<![CDATA[Chronic obstructive pulmonary disease (COPD) is a preventable and treatable disease, characterized by airflow limitationthat is not fully reversible. The airflow limitation is usually progressive and associated with an abnormal inflammatory responseof the lung to noxious particle or gases. There is a chronic inflammation that leads to fixed narrowing of small airways andalveolar wall destruction (emphysema). This characterized by increased number of alveolar macrophages, neutrophils and cytotoxicT-lymphocytes, and the release of multiple inflammatory mediators. A high level of oxidative stress may amplify thisinflammation. There is also increased elastolysis and evidence for involvement of several elastolytic enzymes, including serineproteases, cathepsins and matrix metalloproteinasses. The Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelinesrecommend a stepwise approach to disease management, with bronchodilators being the mainstay of treatment. 2-Adrenergicagonists induce bronchodilatation through stimulation of 2-receptors, leading to an increase in cyclic adenosine monophosphate.In addition to prolonged bronchodilatation, long-acting 2-agonists (LABAs) exert other effects that may be of clinicalrelevance. These include inhibition of airway smooth-muscle cell proliferation and inflammatory mediator release, as well asnonsmooth-muscle effects, such as stimulation of mucociliary transport, cytoprotection of the respiratory mucosa, and attenuationof neutrophil recruitment and activation.]]>
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