Copyright ©ERS Journals Ltd 1998 European Respiratory Journal

Platelet-activating factor (PAF) [1] is a potent ether-linked phospholipid mediator of inflammation which is considered to have a potential role in the pathogenesis of bronchial asthma. Recently, we have shown that PAF (dos-age range 24–12 µg) disturbed pulmonary gas exchange in normal individuals [2–4] and in patients with mild asthma [5, 6] in an identical manner to the entire spectrum of ven-tilation-perfusion (V 'A/Q ') mismatching shown in patients with bronchial asthma [7, 8]. We suggested that the V 'A/Q ' defects could be preferentially related to an augmented bronchial vascular permeability due to post-capillary ven-oconstriction induced by PAF, thereby supporting the no-tion that PAF may play a key role, as a putative potent mediator of inflammation in human airways [5, 8]. How-ever, negative results have been obtained over the last few years, in stable patients with mild to moderate asthma with different PAF antagonists, and these question the role of PAF in the pathobiology of asthma. The compound SR 27417A (N-(2-dimethylaminoe-thyl)-N-(pyridinylmethyl)(4-(2,4,6 triisopropylphenyl) thia-zol-2-yl)) amine difumarate is a novel class of anti-PAF medication that has been shown to be a potent, long-last-ing and selective second generation PAF antagonist [9, 10]. The present study was undertaken to assess the effi-cacy of this new PAF receptor antagonist, SR 27471A, in attenuating or preventing the PAF-induced systemic, neu-tropenic, lung mechanical and pulmonary gas exchange effects observed in patients with mild asthma [5, 6]. To our knowledge, the efficacy of this class of anti-asthma compounds on pulmonary gas exchange abnormalities provoked by PAF has not been investigated previously