Am. J. Respir. Crit. Care Med., Vol 151, No. 6, Jun 1995, 1740-1744.
Salbutamol inhibits pulmonary effects of platelet activating factor in man
J Roca, MA Felez, KF Chung, JA Barbera, M Rotger, C Santos and R Rodriguez-Roisin
Servei de Pneumologia i Al.lergia Respiratoria, Hospital Clinic, Barcelona, Spain.
Inhaled platelet-activating factor (PAF) provokes considerable pulmonary
gas exchange disturbances in normal man and in patients with mild asthma,
similar to those observed in acute severe asthma. To further examine the
mechanisms involved in PAF-induced ventilation- perfusion (VA/Q) mismatch,
eight healthy, non-atopic, nonsmoking subjects were studied after
administration of PAF aerosol (24 micrograms). They had been previously
treated with inhaled salbutamol (300 micrograms) in a randomized,
double-blind, cross-over, placebo- controlled design. After placebo, PAF
provoked a fall in total arterial white cell count with a rebound
leukocytosis. As shown in a previous study, an overall index of VA/Q
inequality (DISP R-E*, 1.64 +/- 0.10) showed a threefold increase (P <
0.006) that accounted for the increase (79%) in AaPO2 (p < 0.04) after
PAF, while the respiratory system resistance (Rrs) rose by 16% (p <
0.02). In contrast, after pretreatment with salbutamol inhaled PAF had no
effects on pulmonary gas exchange, Rrs, or white cell count; facial
flushing and cough were also hindered. The results are consistent with the
hypothesis that salbutamol inhibits PAF-induced venoconstriction in both
the airway and pulmonary microcirculation.