Department of Physics and the Translational Science Center, Wake Forest University, Winston-Salem, North Carolina 27109, USA.
Transfusion. 2011 Apr;51(4):844-51. doi: 10.1111/j.1537-2995.2011.03100.x.
As stored blood ages intraerythrocytic energy sources are depleted resulting in reduced structural integrity of the membrane. Thus, stored red blood cells (RBCs) become less deformable and more fragile as they age. This fragility leads to release of cell-free hemoglobin (Hb) and formation of microparticles, submicron Hb-containing vesicles. Upon transfusion, it is likely that additional hemolysis and microparticle formation occurs due to breakdown of fragile RBCs. Release of cell-free Hb and microparticles leads to increased consumption of nitric oxide (NO), an important signaling molecule that modulates blood flow, and may promote inflammation. Stored blood may also be deficient in recently discovered blood NO synthase activity. We hypothesize that these factors play a potential role in the blood storage lesion.
随着储存血液的衰老，细胞内的能量来源被耗尽，导致膜的结构完整性降低。因此，储存的红细胞（RBC）随着年龄的增长变得更不易变形和更脆弱。这种脆弱性导致无细胞血红蛋白（Hb）的释放和形成微颗粒，亚微米级含 Hb 的囊泡。在输血过程中，由于脆弱的 RBC 破裂，可能会发生额外的溶血和微颗粒形成。无细胞 Hb 和微颗粒的释放导致一氧化氮（NO）的消耗增加，NO 是一种重要的信号分子，调节血流，并可能促进炎症。储存的血液可能也缺乏最近发现的血液一氧化氮合酶活性。我们假设这些因素在血液储存损伤中发挥潜在作用。
