Department of Surgery, University of Tennessee Health Science Center, 910 Madison Avenue, #224, Memphis, TN 38103, USA.
Transfusion. 2011 Apr;51(4):867-73. doi: 10.1111/j.1537-2995.2011.03098.x.
The specific negative clinical manifestations associated with the transfusion of stored red blood cells (RBCs) and the corresponding mechanisms responsible for such phenomena remain poorly defined. Our recent studies document that leukoreduced older RBC units potentiate transfusion-related toxicity in trauma patients. It is our hypothesis that the transfusion of relatively older blood impedes microvascular perfusion. The central mechanisms proposed to mediate this microcirculatory alteration include: 1) the loss of RBC-dependent control of nitric oxide-mediated homeostasis concerning vasodilation and 2) immune cell and complement activation. In this review, we outline the background for our hypothesis and detail our current investigations toward the understanding of this pathophysiology.
与输注储存的红细胞（RBC）相关的具体临床负面表现及其导致这些现象的相应机制仍未明确界定。我们最近的研究证明，去白细胞的较陈旧 RBC 单位会增强创伤患者的输血相关毒性。我们的假设是，输注相对陈旧的血液会阻碍微血管灌注。提出的介导这种微循环改变的中心机制包括：1）RBC 依赖性控制一氧化氮介导的血管舒张和 2）免疫细胞和补体激活的丧失。在这篇综述中，我们概述了我们假设的背景，并详细介绍了我们目前对理解这种病理生理学的研究。
