Louis R, Bury T, Corhay J L, Radermecker M
Department of Pneumology C.H.U., University of Liege, Sart-Tilman, Belgium.
Chest. 1993 Sep;104(3):806-10. doi: 10.1378/chest.104.3.806.
To investigate the possible role of mast cell or basophil histamine release in mediating platelet-activating factor (PAF) airway obstruction, we studied the effect of inhaled PAF (30 micrograms, single dose) on plasma histamine, bronchial caliber, and leukocyte and platelet counts in six patients with mild or moderate allergic asthma (mean age, 27 +/- 1.3 years; mean FEV1, 95 +/- 5 percent of predicted; mean PC20 methacholine, 1.46 +/- 0.36 mg/ml). Specific conductance (SGaw) FEV1, FEF25-75 percent, differential leukocyte and platelet counts, and plasma histamine (radioimmunoassay) were measured before and 5, 10, 15, and 20 min after PAF inhalation. Mean basal plasma histamine level was 0.28 +/- 0.04 ng/ml. Inhalation of PAF caused a fall in SGaw peaking at 5 min (43 +/- 9 percent) and a fall in FEV1 and FEF25-75 peaking at 10 min (19 +/- 10 percent and 30 +/- 13 percent, respectively). There was also a rapid and transient fall in circulating neutrophils at 5 min (from 3,096 +/- 204/mm3 to 2,551 +/- 158/mm3, p < 0.05) followed by a rebound neutrophilia. In contrast, plasma histamine level did not change significantly at any time measured. Conversely in the same asthmatics, a rapid rise in plasma histamine level (from 0.29 +/- 0.03 ng/ml at baseline to 0.53 +/- 0.06 ng/ml at 5 min; p < 0.01) was observed after an allergenic challenge (Dermatophagoides pteronyssinus) causing a fall in FEV1 peaking at 10 min (22 +/- 4 percent). Thus, inhaled PAF may induce airway obstruction and neutropenia in asthmatics without any significant change of plasma histamine level. These results indicate that it is unlikely that lung mast cells or basophils degranulate during PAF-induced bronchoconstriction.
为了研究肥大细胞或嗜碱性粒细胞组胺释放可能在介导血小板活化因子（PAF）气道阻塞中所起的作用，我们研究了吸入PAF（30微克，单剂量）对6例轻度或中度过敏性哮喘患者（平均年龄27±1.3岁；平均第一秒用力呼气容积[FEV1]为预测值的95±5%；平均乙酰甲胆碱激发试验浓度[PC20]为1.46±0.36毫克/毫升）血浆组胺、支气管管径、白细胞及血小板计数的影响。在吸入PAF前及吸入后5、10、15和20分钟测量比气道传导率（SGaw）、FEV1、用力呼气中期流速（FEF25 - 75%）、白细胞分类计数、血小板计数及血浆组胺（放射免疫测定法）。平均基础血浆组胺水平为0.28±0.04纳克/毫升。吸入PAF导致SGaw下降，在5分钟时达到峰值（43±9%），FEV1和FEF25 - 75%下降，在10分钟时达到峰值（分别为19±10%和30±13%）。循环中的中性粒细胞在5分钟时也迅速短暂下降（从3096±204/立方毫米降至2551±158/立方毫米，p<0.05），随后出现中性粒细胞增多。相比之下，在任何测量时间血浆组胺水平均无显著变化。相反，在同一组哮喘患者中，变应原激发试验（屋尘螨）后观察到血浆组胺水平迅速升高（从基线时的0.29±0.03纳克/毫升升至5分钟时的0.53±0.06纳克/毫升；p<0.01），同时FEV1下降，在10分钟时达到峰值（22±4%）。因此，吸入PAF可能在不引起血浆组胺水平显著变化的情况下诱发哮喘患者的气道阻塞和中性粒细胞减少。这些结果表明，在PAF诱导的支气管收缩过程中，肺肥大细胞或嗜碱性粒细胞不太可能发生脱颗粒。
