Neutropenia, inflammation, and the kinetics of transfused neutrophils in rabbits.
Neutropenia, inflammation, and the kinetics of transfused neutrophils in rabbits.
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兔子中性粒细胞减少症、炎症和输注中性粒细胞的动力学。
DOI：
10.1172/jci109496
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发表时间：
1979
期刊：
影响因子：
--
通讯作者：
D. Dale
中科院分区：
文献类型：
--
作者：
M. Rosenshein;T. Price;D. Dale
采用兔模型研究中性粒细胞减少和炎症对输注中性粒细胞血管内分布、存活和组织积累的影响。用[(3)H]胸腺嘧啶标记的供体血液输注到正常或中性粒细胞减少（长春碱处理）的动物体内。炎症是由皮下植入的聚氯乙烯海绵引起的，其中一些添加了内毒素。测量初始循环中性粒细胞池恢复、存活和标记中性粒细胞炎症部位积累。中性粒细胞减少与边际池大小的相对增加有关，表现为输血细胞的初始循环池（CNP）恢复减少。CNP恢复与受体中性粒细胞计数成正比。中性粒细胞减少对输注细胞的血管内存活没有影响，并伴有输注中性粒细胞炎症部位恢复的适度下降（10.4+/-5.4 vs.正常人14.4+/-4.0%）。皮下聚苯乙烯海绵的炎症形式伴随着边缘的增加，在植入后0和4小时的初始CNP回收率分别为24.3+/-4.7和27.6+/-8.8%（正常，38.2+/-9.9%）。炎症加速了CNP的转运，t（(1/2)）为2.02+/-0.72 h（正常，3.2+/-1.0 h）。向海绵中添加内毒素进一步扰乱了细胞动力学。内毒素海绵植入后的CNP回收率相当低，半衰期最初较短，随后无法解释。在内毒素海绵动物中，炎症部位的积累明显减少到注射中性粒细胞标记的7.4+/-1.9%，这表明许多输入的细胞在功能上不可用，而不是边缘。这些研究表明，中性粒细胞减少和有或没有内毒素的炎症显著改变输注中性粒细胞的动力学，输注细胞的CNP恢复不一定能预测其炎症部位的积累。
A rabbit model was used to study the effects of neutropenia and inflammation on the intravascular distribution, survival, and tissue accumulation of transfused neutrophils. Donor blood labeled with [(3)H]thymidine was infused into normal or neutropenic (vinblastine treated) animals. Inflammation was created by subcutaneous implantation of polyvinyl sponges, some with added endotoxin. Initial circulating neutrophil pool recovery, survival, and inflammatory site accumulation of labeled neutrophils were measured. Neutropenia was associated with a relative increase in the marginal pool size, manifested by a diminished initial circulating pool (CNP) recovery of transfused cells. The CNP recovery was directly proportional to recipient neutrophil count. Neutropenia had no effect on the intravascular survival of transfused cells and was accompanied by only a modest decrease in the inflammatory site recovery of the transfused neutrophils (10.4+/-5.4 vs. 14.4+/-4.0% in normals). Inflammation in the form of subcutaneous polyvinyl sponges was accompanied by an increase in margination with initial CNP recoveries of 24.3+/-4.7 and 27.6+/-8.8% at zero and 4 h after implantation respectively (normal, 38.2+/-9.9%). Transit through the CNP was hastened by inflammation with a t((1/2)) of 2.02+/-0.72 h (normal, 3.2+/-1.0 h). Addition of endotoxin to the sponges further perturbed cell kinetics. CNP recoveries were considerably lower and half-lifes were initially shorter and subsequently uninterpretable in studies done after endotoxin sponge insertion. Inflammatory site accumulation was markedly diminished to 7.4+/-1.9% of injected neutrophil label in the endotoxin sponge animals, suggesting that many of the transfused cells were functionally unavailable rather than marginated. These studies demonstrate that neutropenia and inflammation with or without endotoxin markedly alter the kinetics of transfused neutrophils and that CNP recovery of transfused cells is not necessarily predictive of their inflammatory site accumulation.