The effects of salbutamol on neutrophil function

Background

Polymorphonuclear cell (PMN) activation, adhesion and transpulmonary emigration to the alveolar space are important steps in the pathogenesis of the acute respiratory distress syndrome (ARDS). β₂ agonists accelerate alveolar fluid clearance and have been suggested as a potential treatment for patients with ARDS. In addition, these agents have a variety of effects on polymorphonuclear cells (PMN). In animal models of sepsis, treatment with β₂ agonists has been shown to reduce pulmonary neutrophil sequestration and ameliorate the development of lung injury. The aim of this study was to investigate the effect of the β₂ agonist salbutamol on three aspects of PMN function: PMN activation (CD 64 expression), chemotaxis, and adhesion molecule expression (VLA-4).

Methods

PMNs from 10 healthy volunteers were separated using Ficoll-histopaque gradients and incubated with RPMI or salbutamol (10^-4 to 10^-10 M). PMN chemotaxis to FMLP (10^-6) was determined using the under agarose method. The effects of salbutamol (10^-5 M and 10^-9 M) on unstimulated PMN VLA-4 and CD 64 expression were determined using flow cytometry on whole blood.

Results

There was no effect on VLA-4 or CD 64 expression. However, salbutamol did reduce PMN chemotaxis (see Table 1).

Table 1

Conclusion

Salbutamol reduced PMN chemotaxis but had no effect on VLA-4 adhesion molecule expression or CD 64 expression (PMN activation). β₂ agonists may have beneficial effects beyond simply enhancing alveolar fluid clearance in patients with ARDS.