Schrier S L, Sohmer P R, Moore G L, Ma L, Junga I
Transfusion. 1982 Jul-Aug;22(4):261-5. doi: 10.1046/j.1537-2995.1982.22482251202.x.
Experiments with citrate-phosphate-dextrose supplemented with adenine, 0.5 mM final concentration (CPD-A2), provided an opportunity for study of red blood cells (RBC) membrane storage lesions which could limit extension of storage. Impairment in drug-induced endocytosis in intact RBC occurred with storage, but the changes produced did not quantitatively predict or reflect the 24-hour in vivo 51Cr-labelled RBC survival. Abnormalities in RBC membrane protein did appear after storage, but these alterations neither paralleled nor predicted the in vivo 24-hour 51Cr-labelled RBC survival. The RBC membrance protein changes were not reminiscent of those produced by either acute adenosine triphosphate depletion, oxidative attack, or calcium accumulation. Therefore, while storage produces significant alterations in RBC membrane protein and function, the changes detected were not those that determined in vivo RBC survival.
用添加了腺嘌呤(终浓度为0.5 mM)的枸橼酸盐-磷酸盐-葡萄糖(CPD-A2)进行的实验,为研究可能限制储存时间延长的红细胞(RBC)膜储存损伤提供了机会。完整红细胞中药物诱导的内吞作用在储存过程中会受损,但所产生的变化并不能定量预测或反映51Cr标记的红细胞在体内24小时的存活率。储存后红细胞膜蛋白确实出现了异常,但这些改变既不与体内24小时51Cr标记的红细胞存活率平行,也不能预测该存活率。红细胞膜蛋白的变化与急性三磷酸腺苷耗竭、氧化攻击或钙积累所产生的变化不同。因此,虽然储存会使红细胞膜蛋白和功能发生显著改变,但检测到的变化并非决定红细胞在体内存活率的因素。