Bateman Ryon M, Sharpe Michael D, Singer Mervyn, Ellis Christopher G
Department of Medical Biophysics, University of Western Ontario, London, ON N6A 5C1, Canada.
Department of Anesthesia and Critical Care Western, University of Western Ontario, London, ON N6A 5C1, Canada.
Int J Mol Sci. 2017 Sep 8;18(9):1932. doi: 10.3390/ijms18091932.
Sepsis induces a wide range of effects on the red blood cell (RBC). Some of the effects including altered metabolism and decreased 2,3-bisphosphoglycerate are preventable with appropriate treatment, whereas others, including decreased erythrocyte deformability and redistribution of membrane phospholipids, appear to be permanent, and factors in RBC clearance. Here, we review the effects of sepsis on the erythrocyte, including changes in RBC volume, metabolism and hemoglobin's affinity for oxygen, morphology, RBC deformability (an early indicator of sepsis), antioxidant status, intracellular Ca homeostasis, membrane proteins, membrane phospholipid redistribution, clearance and RBC O₂-dependent adenosine triphosphate efflux (an RBC hypoxia signaling mechanism involved in microvascular autoregulation). We also consider the causes of these effects by host mediated oxidant stress and bacterial virulence factors. Additionally, we consider the altered erythrocyte microenvironment due to sepsis induced microvascular dysregulation and speculate on the possible effects of RBC autoxidation. In future, a better understanding of the mechanisms involved in sepsis induced erythrocyte pathophysiology and clearance may guide improved sepsis treatments. Evidence that small molecule antioxidants protect the erythrocyte from loss of deformability, and more importantly improve septic patient outcome suggest further research in this area is warranted. While not generally considered a critical factor in sepsis, erythrocytes (and especially a smaller subpopulation) appear to be highly susceptible to sepsis induced injury, provide an early warning signal of sepsis and are a factor in the microvascular dysfunction that has been associated with organ dysfunction.
脓毒症对红细胞（RBC）会产生广泛影响。其中一些影响，包括代谢改变和2,3-二磷酸甘油酸减少，可通过适当治疗预防，而其他影响，如红细胞变形性降低和膜磷脂重新分布，似乎是永久性的，并且是红细胞清除的因素。在此，我们综述脓毒症对红细胞的影响，包括红细胞体积、代谢、血红蛋白对氧气的亲和力、形态、红细胞变形性（脓毒症的早期指标）、抗氧化状态、细胞内钙稳态、膜蛋白、膜磷脂重新分布、清除以及红细胞氧依赖性三磷酸腺苷外流（一种参与微血管自动调节的红细胞缺氧信号机制）的变化。我们还考虑宿主介导的氧化应激和细菌毒力因子导致这些影响的原因。此外，我们考虑脓毒症诱导的微血管失调导致的红细胞微环境改变，并推测红细胞自氧化的可能影响。未来，更好地理解脓毒症诱导的红细胞病理生理学和清除所涉及的机制可能会指导改进脓毒症治疗。小分子抗氧化剂可保护红细胞免于变形性丧失，更重要的是改善脓毒症患者预后的证据表明该领域值得进一步研究。虽然红细胞（尤其是较小的亚群）通常不被视为脓毒症的关键因素，但它们似乎对脓毒症诱导的损伤高度敏感，可提供脓毒症的早期预警信号，并且是与器官功能障碍相关的微血管功能障碍的一个因素。
