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2
Alterations of red blood cell metabolome during cold liquid storage of erythrocyte concentrates in CPD-SAGM.CPD-SAGM 中红细胞浓缩液低温液体储存过程中红细胞代谢组的改变。
J Proteomics. 2012 Dec 5;76 Spec No.:168-80. doi: 10.1016/j.jprot.2012.03.012. Epub 2012 Mar 20.
3
Red blood cell age and potentiation of transfusion-related pathology in trauma patients.红细胞年龄与创伤患者输血相关病理的增强作用。
Transfusion. 2011 Apr;51(4):867-73. doi: 10.1111/j.1537-2995.2011.03098.x.
4
Storage lesion: role of red blood cell breakdown.贮存损伤：红细胞破坏的作用。
Transfusion. 2011 Apr;51(4):844-51. doi: 10.1111/j.1537-2995.2011.03100.x.
5
Association between length of storage of transfused red blood cells and multiple organ dysfunction syndrome in pediatric intensive care patients.输血量与小儿重症监护患者多器官功能障碍综合征的关系。
Transfusion. 2010 Sep;50(9):1902-13. doi: 10.1111/j.1537-2995.2010.02661.x.
6
Complement and coagulation: strangers or partners in crime?补体与凝血：是陌生人还是共犯？
Trends Immunol. 2007 Apr;28(4):184-92. doi: 10.1016/j.it.2007.02.006. Epub 2007 Mar 1.
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Universal leucodepletion: an overview of some unresolved issues and the highlights of lessons learned.全血白细胞去除术：一些未解决问题的概述及经验教训要点
Transfus Apher Sci. 2003 Oct;29(2):105-17. doi: 10.1016/S1473-0502(03)00112-5.
8
Complement activation during storage of whole blood, red cells, plasma, and buffy coat.全血、红细胞、血浆和 Buffy 层储存期间的补体激活。
Transfusion. 1997 Mar;37(3):264-8. doi: 10.1046/j.1537-2995.1997.37397240207.x.
9
The membrane attack complex of complement. Assembly, structure and cytotoxic activity.补体膜攻击复合物。组装、结构与细胞毒性活性。
Toxicology. 1994 Feb 28;87(1-3):229-47. doi: 10.1016/0300-483x(94)90253-4.
10
Activation of blood coagulation, fibrinolytic and kallikrein systems during storage of plasma.血浆储存期间凝血、纤维蛋白溶解和激肽释放酶系统的激活。
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膜攻击复合物的生成随储存血液中时间的变化而增加。

Membrane attack complex generation increases as a function of time in stored blood.

作者信息

Hu X, Patel R P, Weinberg J A, Marques M B, Ramos T N, Barnum S R

机构信息

Department of Microbiology.

出版信息

Transfus Med. 2014 Apr;24(2):114-6. doi: 10.1111/tme.12109. Epub 2014 Mar 4.

DOI:10.1111/tme.12109
PMID:24588971
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5847664/
Abstract

OBJECTIVE

To determine if the complement system, a potent mediator of inflammation, contributes to haemolysis during red blood cell (RBC) storage.

BACKGROUND

RBCs in storage undergo structural and biochemical changes that may result in adverse patient outcomes post-transfusion. Complement activation on leukodepletion and during storage may contribute to the RBC storage lesion.

METHODS/MATERIALS: We performed a cross-sectional analysis of aliquots of leukoreduced RBC units, stored for 1-6 weeks, for the levels of C3a, C5a, Bb, iC3b, C4d and C5b-9 [membrane attack complex (MAC)] by enzyme-linked immunosorbent assay (ELISA).

RESULTS

We observed that only MAC levels significantly increased in RBC units as a function of storage time. We also observed that the level of C5b-9 bound to RBCs increased as a function of storage time.

CONCLUSION

MAC levels increased over time, suggesting that MAC is the primary complement-mediated contributor to changes in stored RBCs. Inhibition of the terminal complement pathway may stabilise RBC functionality and extend shelf life.

摘要

目的

确定补体系统（一种强大的炎症介质）是否在红细胞（RBC）储存期间导致溶血。

背景

储存中的红细胞会发生结构和生化变化，这可能导致输血后患者出现不良后果。白细胞去除过程中和储存期间的补体激活可能导致红细胞储存损伤。

方法/材料：我们对储存1 - 6周的白细胞去除红细胞单位的等分试样进行了横断面分析，通过酶联免疫吸附测定（ELISA）检测C3a、C5a、Bb、iC3b、C4d和C5b - 9[膜攻击复合物（MAC）]的水平。

结果

我们观察到，仅MAC水平随储存时间显著增加。我们还观察到与红细胞结合的C5b - 9水平随储存时间增加。

结论

MAC水平随时间升高，表明MAC是补体介导的储存红细胞变化的主要促成因素。抑制末端补体途径可能会稳定红细胞功能并延长保质期。