Oh S O, Ibe B O, Johnson C, Kurantsin-Mills J, Raj J U
Department of Pediatrics, University of California at Los Angeles School of Medicine, Torrance, USA.
J Lab Clin Med. 1997 Aug;130(2):191-6. doi: 10.1016/s0022-2143(97)90095-0.
The role of platelet-activating factor (PAF) in the pathogenesis of microvascular vaso-occlusion in sickle cell disease (SCD) is not known. In order to assess a role for PAF in vaso-occlusion in patients with SCD in steady state conditions, we measured plasma PAF level and plasma PAF acetylhydrolase activity as indices of PAF metabolism in vivo. We also studied PAF synthesis, from (3H)-acetate, by purified platelets stimulated with A23187. PAF was extracted from plasma of ten patients with SCD in steady state and from age-matched controls. PAF, purified by thin-layer chromatography, was quantitated by radioimmunoassay. PAF level (mean +/- SEM, pg/ml) in plasma of controls was 393 +/- 65, which was significantly lower than the 797 +/- 62 measured in plasma of patients with SCD. There was no difference in acetylhydrolase activity between the two groups. PAF synthesis (mean +/- SEM, nmol/10(6) cells) by platelets of controls without exogenous lyso-PAF was 1.69 +/- 0.24, higher than the 0.59 +/- 0.038 synthesized by platelets of patients with SCD. Incubation of platelets with 1.0 micromol/L lyso-PAF increased PAF synthesis by controls to 8.93 +/- 1.76, still higher than the 4.59 +/- 0.98 synthesized by platelets of patients with SCD. Our data show that patients with SCD are susceptible to a higher circulating levels of PAF in vivo during steady-state conditions. We speculate that higher levels of PAF may be a contributing factor to the persistent stress and inflammatory state of the microcirculation of patients with SCD.
血小板活化因子（PAF）在镰状细胞病（SCD）微血管血管阻塞发病机制中的作用尚不清楚。为了评估PAF在稳态条件下SCD患者血管阻塞中的作用，我们测量了血浆PAF水平和血浆PAF乙酰水解酶活性，作为体内PAF代谢的指标。我们还研究了用A23187刺激的纯化血小板从（3H）-乙酸盐合成PAF的情况。从10例稳态SCD患者和年龄匹配的对照者的血浆中提取PAF。通过薄层色谱法纯化的PAF，采用放射免疫分析法进行定量。对照组血浆中PAF水平（平均值±标准误，pg/ml）为393± 65，显著低于SCD患者血浆中测得的797±62。两组之间的乙酰水解酶活性没有差异。无外源性溶血PAF时，对照组血小板合成PAF（平均值±标准误，nmol/10(6)细胞）为1.69±0.24，高于SCD患者血小板合成的0.59±0.038。用1.0 μmol/L溶血PAF孵育血小板可使对照组PAF合成增加至8.93±1.76，仍高于SCD患者血小板合成的4.59±0.98。我们的数据表明，SCD患者在稳态条件下体内循环PAF水平较高。我们推测，较高水平的PAF可能是SCD患者微循环持续应激和炎症状态的一个促成因素。
