Platelet-activating factor impairs mucociliary transport and increases plasma leukotriene B4 in man.

We assessed the effect of inhaled platelet-activating factor (PAF) on tracheobronchial clearance, pulmonary function and blood pressure in seven healthy volunteers. After inhalation of 500 micrograms of PAF, retention of radioaerosol in ciliated airways measured at 4 h was 80% higher than in the control recording, and the clearance was reduced by 33% (p less than 0.005). Acetylsalicylic acid (ASA) did not abolish the phenomenon. PAF also decreased forced expiratory volume in one second (FEV1) by 16% (p less than 0.01), which was markedly attenuated by acetylsalicylic acid. The decrease in blood pressure after PAF (p less than 0.01) was not influenced by acetylsalicylic acid. Plasma leukotriene B4 (LTB4) was increased at 20 min after PAF inhalation (without and with ASA: mean 240 and 299 pg.ml.1, respectively) as compared to the baseline (144 and 166 pg.ml.1) and the values at 60 min after the challenge (133 and 178 pg.ml.1; p less than 0.05 and p less than 0.01, respectively). Only three out of seven subjects showed a bronchial hyperresponsiveness to methacholine measured 24 h after PAF. The PAF-induced reduction of mucociliary transport seems to be independent of cyclo-oxygenase products of arachidonic acid metabolism. These autacoids are, however, believed to contribute to the acute bronchial obstruction after PAF inhalation. In addition, inhaled PAF causes a transient increase in plasma LTB4.