Hemanext, Lexington, MA, United States of America.
Laboratoire de Recherche sur les Produits Sanguins, Transfusion Interrégionale CRS, Epalinges, Switzerland.
Blood Transfus. 2019 Jan;17(1):27-52. doi: 10.2450/2019.0217-18.
Red blood cells (RBCs) are a specialised organ that enabled the evolution of multicellular organisms by supplying a sufficient quantity of oxygen to cells that cannot obtain oxygen directly from ambient air via diffusion, thereby fueling oxidative phosphorylation for highly efficient energy production. RBCs have evolved to optimally serve this purpose by packing high concentrations of haemoglobin in their cytosol and shedding nuclei and other organelles. During their circulatory lifetimes in humans of approximately 120 days, RBCs are poised to transport oxygen by metabolic/redox enzymes until they accumulate damage and are promptly removed by the reticuloendothelial system. These elaborate evolutionary adaptions, however, are no longer effective when RBCs are removed from the circulation and stored hypothermically in blood banks, where they develop storage-induced damages ("storage lesions") that accumulate over the shelf life of stored RBCs. This review attempts to provide a comprehensive view of the literature on the subject of RBC storage lesions and their purported clinical consequences by incorporating the recent exponential growth in available data obtained from "omics" technologies in addition to that published in more traditional literature. To summarise this vast amount of information, the subject is organised in figures with four panels: i) root causes; ii) RBC storage lesions; iii) physiological effects; and iv) reported outcomes. The driving forces for the development of the storage lesions can be roughly classified into two root causes: i) metabolite accumulation/depletion, the target of various interventions (additive solutions) developed since the inception of blood banking; and ii) oxidative damages, which have been reported for decades but not addressed systemically until recently. Downstream physiological consequences of these storage lesions, derived mainly by in vitro studies, are described, and further potential links to clinical consequences are discussed. Interventions to postpone the onset and mitigate the extent of the storage lesion development are briefly reviewed. In addition, we briefly discuss the results from recent randomised controlled trials on the age of stored blood and clinical outcomes of transfusion.
红细胞（RBC）是一种专门的器官，通过向不能直接通过扩散从周围空气中获取氧气的细胞提供足够的氧气量，从而为高效的能量产生提供氧化磷酸化，使多细胞生物的进化成为可能。RBC 通过在细胞质中包装高浓度的血红蛋白并去除细胞核和其他细胞器，从而进化到最佳地服务于这一目的。在人类大约 120 天的循环寿命中，RBC 准备通过代谢/氧化还原酶来运输氧气，直到它们积累损伤并被网状内皮系统迅速清除。然而，当 RBC 从循环中取出并在低温下储存在血库中时，这些精细的进化适应不再有效，在血库中，它们会发展出“储存损伤”（“储存损伤”），这些损伤会在储存 RBC 的保质期内积累。本综述试图通过整合除了更传统文献中发表的文献之外，还整合了“组学”技术获得的可用数据的最近指数增长，提供有关 RBC 储存损伤及其所谓的临床后果的文献的综合观点。为了总结这些大量信息，该主题以四个面板的形式组织：i）根本原因；ii）RBC 储存损伤；iii）生理影响；iv）报告的结果。储存损伤的发展驱动力大致可分为两个根本原因：i）代谢物积累/耗竭，这是自血库成立以来开发的各种干预措施（添加剂解决方案）的目标；ii）氧化损伤，几十年来一直有报道，但直到最近才系统地解决。描述了这些储存损伤的主要来源于体外研究的下游生理后果，并进一步讨论了与临床后果的潜在联系。简要回顾了推迟发病和减轻储存损伤发展程度的干预措施。此外，我们还简要讨论了最近关于储存血液年龄和输血临床结果的随机对照试验的结果。
