythropoiesis and myeloid cell numbers among control, muscle trauma, and polytrauma groups. More reticulocytes at 1.7 days (40 h) post-trauma (dpt) and neutrophils at 4 dpt were produced in the muscle trauma mice than corresponding control mice. In contrast to muscle trauma, polytrauma led to a reduced red blood cell count and elevated serum erythropoietin levels at 1.7 dpt. There were more erythroid subsets and apoptotic reticulocytes in the polytrauma mice than muscle trauma mice at 4 and 8 dpt. At 14 dpt, the red blood cell count of the polytrauma + normobaric normoxia mice was 12% lower than that of the control + normobaric normoxia mice; however, no difference was observed between polytrauma + hypobaric hypoxia and control + hypobaric hypoxia mice. Our findings suggest muscle trauma alone induces stress erythropoiesis; in a polytrauma model, hypobaric hypoxia exposure may result in the dysregulation of splenic cells, requiring a treatment plan to ensure adequate immune functioning.
组织创伤和失血性休克是常见的战场损伤，可导致缺氧、炎症和/或贫血。炎症和缺氧会引发适应性机制，如脾脏中的应激性红细胞生成，以产生红细胞并恢复氧气供应。在军事环境中，轻度低压低氧（航空医疗后送或途中护理期间的环境因素之一）可能会影响适应性机制，如应激性红细胞生成和宿主防御。在本研究中，健康（对照）、肌肉创伤和多发伤（肌肉创伤和失血性休克）小鼠分别暴露于常压低氧或低压缺氧环境中约 17.5 小时，以测试低压低氧暴露是否会影响多发伤后的脾脏红细胞生成和脾脏炎症的假设。该假设得到了部分支持。与多发伤+常压低氧组相比，多发伤+低压低氧组的脾脏中性粒细胞更多，总脾细胞更少，增殖细胞更少；然而，两组间脾脏红细胞生成无差异。我们还比较了对照组、肌肉创伤组和多发伤组之间的脾脏红细胞生成和髓样细胞数量。与相应的对照组相比，肌肉创伤组在创伤后 1.7 天（40 小时）时产生更多的网织红细胞，在 4 天时有更多的中性粒细胞。与肌肉创伤相反，多发伤导致创伤后 1.7 天红细胞计数减少和血清促红细胞生成素水平升高。与肌肉创伤相比，多发伤组在 4 天和 8 天时有更多的红系亚群和凋亡网织红细胞。在 14 天，多发伤+常压低氧组的红细胞计数比对照组+常压低氧组低 12%；然而，多发伤+低压低氧组和对照组+低压低氧组之间没有差异。我们的研究结果表明，单独的肌肉创伤会引起应激性红细胞生成；在多发伤模型中，低压低氧暴露可能导致脾脏细胞失调，需要制定治疗计划以确保充分的免疫功能。
