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To investigate whether salbutamol inhibits platelet-activating factor (PAF)-induced neutrophil sequestration in the lungs, we studied eight nonatopic, nonsmoking, healthy subjects (six men; aged 27.0 +/- 1.5 (SE) yr) with PAF-induced bronchial response. Prior to PAF challenge (24 micrograms), they inhaled either salbutamol (300 micrograms) or placebo in a randomized, double-blind, crossover manner two weeks apart. Respiratory system resistance (Rrs), arterial blood gases, and neutrophil counts were measured 4, 8, 12 and 30 min after PAF. Neutrophil kinetics in the lungs were assessed by tracking autologous 99mTc-erythrocytes and 111in-neutrophils. Compared with salbutamol, arterial blood neutrophil counts fell (p < 0.04) maximally at 4 min after PAF, followed by a mild rebound neutrophilia, whereas Rrs increased (p < 0.01) and Pao2 decreased (p < 0.05) at 4 min only. The intrapulmonary activity of 111in-neutrophils after pretreatment with placebo was higher compared with salbutamol (1.98 +/- 0.15 versus 1.33 +/- 0.23 cps/mCi/pixel) (p < 0.01) although both their initial sequestration (first-pass) and subsequent washout were not significantly different. Inhaled salbutamol blocks pulmonary neutrophil sequestration and lung function abnormalities following PAF challenge in humans.
Masclans et al. (Thu,) studied this question.
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