Fäldt R, Ankerst J, Zoucas E
Department of Internal Medicine, University of Lund, Sweden.
Br J Haematol. 1987 Aug;66(4):529-34. doi: 10.1111/j.1365-2141.1987.tb01339.x.
The effect of myeloid leukaemic cells, cells of the promyelocytic cell line HL-60 and normal polymorphonuclear granulocytes (PMN), enclosed in dialysis tubes, on the aggregation of allogeneic normal platelets after induction with arachidonic acid (AA) and with adenosine diphosphate (ADP) was investigated in vitro. Inhibition of aggregation was seen after preincubation of the platelets with leukaemic blood or bone marrow cells from 7/14 patients belonging to various FAB groups and with HL-60 cells, but not with normal PMN (14/14 cases). A dose-dependent inhibition was seen after lysis of some leukaemic cells with anti-human rabbit antiserum and active complement. Lysis of normal PMN inhibited platelet aggregation slightly and inconstantly and only at higher cell concentrations. Platelet inhibitory activity was not related to a higher rate of metabolism of the leukaemic cells which inhibited platelet aggregation since they did not differ from the cells not inhibiting aggregation with respect to heat production. Neither was a non-specifically increased cell membrane permeability the cause of the release of platelet inhibitory factor(s) since the release of 51Cr-labelled leukaemic cells was not related to the inhibition of platelet aggregation.
在体外研究了包封在透析管中的髓样白血病细胞、早幼粒细胞系HL-60细胞和正常多形核粒细胞（PMN）对花生四烯酸（AA）和二磷酸腺苷（ADP）诱导的同种异体正常血小板聚集的影响。在用来自7/14例属于不同FAB组的患者的白血病血液或骨髓细胞以及HL-60细胞预孵育血小板后，可见聚集受到抑制，但正常PMN（14/14例）预孵育后未出现抑制。在用抗人兔抗血清和活性补体裂解一些白血病细胞后，可见剂量依赖性抑制。正常PMN的裂解仅在较高细胞浓度时轻微且不稳定地抑制血小板聚集。血小板抑制活性与抑制血小板聚集的白血病细胞较高的代谢率无关，因为它们在产热方面与不抑制聚集的细胞没有差异。非特异性增加的细胞膜通透性也不是血小板抑制因子释放的原因，因为51Cr标记的白血病细胞的释放与血小板聚集的抑制无关。
